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1 | name | aliases | url | body_area | category | class | fda_status | evidence_strength | evidence_note | what_it_is | research_at_a_glance | key_takeaway | mechanism | human_study_findings | study_table_rows | study_rows_human | study_rows_animal_or_cell | dosing_info | side_effects_safety | num_citations | pmids | citation_urls | reviewed_by | last_updated | Taken from @MeesesRfriends on X | ||
2 | 5-Amino-1MQ | https://superpower.com/guides/peptides/5-amino-1mq | Digestive & weight | Wellness and performance | Small-molecule NNMT inhibitor | Marketed in the wellness and longevity space for metabolism and fat loss, but not FDA-approved for any use | Low research | Its evidence is limited to animal and cell studies of NNMT inhibition and fat loss, with no completed human trials. | Blocks an enzyme called NNMT; despite being sold alongside peptides, not technically a peptide | Almost all in animals, with no completed human trials | 5-Amino-1MQ is a small-molecule NNMT inhibitor that, in cell studies, increases NAD+ and SAM and suppresses fat production in fat cells. In diet-induced obese mice, a potent NNMT inhibitor reduced body weight and fat mass without changing food intake. As of 2026, no human trials have been published, and it is not a peptide. It is not approved by the FDA. | NNMT is an enzyme that becomes more active in fat tissue in obesity. In cell studies, inhibiting it increases NAD+ and SAM and suppresses fat production in fat cells. In diet-induced obese mice, a potent NNMT inhibitor reduced body weight and fat mass without changing how much the animals ate. These findings come from animal and cell studies, not from humans. | The research is almost entirely preclinical. The main evidence comes from animal and cell work, including these two studies: Study | Model | Finding Foundational NNMT-inhibitor study | Mice | First showed NNMT inhibitors reduce obesity 2022 study | Obese mice | NNMT inhibition combined with a low-fat diet reduced body weight and adiposity There are no completed randomized controlled human trials, so its effects and safety in people remain unknown. | 2 | 0 | 2 | What are the risks of using 5-Amino-1MQ? The human risk profile is unknown because no human safety studies have been conducted. Theoretical concerns include off-target effects of sustained SAM elevation on methylation biology and unknown drug interactions. Long-term effects , including any implications for cancer biology, given NNMT's roles in various cancers , have not been characterized. Gray-market products carry additional risks related to undetermined purity, dose accuracy, and contamination. | 9 | 29155147; 39161060; 39531138; 29992272; 35338115 | https://doi.org/10.1016/j.bcp.2017.11.007 ; https://doi.org/10.1038/s41598-021-03670-5 ; https://pubmed.ncbi.nlm.nih.gov/29155147/ ; https://pubmed.ncbi.nlm.nih.gov/39161060/ ; https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=213051 ; https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=215866 ; https://pubmed.ncbi.nlm.nih.gov/39531138/ ; https://pubmed.ncbi.nlm.nih.gov/29992272/ ; https://pubmed.ncbi.nlm.nih.gov/35338115/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
3 | Abaloparatide | https://superpower.com/guides/peptides/abaloparatide | Bones & muscles | FDA-approved | PTHrP analog | FDA-approved peptide injection | FDA approved | It is approved by the FDA for osteoporosis in postmenopausal women and men at high fracture risk, backed by the pivotal ACTIVE double-blind, placebo-controlled trial. | Performs better than teriparatide in placebo trials | Abaloparatide is a synthetic 34-amino acid analog of parathyroid hormone-related protein (PTHrP) that activates the PTH1 receptor to stimulate new bone formation. FDA-approved in 2017 as Tymlos, it is a daily injection for postmenopausal women and men with osteoporosis at high fracture risk, and it is capped at two years of use. In the pivotal ACTIVE trial, it cut the risk of new spine fractures by about 86% versus placebo. | Bone is constantly being torn down (resorption) and rebuilt (formation). Abaloparatide ramps up the build-up faster than the tear-down so that new bone is created quicker than old bone is removed. This creates what's called an anabolic window, the stretch where bone formation outpaces bone resorption. Abaloparatide also influences the calcium and phosphate balance in the body, both of which are minerals that contribute to bone health. In trials, abaloparatide reduced the risk of major fractures; in the spine, the relative risk reduction for new fractures was 86%, and in nonvertebral fractures it was 43%. In addition to reducing fractures, abaloparatide increases bone mineral density, which measures the amount of calcium and other minerals in your bones to determine the bones’ strength and fracture risk. In a large trial abbreviated ACTIVE, it had a statistically significant impact on the hip, lower spine, and femoral neck (the bone that connects the femur to the hip). In comparison to… | 0 | 0 | 0 | Tymlos lists the potential side effects as: - Dizziness - Nausea - Headache - Fast heartbeat - Fatigue - Vertigo - Redness, swelling, and/or bruising at injection site - Joint and/or bone pain - Abdominal bloating or pain - Diarrhea - Nausea Serious side effects can include: - Increased blood calcium (hypercalcemia) - Increased urine calcium (hypercalciuria), which may cause kidney stones | 8 | https://www.ncbi.nlm.nih.gov/books/NBK587447/ ; https://pmc.ncbi.nlm.nih.gov/articles/PMC6182596/ ; https://www.ncbi.nlm.nih.gov/books/NBK499863/ ; https://www.niams.nih.gov/health-topics/bone-mineral-density-tests-what-numbers-mean ; https://jamanetwork.com/journals/jama/fullarticle/2544640 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/208743Orig1s015lbl.pdf ; https://www.tymlos.com/?gad_source=1&gad_campaignid=21055082327&gbraid=0AAAAADNsb4qCJgnxNB5pTWCD3N2p3Zm6C&gclid=CjwKCAjw_KjVBhAHEiwAnC0N9Ap1pWaetNr-4XCLa4_tM5peCP-VQTDHPPoLXABXJH0HzzOqanVymRoCXVQQAvD_BwE ; http://sciencedirect.com/science/article/abs/pii/S0006295219302126 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
4 | Acetyl hexapeptide-8 | Argireline | https://superpower.com/guides/peptides/acetyl-hexapeptide-8 | Skin & aging | Cosmetic and topical | Neurotransmitter-inhibiting peptide | Cosmetic ingredient rather than a drug, so does not require FDA approval | Moderate research | It has human trial evidence, including a 2013 randomized, placebo-controlled study, but that evidence is limited, since the studies are small, often manufacturer-associated, and complicated by real questions about how well the peptide penetrates the skin. | Synthetic peptide used in anti-aging skincare, best known by the trade name Argireline | Acetyl hexapeptide-8, sold in skincare as Argireline, is a synthetic peptide modeled on the nerve protein SNAP-25 and marketed as a topical, "Botox-like" way to soften the appearance of expression lines. In lab and small clinical studies it interferes with the SNARE complex that nerves use to trigger muscle contraction, and a 2013 randomized study found it reduced the appearance of peri-orbital wrinkles over four weeks. It is a cosmetic ingredient rather than a drug, so it does not require FDA approval, and its evidence is rated Moderate. | Acetyl hexapeptide-8 softens the look of expression lines by reducing the small muscle contractions that create them. Nerves trigger those contractions by releasing a chemical signal, and that release depends on a group of proteins called the SNARE complex, of which SNAP-25 is a part. In laboratory studies, acetyl hexapeptide-8 mimics the end of SNAP-25 and competes with it, which interferes with SNARE complex formation and reduces the release of the signal that tells the muscle to contract. This is the same broad target as Botox, but acetyl hexapeptide-8 is applied topically and is far milder, not an injection that blocks the nerve. One important limit is delivery. Because it is a relatively large, water-loving peptide, how well it crosses the skin barrier to reach the nerves underneath is debated, and that penetration question is a major reason its effect is modest. | The main controlled evidence is a 2013 randomized, placebo-controlled study in 60 people, in which a topical argireline product reduced the appearance of peri-orbital wrinkles over four weeks compared with placebo. A 2025 review and other small studies report similar modest improvements, while noting that many studies are small or manufacturer-associated and that skin penetration is a genuine question. The research supports a modest cosmetic benefit, not a result like injectable Botox. | 0 | 0 | 0 | Topical acetyl hexapeptide-8 is generally well tolerated, and a cosmetic-industry safety review assessed it as safe as used in cosmetics. As with any skincare ingredient, some people can still experience: - Mild redness - Irritation - An allergic reaction For that reason, a patch test before regular use is sensible. Because the peptide is applied to the skin rather than injected, its safety considerations are those of a typical cosmetic ingredient. || Is argireline safe to use? Across published studies, argireline has shown a low-irritation profile. Early testing found no primary irritation at high doses, and no allergic reactions were reported in a 26-patient case series or a small 2023 double-blind study. The CIR Expert Panel formally assessed acetyl hexapeptide-8 amide as safe for cosm… | 17 | 23417317; 38024099; 29371611; 24754410; 40673537; 18498523; 33482052; 33151254; 35950860; 18492182; 25497319 | https://doi.org/10.1007/s40257-013-0009-9 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC12193160/ ; https://www.fda.gov/cosmetics/cosmetics-laws-regulations/fda-authority-over-cosmetics-how-cosmetics-are-not-fda-approved-are-fda-regulated ; https://www.fda.gov/cosmetics/cosmetics-laws-regulations/it-cosmetic-drug-or-both-or-it-soap ; https://www.cir-safety.org/sites/default/files/acetyl122020revTR.pdf ; https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=485d9b71-6881-42c5-a620-a4360c7192ab ; https://pubmed.ncbi.nlm.nih.gov/23417317/ ; https://pubmed.ncbi.nlm.nih.gov/38024099/ ; https://pubmed.ncbi.nlm.nih.gov/29371611/ ; https://pubmed.ncbi.nlm.nih.gov/24754410/ ; https://pubmed.ncbi.nlm.nih.gov/40673537/ ; https://pubmed.ncbi.nlm.nih.gov/18498523/ ; https://pubmed.ncbi.nlm.nih.gov/33482052/ ; https://pubmed.ncbi.nlm.nih.gov/33151254/ ; https://pubmed.ncbi.nlm.nih.gov/35950860/ ; https://pubmed.ncbi.nlm.nih.gov/18492182/ ; https://pubmed.ncbi.nlm.nih.gov/25497319/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
5 | Acetyl octapeptide-3 | SNAP-8 | https://superpower.com/guides/peptides/acetyl-octapeptide-3 | Skin & aging | Cosmetic and topical | Neurotransmitter-inhibiting peptide | Cosmetic ingredient rather than a drug, so does not require FDA approval | Low research | Its human evidence is limited mainly to manufacturer testing, with no independent, peer-reviewed clinical trial, so the cosmetic benefit is largely unverified despite a plausible mechanism shared with Argireline. | Synthetic peptide used in anti-aging skincare, best known by the trade name SNAP-8 | Acetyl octapeptide-3, sold in skincare as SNAP-8, is a synthetic eight-amino acid peptide modeled on the nerve protein SNAP-25 and marketed as a stronger successor to Argireline for softening the appearance of expression lines. Like Argireline, it is designed to interfere with the SNARE complex that nerves use to trigger muscle contraction, but its own published human evidence is thin and comes mostly from the manufacturer. It is a cosmetic ingredient rather than a drug, so it does not require FDA approval, and its evidence is rated Low. | Acetyl octapeptide-3 softens the look of expression lines by reducing the small muscle contractions that create them. Nerves trigger those contractions by releasing a chemical signal, and that release depends on a group of proteins called the SNARE complex, of which SNAP-25 is a part. In laboratory studies, peptides in this family mimic the end of SNAP-25 and compete with it, which interferes with SNARE complex formation and reduces the release of the signal that tells the muscle to contract. It is marketed as more potent than Argireline, though it is still a topical, far milder approach than an injection like Botox. As with other topical peptides, a major limit is delivery. How well a large, water-loving peptide crosses the skin barrier to reach the nerves underneath is uncertain, and that caps how strong the effect can be. Acetyl octapeptide-3 and acetyl hexapeptide-8 (Argireline) are close relatives, and the main practical difference between them is the strength of their published … | The published human evidence for acetyl octapeptide-3 is thin. Most of the efficacy data comes from the ingredient's manufacturer, which reports reductions in the depth of wrinkles, rather than from independent, peer-reviewed clinical trials. Its close relative Argireline has a published randomized trial, but acetyl octapeptide-3 has not been tested to the same standard, so its benefit rests largely on manufacturer testing and its shared mechanism rather than strong independent evidence. | 0 | 0 | 0 | Topical acetyl octapeptide-3 is generally considered well tolerated, with the low potential for irritation typical of cosmetic peptides. As with any skincare ingredient, some people can still experience mild redness, irritation, or an allergic reaction, so a patch test before regular use is sensible. Because the peptide is applied to the skin rather than injected, its safety considerations are those of a typical cosmetic ingredient. | 4 | https://doi.org/10.1007/s40257-013-0009-9 ; https://www.fda.gov/cosmetics/cosmetics-laws-regulations/fda-authority-over-cosmetics-how-cosmetics-are-not-fda-approved-are-fda-regulated ; https://www.fda.gov/cosmetics/cosmetics-laws-regulations/it-cosmetic-drug-or-both-or-it-soap ; https://doi.org/10.1111/jocd.12314 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
6 | Acetyl tetrapeptide-5 | Eyeseryl | https://superpower.com/guides/peptides/acetyl-tetrapeptide-5 | Skin & aging | Cosmetic and topical | Signal peptide | Cosmetic ingredient rather than a drug, so does not require FDA approval | Low research | Its human evidence is limited mainly to manufacturer panel studies, with no independent, peer-reviewed clinical trial, so the cosmetic benefit is largely unverified despite a plausible anti-edema mechanism. | Synthetic peptide used in anti-aging and eye-care skincare, best known by the trade name Eyeseryl | Acetyl tetrapeptide-5, sold in skincare as Eyeseryl, is a synthetic four-amino acid peptide used in eye creams to soften the look of under-eye bags and puffiness. It is thought to work in two ways, by easing the fluid buildup that makes the under-eye area look swollen and by limiting the glycation that stiffens collagen, though its published evidence comes almost entirely from the manufacturer. It is a cosmetic ingredient rather than a drug, so it does not require FDA approval, and its evidence is rated Low. | Acetyl tetrapeptide-5 is thought to reduce the appearance of under-eye bags through two proposed actions: - An anti-edema effect. Puffiness under the eyes is partly caused by fluid pooling in the tissue, and in the manufacturer's testing the peptide reduced that fluid buildup, in part by lowering the leakiness of small blood vessels, their vascular permeability, so that less fluid escapes into the surrounding skin. - An effect on glycation, the process in which sugars bind to and stiffen collagen. By limiting glycation, the peptide is proposed to help the thin skin under the eyes stay more elastic and less prone to the slackening that deepens the look of bags. Both of these are findings from laboratory and manufacturer studies rather than independent clinical research. As with any topical peptide, how much of it actually crosses the skin barrier to reach the tissue underneath is uncertain, and that places a ceiling on how strong the effect can be. | The published evidence for acetyl tetrapeptide-5 is thin and comes mostly from its manufacturer. Lipotec's own panel studies report a visible reduction in the appearance of under-eye bags and puffiness in volunteers who used a formulation containing the peptide, but those results have not been reproduced in independent, peer-reviewed clinical trials. So while the proposed mechanism is reasonable and the manufacturer data is encouraging, the cosmetic benefit rests largely on the company's own testing rather than on strong outside evidence. | 0 | 0 | 0 | Topical acetyl tetrapeptide-5 is generally considered well tolerated, with the low potential for irritation typical of cosmetic peptides, and it is used on the especially delicate skin around the eyes. As with any skincare ingredient, some people can still experience mild redness, stinging, or an allergic reaction, so patch testing before regular use and keeping the product out of the eyes themselves is sensible. | 4 | https://www.lubrizol.com/Personal-Care/Products/Product-Finder/Products-Data/Eyeseryl-peptide-solution-G ; https://incidecoder.com/ingredients/acetyl-tetrapeptide-5 ; https://www.fda.gov/cosmetics/cosmetics-laws-regulations/fda-authority-over-cosmetics-how-cosmetics-are-not-fda-approved-are-fda-regulated ; https://www.fda.gov/cosmetics/cosmetics-laws-regulations/it-cosmetic-drug-or-both-or-it-soap | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
7 | Afamelanotide | https://superpower.com/guides/peptides/afamelanotide | Skin & aging | FDA-approved | MC1R agonist | FDA-approved peptide, sold as Scenesse, given as a subcutaneous implant | FDA approved | It is approved by the FDA for erythropoietic protoporphyria, backed by two multicenter, randomized, double-blind, placebo-controlled trials showing increased pain-free light exposure. | Afamelanotide is a synthetic, longer-lasting analog of alpha-melanocyte-stimulating hormone (α-MSH) that activates the MC1R receptor on pigment cells to boost the skin's own protective eumelanin. The FDA approved it in 2019 as Scenesse, a subcutaneous implant for adults with erythropoietic protoporphyria (EPP), a rare light-sensitivity disorder. In the pivotal 2015 placebo-controlled trials, U.S. patients (94) logged a median 69.4 pain-free hours in direct sunlight versus 40.8 on placebo (P = 0.04). EU patients (74) logged 6.0 versus 0.8 hours (P = 0.005). | Afamelanotide works by switching on the skin's own pigment system to build a protective layer of melanin. It is a potent agonist of the melanocortin-1 receptor, or MC1-R, which sits on melanocytes, the pigment-producing cells of the skin. Activating MC1R drives those cells to make more eumelanin, the dark form of melanin that acts as the body's natural sunscreen, absorbing and scattering light and neutralizing the reactive oxygen species that light can generate in the skin. Because the drug triggers this through the receptor rather than through sun exposure, it raises eumelanin without requiring the UV damage that normally produces a tan. In erythropoietic protoporphyria, that extra pigment matters for a specific reason. People with EPP build up a molecule called protoporphyrin IX, which reacts with visible light to produce bursts of reactive oxygen that damage tissue and cause severe burning pain after even brief light exposure. By increasing eumelanin, afamelanotide reduces how much… | 3 | 3 | 0 | According to the prescribing information, the most common side effects are: - Implant-site reactions - Nausea - Throat pain and cough - Fatigue - Skin hyperpigmentation and darkening of existing moles - Dizziness or drowsiness - Respiratory tract infection - Skin irritation The label also warns that serious hypersensitivity reactions, including anaphylaxis, have been reported with postmarket use. Because afamelanotide increases skin pigmentation, the label calls for regular full-body skin exams so that moles and any suspicious lesions can be monitored over time. | 9 | 26132941; 32186677; 36041558 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/210797s000lbl.pdf ; https://www.mcgill.ca/oss/article/medical-critical-thinking-student-contributors-pseudoscience/barbie-drug-your-dermatologist-has-never-heard ; https://www.ema.europa.eu/en/medicines/human/EPAR/scenesse ; https://www.biospace.com/fda-approves-first-treatment-to-increase-pain-free-light-exposure-in-patients-with-a-rare-disorder ; https://pubmed.ncbi.nlm.nih.gov/26132941/ ; https://pubmed.ncbi.nlm.nih.gov/32186677/ ; https://pubmed.ncbi.nlm.nih.gov/36041558/ ; https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=94f53286-11dd-7fbb-e053-2a95a90a7c48 ; https://doi.org/10.1056/NEJMoa1411481 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
8 | Albiglutide | https://superpower.com/guides/peptides/albiglutide | Hormones & metabolism | FDA-approved | GLP-1 receptor agonist | FDA-approved GLP-1 peptide, formerly sold as Tanzeum for type 2 diabetes | FDA approved | it is approved by the FDA for type 2 diabetes, supported by the HARMONY trial program including the HARMONY OUTCOMES cardiovascular trial, although the manufacturer no longer markets it. | Albiglutide is a once-weekly GLP-1 receptor agonist made by fusing GLP-1 analog chains to human albumin, approved for type 2 diabetes in 2014 as Tanzeum. It had a somewhat weaker effect on gastric emptying and appetite than some other GLP-1 drugs but showed a cardiovascular benefit in the HARMONY OUTCOMES trial. Despite that, GSK withdrew it from the market in 2018 for commercial reasons, so it remains FDA-approved but is no longer available. | Albiglutide lowers blood sugar by activating the GLP-1 receptor, mimicking a gut hormone the body releases after eating. Through that receptor it: - Drives glucose-dependent insulin release, which keeps the risk of hypoglycemia low on its own - Lowers glucagon - Slows the rate at which the stomach empties, though it has a somewhat weaker effect on gastric emptying and appetite than some other GLP-1 drugs Fusing the peptide to albumin is what gave it a long half-life and once-weekly dosing. In the HARMONY OUTCOMES trial, albiglutide reduced major cardiovascular events in people with type 2 diabetes and established heart disease. | 0 | 0 | 0 | The most common side effects were: - Diarrhea - Nausea - Injection-site reactions - Upper respiratory infection Less common but more serious risks included: - Thyroid C-cell tumors: albiglutide carried a boxed warning based on rodent studies. It is not known whether this happens in humans. - Pancreatitis, or inflammation of the pancreas - Severe allergic reactions, including anaphylaxis - Low blood sugar, especially when combined with insulin or a sulfonylurea - Acute kidney injury, usually from dehydration caused by vomiting or diarrhea | 3 | https://pmc.ncbi.nlm.nih.gov/articles/PMC4665069/ ; https://doi.org/10.1016/S0140-6736(18)32261-X ; https://www.drugs.com/tanzeum.html | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||||
9 | Amycretin | https://superpower.com/guides/peptides/amycretin | Digestive & weight | In clinical trials | Amylin + GLP-1 co-agonist | Investigational peptide, not approved by the FDA or any regulator | Moderate research | It has shown dose-dependent weight loss, but only in small, short, early-phase trials with high dropout, and no Phase 3 efficacy data exist. | GLP-1 and amylin receptor co-agonist, studied as both an injection and a tablet | Human evidence from early-phase (Phase 1/2a) trials in overweight and obesity | Amycretin is an investigational single-molecule drug that activates both the GLP-1 receptor and the amylin receptor, being developed by Novo Nordisk in subcutaneous and oral forms for weight management. In a 2025 phase 1b/2a trial of 125 adults with overweight or obesity, the 60 mg group lost 24.3% of body weight at 36 weeks versus 1.1% on placebo (p < 0.0001), though many participants withdrew. As of 2026 it is not approved anywhere and is moving into Phase 3 testing. | Amycretin combines two appetite-signaling actions in one molecule. The first is activation of the GLP-1 receptor, the same incretin target as drugs like semaglutide. Switching it on: - Raises insulin release when blood sugar is high - Slows how fast the stomach empties - Reduces appetite The second is activation of the amylin receptor, which responds to amylin, a pancreatic hormone that promotes a feeling of fullness. Each pathway curbs eating on its own, and the reason for building both into a single drug is that the two fullness signals may add together to reduce food intake more than either does alone. This is the proposed mechanism; whether it produces lasting benefit is what clinical trials are meant to establish. | The human data so far come from early-phase trials. According to PubMed, the two published trials reported the following: Trial | Duration | Findings Phase 1b/2a trial of the subcutaneous form in 125 adults with overweight or obesity | Up to 36 weeks | Dose-dependent weight reductions; weight fell 24.3% on 60 mg versus 1.1% on placebo at 36 weeks (p < 0.0001); mostly mild to moderate gastrointestinal side effects but a notably high rate of withdrawal and discontinuation First-in-human trial of the oral form | 12 weeks | Focused mainly on safety and drug levels, with exploratory weight-change signals These are small, short studies; no Phase 3 efficacy data are available yet, so amycretin's longer-term effect and tolerability remain unproven. | 2 | 2 | 0 | 3% on 60 mg versus 1. | 5 | https://doi.org/10.1016/S0140-6736(26)01247-X ; https://www.ncbi.nlm.nih.gov/books/NBK551568/ ; https://doi.org/10.1016/S0140-6736(25)01185-7 ; https://clinicaltrials.gov/study/NCT07339423 ; https://doi.org/10.1016/S0140-6736(25)01176-6 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
10 | Angiotensin II | https://superpower.com/guides/peptides/angiotensin-ii | Heart & blood | FDA-approved | Vasopressor peptide | FDA-approved peptide, sold as Giapreza, given as an intravenous infusion in intensive care | FDA approved | It is approved by the FDA for septic or other distributive shock, supported by the randomized, double-blind, placebo-controlled ATHOS-3 trial. | Angiotensin II is a natural peptide hormone and the main active signal of the renin-angiotensin system, which the body uses to raise blood pressure by tightening blood vessels. A synthetic version is FDA-approved as Giapreza, an intravenous drug given in intensive care to raise dangerously low blood pressure in adults with septic or other distributive shock. In its pivotal ATHOS-3 trial it raised blood pressure in about 70% of patients compared with 23% on placebo, though it also carries a risk of blood clots. | Angiotensin II raises blood pressure by binding to receptors on the muscle lining the blood vessels and making them tighten. It acts mainly through the AT1 receptor on vascular smooth muscle, and activating it constricts the vessels, which raises blood pressure quickly. This is the final active step of the renin-angiotensin system: the kidney releases renin, which starts a chain that produces angiotensin I, and an enzyme called ACE converts that into angiotensin II, the potent form. Beyond directly tightening vessels, angiotensin II signals the adrenal glands to release aldosterone, a hormone that makes the body hold on to sodium and water, and it promotes the release of vasopressin, another blood-pressure hormone. In shock, this matters because it gives clinicians a way to raise blood pressure through a pathway separate from the standard catecholamine drugs such as norepinephrine, which helps when those drugs alone are not enough. In the pivotal ATHOS-3 trial of patients with vasodil… | 0 | 0 | 0 | The most important safety concern is a risk of blood clots. In its trial, angiotensin II was associated with thrombotic events, including deep vein thrombosis, and the label recommends giving clot-prevention treatment (venous thromboembolism prophylaxis) while a patient is receiving it. According to the prescribing information, other reported effects included: - Low platelet counts - A fast heart rate - Fungal infection - Delirium - Acidosis - High blood sugar - Reduced blood flow to the hands and feet Because it is used only in intensive care, patients receiving it are already under close monitoring. | 5 | 11751697 | https://www.ncbi.nlm.nih.gov/books/NBK470410/ ; https://www.giapreza.com/ ; https://pubmed.ncbi.nlm.nih.gov/11751697/ ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/209360s000lbl.pdf ; https://doi.org/10.1056/NEJMoa1704154 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
11 | AOD-9604 | https://superpower.com/guides/peptides/aod-9604 | Digestive & weight | Wellness and performance | GH fragment (lipolytic) | Non-FDA-approved peptide | Low research | Its human obesity trials failed to beat placebo and development was halted, so there is no sound human evidence that it works for fat loss, despite more human testing than most peptides in this category. | Modified fragment of the growth hormone molecule, studied for fat loss | Human obesity trials did not beat placebo, and development was discontinued | AOD-9604 is a modified fragment of the tail end of human growth hormone, developed as a fat-loss drug. Its human obesity trials failed to beat placebo, and development for obesity was halted. As of 2026 it is not FDA-approved and is banned in sport. | The proposed idea is that the tail region of growth hormone carries its fat-burning activity without the rest of the hormone's effects. In animal and cell studies, AOD-9604 increased both fat breakdown and fat oxidation while it reduced fat storage, reportedly without activating the growth hormone receptor or causing growth or insulin-resistance effects. In rodents, it also raised markers of fat metabolism (here and here). These are animal and laboratory findings; the human trials below tested whether they translate. | Unusually for a wellness peptide, AOD-9604 was tested in real human trials, and they were negative. A 24-week Phase 2b obesity trial of 536 participants did not produce significant weight loss versus placebo, and development for obesity was terminated in 2007; an earlier, smaller signal did not replicate. The supporting mechanism data remain animal and cell-based. So the best human evidence does not support the marketed fat-loss use; it argues against it. | 0 | 0 | 0 | 11 | 23092275; 25208511; 24124033; 18057338 | https://doi.org/10.1159/000053183 ; https://doi.org/10.1038/sj.ijo.0801740 ; https://pubmed.ncbi.nlm.nih.gov/23092275/ ; https://pubmed.ncbi.nlm.nih.gov/25208511/ ; https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1058e17c-9261-459c-a3e6-fae38d196c14 ; https://pubmed.ncbi.nlm.nih.gov/24124033/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://www.wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf ; https://www.fda.gov/media/174456/download ; https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=022505 ; https://pubmed.ncbi.nlm.nih.gov/18057338/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
12 | Apraglutide | https://superpower.com/guides/peptides/apraglutide | Digestive & weight | In clinical trials | GLP-2 analog | Investigational peptide, not approved by the FDA | Moderate research | It has one adequately powered, positive Phase 3 trial supported by Phase 2 data, but the result is from a single unreplicated trial, and the FDA has required a confirmatory trial. | Long-acting GLP-2 analog given as a once-weekly injection for short bowel syndrome | Apraglutide is an investigational long-acting GLP-2 analog, developed by Ironwood Pharmaceuticals as a once-weekly injection for short bowel syndrome, a condition in which people depend on intravenous nutrition because their intestine cannot absorb enough. In a Phase 3 trial it reduced the need for that intravenous support compared with placebo. As of 2026 it is not approved, and the FDA has asked for an additional confirmatory trial. | Apraglutide activates the GLP-2 receptor in the gut. GLP-2 signaling has these effects: - Promotes growth and adaptation of the intestinal lining - Slows how fast the stomach empties and food transits - Increases absorption of fluid and nutrients In short bowel syndrome, the goal is to help the remaining intestine absorb more so that patients can reduce their dependence on intravenous feeding. This describes the mechanism, separate from the trial outcomes below. | The main evidence is one Phase 3 trial, with a supporting Phase 2 study. According to PubMed, the two studies found: Study | Phase and population | Result STARS trial | Phase 3, adults with short bowel syndrome | Met its primary endpoint, with a greater reduction in weekly intravenous support volume on apraglutide than placebo, and more participants achieving at least 1 day per week off intravenous support Supporting study | Phase 2 | Reported improved absorption and reduced parenteral support over a year The evidence is from a single pivotal trial that has not been replicated, and the FDA has asked for a confirmatory study. | 2 | 2 | 0 | 2 | https://doi.org/10.1016/j.cgh.2026.08.026 ; https://doi.org/10.1016/j.clnu.2024.10.011 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
13 | Aviptadil | https://superpower.com/guides/peptides/aviptadil | Immune & defense | In clinical trials | Vasoactive intestinal peptide | Investigational drug, not approved by the FDA for any use; studied mainly for severe respiratory failure in COVID-19 | Low research | Although it has been tested in randomized controlled human trials, the results do not support a benefit. Since the largest independent trial found no significant improvement and was stopped for futility, there is no sound human evidence that it works for its studied uses. | Synthetic version of vasoactive intestinal peptide (VIP), also known by the development code RLF-100 and the name Zyesami | Mixed human evidence: the largest independent randomized trial found no significant benefit and was halted early for futility | Aviptadil is a synthetic form of vasoactive intestinal peptide (VIP), a signaling molecule that acts on lung receptors, and it has been studied mainly for severe COVID-19 respiratory failure. In the NIH-funded TESICO trial of 461 patients, aviptadil did not beat placebo on the 90-day recovery scale (odds ratio 1.11, 95% CI 0.80 to 1.55, p = 0.54). Ninety-day mortality was 38% with aviptadil versus 36% with placebo (p = 0.78), and the trial stopped early for futility. As of 2026 it is not FDA-approved for any use. | Aviptadil works by mimicking vasoactive intestinal peptide, the natural signaling molecule the body uses to relax blood vessels and calm inflammation, particularly in the lungs. VIP binds to two receptors, VPAC1 and VPAC2, that are common on lung tissue, and activating them relaxes the smooth muscle in blood vessels and airways and triggers signals that lower inflammation. Those receptors are not limited to the lungs. VPAC1 and VPAC2 sit on T cells and macrophages, and VPAC1 receptors couple to adenylyl cyclase, the enzyme that makes the signaling molecule cAMP. A 2013 review of VIP's immune effects describes work in mice, where VIP: - Inhibited TNF, IL-6, and IL-12 and raised IL-10 - Blocked NF-κB movement into the nucleus - Induced Foxp3-positive regulatory T cells through tolerogenic dendritic cells These are animal findings, and they do not show the same effects in patients. Much of the therapeutic rationale centers on a specific lung cell. In laboratory studies, VIP helps protect… | The strongest research shows that aviptadil has not been proven to work for the condition it was most studied in. It was tested primarily in critically ill COVID-19 patients with acute hypoxemic respiratory failure. The companies developing it reported favorable early findings from a company-sponsored phase 2b/3 study in 2021, but the pivotal independent test was the NIH-funded TESICO trial, a randomized, placebo-controlled study of 461 patients. According to PubMed, that trial found that aviptadil did not significantly improve a patient's clinical status at 90 days, showed no reduction in mortality, and was stopped early for futility on the recommendation of its independent safety monitoring board. TESICO's two headline results, up to day 90, were: Outcome | Aviptadil vs placebo | Significance Better category on the primary 90-day recovery scale | Odds ratio 1.11 (95% CI 0.80 to 1.55) | p = 0.54 Death up to day 90 | 38% of patients on aviptadil died versus 36% on placebo (hazard ratio 1.04) | p = 0.78 In short, the human evidence is real but conflicting, and the best-designed independent study did not confirm a benefit. Outside the respiratory-failure setting, published human evidence is limited. Aviptadil is best understood as an investigational compound whose effectiveness for its studied uses has not been established. | 0 | 0 | 0 | 11 | 5450698; 12409234; 21951273; 22139413 | https://pubmed.ncbi.nlm.nih.gov/5450698/ ; https://pmc.ncbi.nlm.nih.gov/articles/PMC10527239/ ; https://pmc.ncbi.nlm.nih.gov/articles/PMC8630992 ; https://pubmed.ncbi.nlm.nih.gov/12409234/ ; https://pubmed.ncbi.nlm.nih.gov/21951273/ ; https://pubmed.ncbi.nlm.nih.gov/22139413/ ; https://thepharmaletter.com/pharmaceutical/fda-declines-eua-for-aviptadil-for-patients-with-critical-covid-19-at-immediate-risk ; https://www.globenewswire.com/news-release/2020/06/24/2052448/0/en/NeuroRx-and-Relief-Therapeutics-Announce-Fast-Track-Designation-Granted-by-the-FDA-to-RLF-100-Aviptadil-for-the-Treatment-of-Respiratory-Distress-in-COVID-19.html ; https://www.sec.gov/Archives/edgar/data/1719406/000155837022008948/nrxp-20220331x10q.htm ; https://awttc.nhs.wales/files/appraisals-asar-far/final-recommendation-aviptadil-phentolamine-invicorp-3435/ ; https://doi.org/10.1016/S2213-2600(23)00147-9 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
14 | Bacitracin | https://superpower.com/guides/peptides/bacitracin | Skin & aging | FDA-approved | Polypeptide antibiotic | FDA-approved polypeptide antibiotic, sold over the counter as a topical ointment for minor wounds | FDA approved | It is approved by the FDA as a topical antibiotic for preventing infection in minor skin wounds and is sold over the counter, with decades of clinical use behind it. | Bacitracin is a cyclic polypeptide antibiotic produced by Bacillus bacteria that kills gram-positive bacteria by blocking the construction of their cell wall. It is best known as an over-the-counter topical ointment for preventing infection in minor cuts, scrapes, and burns, often combined with neomycin and polymyxin B in "triple antibiotic" products. It is widely available over the counter, but it is also a common cause of allergic skin reactions, and its injectable form was withdrawn over kidney-toxicity concerns. | Bacitracin kills bacteria by blocking the construction of their cell wall. It interferes with a recycling step in wall-building: A lipid carrier molecule (C55 or undecaprenyl pyrophosphate) ferries the building blocks of the wall across the bacterial membrane, and it must shed a phosphate to be reused. Bacitracin binds that carrier and prevents its dephosphorylation, so the carrier is pulled out of circulation and new cell-wall material can no longer be delivered. Because this target matters most in gram-positive bacteria, bacitracin's activity is strongest against organisms such as staphylococci and streptococci. It is poorly absorbed through the skin, which is part of why it works well as a surface antibiotic but is not used orally for body-wide infection. | 0 | 0 | 0 | The most notable side effect of bacitracin is allergy. Its main risks are: - Allergic contact dermatitis: it is a well-recognized cause of this itchy, red, sometimes blistering rash where it is applied, and in 2003, the American Contact Dermatitis Society named it "Allergen of the Year." - Anaphylaxis: more rarely, topical bacitracin has triggered anaphylaxis, a severe whole-body allergic reaction, which is unusual for an over-the-counter ointment. - Kidney damage: when given by injection, bacitracin can cause serious kidney damage, which is why that form was taken off the U.S. market. Applied topically to small areas, it is generally well tolerated apart from the allergy risk. | 5 | 8805732 | https://go.drugbank.com/drugs/DB00626 ; https://www.statpearls.com/point-of-care/18087 ; https://reference.medscape.com/drug/baciguent-bacitracin-topical-343464 ; https://pubmed.ncbi.nlm.nih.gov/8805732/ ; https://www.pharmacytimes.com/view/bacitracin-and-boo-boos-becoming-a-no-no | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
15 | Balixafortide | https://superpower.com/guides/peptides/balixafortide | Heart & blood | In clinical trials | CXCR4 antagonist peptide | Investigational peptide, not approved by the FDA | Low research | A randomized Phase 3 trial failed to show benefit over standard chemotherapy, which outweighs the earlier uncontrolled Phase 1 signal. | CXCR4 antagonist studied with the chemotherapy eribulin in metastatic breast cancer | A Phase 1 trial suggested activity, but the Phase 3 trial (FORTRESS) failed to show benefit | Balixafortide is an investigational peptide that blocks the CXCR4 receptor, studied by Polyphor in combination with chemotherapy for metastatic breast cancer. An early single-arm trial suggested activity, but the pivotal Phase 3 trial did not show a benefit over chemotherapy alone, and development has effectively stopped. As of 2026 it is not approved. | Balixafortide blocks the CXCR4 receptor and interrupts its signaling with a partner molecule called CXCL12 (SDF-1α). This pathway influences the trafficking of tumor cells, the tumor's surrounding environment, and immune cell behavior. In laboratory work, blocking CXCR4 was proposed to make tumors more responsive to chemotherapy, which is the rationale for combining it with eribulin. This describes the proposed mechanism, separate from the patient outcomes below. | The decisive evidence is negative. Two trials tested balixafortide plus eribulin in metastatic breast cancer: Trial | Design | Result Phase 1 trial, according to PubMed | Early single-arm study in heavily pretreated metastatic breast cancer | Partial responses in about 30% of evaluable patients, encouraging for an uncontrolled study Phase 3 FORTRESS trial, reported by the company in 2021 | Randomized, compared with eribulin alone | Did not meet its primary endpoint; response and clinical-benefit rates were similar to eribulin alone, showing no meaningful improvement from adding balixafortide The controlled evidence does not support a benefit. | 2 | 2 | 0 | 2 | https://doi.org/10.1016/S1470-2045(18)30147-5 ; https://www.clinicaltrialsarena.com/news/polyphor-balixafortide-fails-breast-cancer-study/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
16 | Bivalirudin | https://superpower.com/guides/peptides/bivalirudin | Heart & blood | FDA-approved | Direct thrombin inhibitor | FDA-approved peptide anticoagulant, sold as Angiomax, given intravenously in the hospital | FDA approved | It is approved by the FDA as an anticoagulant for coronary procedures, supported by large randomized controlled trials including HORIZONS-AMI. | Bivalirudin is a synthetic 20-amino acid peptide anticoagulant, derived in design from the leech protein hirudin, that directly and reversibly blocks thrombin, the central enzyme in blood clotting. Sold as Angiomax, it is given intravenously during coronary procedures such as angioplasty and stenting to prevent clots, including in people who cannot receive heparin. In a large trial of heart-attack patients, using it instead of heparin plus a second blood thinner reduced major bleeding and lowered 30-day death rates. | Bivalirudin works by directly binding and blocking thrombin, the enzyme at the center of blood clotting. Thrombin converts fibrinogen into the fibrin mesh that holds a clot together and also activates platelets, and by occupying thrombin, bivalirudin stops both. It is a bivalent inhibitor: one end binds thrombin's active (catalytic) site, and the other binds a separate docking region, called exosite 1, that normally grips fibrinogen. Because it latches on at two points, it blocks thrombin that is free in the blood as well as thrombin already bound inside a clot, which heparin does less well. Its action is also reversible and short-lived. Thrombin slowly cleaves the bound drug and recovers its function, so the effect fades within roughly 25 minutes of stopping the infusion, which makes it predictable to use during a procedure. In the HORIZONS-AMI trial of 3,602 heart-attack patients undergoing angioplasty, bivalirudin alone reduced 30-day major bleeding and lowered death from cardiac c… | 0 | 0 | 0 | The main risk of bivalirudin, as with any anticoagulant, is bleeding, though in trials it caused less major bleeding than heparin-based regimens. Other effects reported during treatment include: - Back pain - Nausea - Low blood pressure - Headache One specific signal from the HORIZONS-AMI trial was a higher rate of acute stent thrombosis, a clot forming on the new stent, in the first 24 hours; this did not persist at 30 days and is managed by ensuring adequate antiplatelet therapy. Because it is used only in monitored hospital settings, its dosing is carefully controlled. | 4 | https://www.drugs.com/monograph/bivalirudin.html ; https://link.springer.com/article/10.2165/00003495-200565130-00010 ; https://doi.org/10.1056/NEJMoa0708191 ; http://Drugs.com | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||||
17 | BPC-157 | https://superpower.com/guides/peptides/bpc-157 | Digestive & weight | Wellness and performance | Synthetic pentadecapeptide (gastric-derived) | Not approved by the FDA for any use | Low research | Its human evidence is limited to a single small retrospective report (12 patients with chronic knee pain), while the rest of the literature, including all 35 studies in the 2025 systematic review, is preclinical animal or lab work. | Synthetic peptide made of 15 amino acids, based on a protein found in gastric juice | Almost all done in animals rather than in humans | BPC-157 is a synthetic 15-amino-acid peptide studied for tissue and gut repair, and 35 of the 36 studies in a 2025 systematic review were animal or lab work. The one human report, a retrospective series of 12 patients with chronic knee pain, found that seven (58%) described relief lasting more than 6 months. It had no control group, effect size, or safety data. BPC-157 is not FDA-approved, is prohibited in sport, and remains unsettled in FDA compounding review. | The proposed mechanisms come almost entirely from animal and cell studies. The most consistent finding is that BPC-157 promotes angiogenesis, the growth of new blood vessels, mainly through the VEGFR2-Akt-eNOS pathway and by influencing the nitric oxide system, which helps regulate blood flow and vascular health. In laboratory models, researchers have also reported that BPC-157 increases collagen production, activates fibroblasts, reduces inflammatory signaling, and affects pain pathways. In tendon cells, it has been shown to increase expression of the growth hormone receptor. Across rodent studies, it has been associated with faster healing of muscle, tendon, ligament, bone, and gastrointestinal tissue. In animal data, BPC-157 is metabolized in the liver, cleared by the kidneys, and has a short half-life of under 30 minutes. None of these findings have been confirmed in controlled human studies. | The research on BPC-157 is overwhelmingly preclinical. The 2025 systematic review in orthopedic sports medicine screened the literature and included 36 studies, of which 35 were preclinical (animal or laboratory) and only one involved humans. There are no completed randomized controlled human trials, and there is no long-term human data. A 2019 review reached a similar conclusion, describing consistent healing effects in rodents while noting that efficacy is “yet to be confirmed in humans.” The animal research is broad and fairly consistent, but the human research needed to draw firm conclusions has not been done. The most replicated animal findings involve tendons. In rats with a cut Achilles tendon, BPC-157 improved tendon strength, elasticity, and function and shrank the defect by day 14. The one human report is a retrospective, uncontrolled series of 12 patients with chronic knee pain. After a single knee injection, seven of them (58%) reported relief lasting more than 6 months. The report published no effect size or safety data. | 0 | 0 | 0 | 14 | 14554208; 40756949 | https://doi.org/10.3390/ijms27062876 ; https://doi.org/10.3390/ph18060928 ; https://www.statnews.com/2026/06/01/bpc-157-researcher-predrag-sikiric-addesses-skeptics-questions/ ; https://doi.org/10.1177/15563316251355551 ; https://clinicaltrials.gov/study/NCT02637284 ; https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503a-fdc-act ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://www.statnews.com/2026/07/24/fda-peptide-compounding-panel-backs-epitalon-rejects-emideltide/ ; https://www.usada.org/spirit-of-sport/bpc-157-peptide-prohibited/ ; https://doi.org/10.1007/s00441-019-03016-8 ; https://pubmed.ncbi.nlm.nih.gov/14554208/ ; http://ClinicalTrials.gov ; https://pubmed.ncbi.nlm.nih.gov/40756949/ ; https://www.wada-ama.org/en/prohibited-list | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
18 | Bremelanotide | https://superpower.com/guides/peptides/bremelanotide | Brain & sleep | FDA-approved | MC4R agonist | FDA-approved peptide, sold by prescription as Vyleesi, given as a self-injection | FDA approved | It is approved by the FDA for hypoactive sexual desire disorder in premenopausal women, supported by the two randomized, placebo-controlled RECONNECT phase 3 trials, which showed a modest but statistically significant benefit. | Bremelanotide is a synthetic seven-amino acid peptide that activates melanocortin receptors in the brain to increase sexual desire, unlike blood-flow drugs such as sildenafil. In the two RECONNECT phase 3 trials of 1,267 premenopausal women with hypoactive sexual desire disorder (HSDD), it raised the desire score 0.35 points more than placebo and reduced desire-related distress 0.33 points more (both P<.001) over 24 weeks. It is FDA-approved as Vyleesi, a prescription self-injection for acquired, generalized HSDD. Versions sold online as PT-141 are not the FDA-approved product and are not quality-controlled. | Bremelanotide works in the brain rather than on the genitals. It activates melanocortin receptors, chiefly the MC4 receptor, in regions of the central nervous system that help regulate sexual desire. By stimulating this pathway it is thought to shift the balance of brain signals toward excitation, which can increase desire. This is a different mechanism from erectile dysfunction drugs such as sildenafil, which increase blood flow; bremelanotide targets desire itself. It is used on demand rather than daily. In its pivotal RECONNECT trials, two phase 3 studies of 1,267 randomized premenopausal women with HSDD, bremelanotide produced a small but statistically significant gain on both outcomes over 24 weeks (P<.001 for both): Outcome | Change vs placebo Desire score | Raised 0.35 points more Desire-related distress | Cut 0.33 points more An independent reanalysis of the RECONNECT data judged the benefit statistically modest, and found little evidence that the desire and distress scales… | 0 | 0 | 0 | The most common side effect is nausea, which was frequent in trials and sometimes required anti-nausea treatment. Other common effects include flushing, headache, vomiting, and injection-site reactions. Two effects deserve specific mention: Bremelanotide causes a transient rise in blood pressure and a brief drop in heart rate after each dose, which is why it is avoided in people with cardiovascular risk, and repeated use can cause focal hyperpigmentation, darkened patches of skin or gums, more likely with frequent dosing and in people with darker skin. | 5 | https://www.sciencedirect.com/topics/medicine-and-dentistry/bremelanotide ; https://palatin.com/press_releases/fda-approves-new-drug-application-for-vyleesi-bremelanotide-injection-2/ ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/210557s000lbl.pdf ; https://doi.org/10.1097/AOG.0000000000003500 ; https://doi.org/10.1080/00224499.2023.2175192 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||||
19 | Brilacidin | https://superpower.com/guides/peptides/brilacidin | Digestive & weight | In clinical trials | Defensin-mimetic host-defense peptide | Investigational defensin-mimetic, not approved by the FDA for any use | Low research | There is no peer-reviewed controlled human efficacy evidence; positive human results exist only as company announcements, with peer-reviewed support confined to laboratory studies. | Published support mostly laboratory and preclinical | Brilacidin is an investigational defensin-mimetic, a small molecule designed to imitate the body's own host-defense peptides, developed by Innovation Pharmaceuticals for oral mucositis and studied as an antibacterial and antiviral agent. Its human results to date have been reported mainly through company announcements rather than peer-reviewed trials, while published support is largely laboratory-based. As of 2026 it is not approved for any use. | Brilacidin's proposed actions differ by target: - Bacteria and fungi: its structure carries a pattern of charge that lets it interact with and disrupt microbial membranes, the proposed basis for its antibacterial and antifungal activity - Viruses: in laboratory studies against SARS-CoV-2, it has been reported to disrupt the virus and interfere with how it enters cells - Oral mucositis: an anti-inflammatory action has been proposed These are mechanisms observed mainly in the laboratory, separate from whether the drug helps patients. | The published human evidence is limited, and according to PubMed, the peer-reviewed literature is mainly laboratory work. The table sorts the evidence by type: Evidence | Setting | Reported result | Peer-reviewed Oral mucositis Phase 2 trial | Human | Described by the company as positive, in a press-release topline | No COVID-19 Phase 2 trial | Human | Described by the company as positive, in a press-release topline | No Laboratory study | Cell culture | Brilacidin inhibits SARS-CoV-2 | Yes Laboratory study | Laboratory | Shows broad antiviral activity against coronaviruses | Yes Without peer-reviewed controlled human efficacy data, its clinical benefit is unestablished. | 4 | 2 | 1 | 2 | https://doi.org/10.3390/v13020271 ; https://doi.org/10.1002/jmv.27616 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
20 | Cagrilintide | https://superpower.com/guides/peptides/cagrilintide | Digestive & weight | In clinical trials | Long-acting amylin analog | Investigational peptide, not approved by the FDA or any regulator | Moderate research | It has one positive but limited Phase 2 trial as a standalone drug, with no completed Phase 3 of cagrilintide alone. | Long-acting amylin analog given as a once-weekly injection | Standalone human evidence is a single Phase 2 trial in overweight and obesity | Cagrilintide is an investigational long-acting amylin analog, developed by Novo Nordisk as a once-weekly injection for weight management. In a Phase 2 trial, it produced weight loss over 26 weeks, but most of its late-stage development is as the amylin component of the combination drug CagriSema, though a standalone Phase 3 trial has started. As of 2026, cagrilintide is not approved on its own. | Cagrilintide acts at amylin and calcitonin receptors, mimicking the natural hormone amylin. Activating these receptors is associated with three effects, which together reduce food intake: - Greater satiety - Slower stomach emptying - Suppression of glucagon after meals Because this is a different pathway from the GLP-1 incretin system, cagrilintide is also studied in combination with GLP-1 drugs on the theory that the two mechanisms complement each other. This describes the proposed mechanism rather than a proven outcome. | The main standalone evidence is one Phase 2 trial. According to PubMed, a 26-week dose-finding trial in people with overweight or obesity without diabetes reported weight reductions across a range of doses compared with placebo, with gastrointestinal effects as the most common side effect. This is a single, limited Phase 2 study; cagrilintide alone has not completed a Phase 3 trial for obesity, so its standalone efficacy and long-term profile are not established. | 0 | 0 | 0 | 9% shown by semaglutide 2.4 mg alone in the STEP 1 trial and the 20. || 9% shown by tirzepatide 15 mg in SURMOUNT-1. || The combination of cagrilintide with semaglutide 2.4 mg produced 17. || A 2024 thorough QT cardiac safety study enrolled 105 healthy participants and found no clinically relevant QTcF prolongation at any measured time point after the final 4.5 mg dose. | What are the side effects of cagrilintide? In the 26-week Phase 2 trial, which assigned 706 participants to cagrilintide, the most common adverse events were gastrointestinal: 41% to 63% of cagrilintide-treated participants had a gastrointestinal event depending on dose, mainly nausea, versus 32% in the placebo group. A 2024 thorough QT cardiac safety study enrolled 105 healthy participants and found no clinically relevant QTcF prolongation at any measured time point after the final 4.5 mg dose. Long-term safety data beyond 26 weeks for cagrilintide monotherapy is limited. | 15 | 34798060; 40544433; 33567185; 35658024; 33894838; 40550231; 39279639; 41207310 | https://doi.org/10.1016/S0140-6736(21)01751-7 ; https://www.ncbi.nlm.nih.gov/books/NBK551568/ ; https://doi.org/10.1056/NEJMoa2502081 ; https://clinicaltrials.gov/study/NCT07220642 ; https://www.fda.gov/drugs/drug-alerts-and-statements/fdas-concerns-unapproved-glp-1-drugs-used-weight-loss ; https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=4aea30ff-eb0d-45c1-b114-3127966328ff ; https://pubmed.ncbi.nlm.nih.gov/34798060/ ; https://pubmed.ncbi.nlm.nih.gov/40544433/ ; https://pubmed.ncbi.nlm.nih.gov/33567185/ ; https://pubmed.ncbi.nlm.nih.gov/35658024/ ; https://pubmed.ncbi.nlm.nih.gov/33894838/ ; https://pubmed.ncbi.nlm.nih.gov/40550231/ ; https://pubmed.ncbi.nlm.nih.gov/39279639/ ; https://pubmed.ncbi.nlm.nih.gov/41207310/ ; https://www.sec.gov/Archives/edgar/data/353278/000035327826000006/caq42025.htm | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||
21 | CagriSema | https://superpower.com/guides/peptides/cagrisema | Digestive & weight | In clinical trials | Amylin + GLP-1 combination | Investigational combination peptide, not yet approved (under FDA review as of 2026) | Deep research | Two large, consistent Phase 3 trials show substantial weight loss versus placebo in both obesity and type 2 diabetes, though it is not FDA-approved, its obesity result came in below expectations, and it did not beat tirzepatide head-to-head. | Combines cagrilintide (amylin analog) and semaglutide (GLP-1 agonist) in one weekly injection | Two large, positive Phase 3 trials versus placebo in obesity and in type 2 diabetes | CagriSema is an investigational once-weekly injection that combines the amylin analog cagrilintide with the GLP-1 drug semaglutide, developed by Novo Nordisk for weight management and type 2 diabetes. In two large Phase 3 trials it produced substantial weight loss compared with placebo, though the headline obesity result came in below market expectations and a later head-to-head trial did not beat tirzepatide. As of 2026, it is under FDA review and not yet approved. | CagriSema pairs two appetite-regulating mechanisms. Semaglutide activates the GLP-1 receptor, enhancing glucose-dependent insulin release, slowing gastric emptying, and reducing appetite. Cagrilintide mimics amylin, adding a separate satiety signal and further slowing stomach emptying and suppressing glucagon. The rationale is that combining an incretin and an amylin pathway drives complementary effects on appetite and blood sugar. This describes the intended mechanism; the trials below are what test whether it helps. | Two large Phase 3 trials tested CagriSema against placebo, with these results according to PubMed. Trial | Population | Mean weight change with CagriSema | Mean weight change with placebo REDEFINE 1 | Obesity or overweight without diabetes | About -20% over 68 weeks | About -3% REDEFINE 2 | Obesity and type 2 diabetes | About -14%, with most participants reaching their blood-sugar target | About -3% Two caveats belong alongside those results. The REDEFINE 1 figure, while clearly positive against placebo, landed below the roughly 25% that markets had anticipated. And, a separate head-to-head trial reported by the company in 2026 (REDEFINE 4) did not meet its goal of showing CagriSema non-inferior to tirzepatide; that result has been reported via press release and is not yet peer-reviewed. | 2 | 1 | 0 | In SURMOUNT-1, tirzepatide 15 mg produced 20. || In REDEFINE 4, cagrisema did not meet its goal of showing non-inferiority to tirzepatide 15 mg at 84 weeks (23. | What are the main side effects of cagrisema? In REDEFINE-1 and REDEFINE-2, gastrointestinal adverse events were the most common, affecting 72.5% to 79.6% of CagriSema-treated participants. These included nausea, vomiting, diarrhea, and constipation; most were described as transient and mild to moderate in severity. The semaglutide component's label warns of acute gallbladder disease, including gallstones, and acute pancreatitis, and carries a boxed warning about thyroid C-cell tumors seen in rodents; it is not used in people with a personal or family history of medullary thyroid carcinoma. In a 2024 thorough QT study in healthy participants, cagrilintide showed no clinically relevant QTc prolongation. | 14 | 35658024; 40544433; 40544432; 39279639; 38937282 | https://www.ncbi.nlm.nih.gov/books/NBK551568/ ; https://doi.org/10.1016/S0140-6736(21)01751-7 ; https://www.sec.gov/Archives/edgar/data/353278/000035327826000006/caq42025.htm ; https://doi.org/10.1056/NEJMoa2502081 ; https://doi.org/10.1056/NEJMoa2502082 ; https://www.fda.gov/drugs/drug-alerts-and-statements/fdas-concerns-unapproved-glp-1-drugs-used-weight-loss ; https://pubmed.ncbi.nlm.nih.gov/35658024/ ; https://www.sec.gov/Archives/edgar/data/353278/000117184326000996/f6k_022326.htm ; https://www.sec.gov/Archives/edgar/data/353278/000117184324007023/f6k_122024.htm ; https://pubmed.ncbi.nlm.nih.gov/40544433/ ; https://pubmed.ncbi.nlm.nih.gov/40544432/ ; https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ee06186f-2aa3-4990-a760-757579d8f77b ; https://pubmed.ncbi.nlm.nih.gov/39279639/ ; https://pubmed.ncbi.nlm.nih.gov/38937282/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||
22 | Calcitonin-salmon | Miacalcin (injection); nasal spray sold as a generic | https://superpower.com/guides/peptides/calcitonin-salmon | Bones & muscles | FDA-approved | Calcitonin receptor agonist | FDA-approved | FDA approved | It is approved by the FDA for postmenopausal osteoporosis, Paget's disease of bone, and hypercalcemia, with the nasal spray's osteoporosis benefit supported by the five-year, placebo-controlled PROOF trial, though the effect on fractures was modest and later reviews narrowed its long-term use. | Calcitonin-salmon is an FDA-approved synthetic version of a natural hormone that slows bone breakdown, used mainly for postmenopausal osteoporosis, Paget's disease of bone, and high blood calcium (hypercalcemia). It comes as an injection, sold as Miacalcin, and as a nasal spray sold as a generic. A modest effect on fractures and a small possible cancer risk with long-term use make it a second-line option today. | It works by putting a brake on the cells that break down bone. Bone is constantly being remodeled: cells called osteoclasts dissolve old bone while others build new bone. Calcitonin-salmon binds to calcitonin receptors on osteoclasts and quiets their activity, which slows the release of calcium from bone into the blood. It also nudges the kidneys to pass more calcium in the urine. Together these effects lower blood calcium and can modestly protect bone. | The strongest evidence comes from a large trial of the nasal spray in osteoporosis. According to PubMed, the five-year PROOF study of 1,255 postmenopausal women found that the 200 IU daily nasal dose reduced the risk of new spinal fractures by about 33% compared with placebo. The result was statistically significant, but the effect was modest and, notably, the higher and lower doses tested did not show the same clear benefit, which left some uncertainty about how robust the finding was. | 0 | 0 | 0 | According to PubMed, the five-year PROOF study of 1,255 postmenopausal women found that the 200 IU daily nasal dose reduced the risk of new spinal fractures by about 33% compared with placebo. | The most important safety development came years after approval. In 2013, a reassessment by European regulators, echoed by an FDA advisory committee, pooled data across trials and found a small but consistent increase in cancer rates among people treated with calcitonin over long periods. Regulators concluded that the modest benefit no longer clearly outweighed this risk for routine, long-term osteoporosis use. As a result, the nasal spray's role in osteoporosis was narrowed, and calcitonin-salmon is now generally reserved for people who cannot take other, better-established bone treatments. More common, milder side effects include nasal irritation with the spray and nausea or flushing with the injection. The injection's label also warns of serious allergic reactions and low blood calcium. | 5 | https://www.drugs.com/monograph/calcitonin-salmon.html ; https://go.drugbank.com/drugs/DB00017 ; https://doi.org/10.1016/s0002-9343(00)00490-3 ; https://www.ema.europa.eu/en/medicines/human/referrals/calcitonin ; http://Drugs.com | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
23 | Carnosine | https://superpower.com/guides/peptides/carnosine | Skin & aging | Cosmetic and topical | Antioxidant dipeptide | Cosmetic ingredient rather than a drug, so does not require FDA approval | Low research | The case for topical carnosine rests on antioxidant and anti-glycation activity seen in laboratory and ex-vivo skin studies, with no sound standalone human trial showing an appearance benefit. | Cosmetic ingredient, a naturally occurring dipeptide used for its antioxidant properties | Lab and ex-vivo studies point to antioxidant and anti-glycation activity; standalone human appearance trials are limited | Carnosine is a naturally occurring dipeptide, made of the amino acids beta-alanine and histidine, used in skincare as an antioxidant ingredient. Laboratory and ex-vivo skin studies suggest it can neutralize reactive oxygen species and limit glycation, a process in which sugars stiffen skin proteins, which is the rationale for using it in products aimed at the appearance of aging skin. As of 2026, the evidence for topical carnosine is largely from lab and ex-vivo studies rather than large human appearance trials. | Laboratory studies suggest carnosine acts mainly as an antioxidant and an anti-glycation agent. As an antioxidant, it can neutralize reactive oxygen species, the unstable molecules generated by UV light and pollution that are associated with the visible signs of skin aging. In an ex-vivo human skin study, topical carnosine reduced markers of UV-induced oxidative stress. Its second proposed role is limiting glycation, a reaction in which sugar molecules bind to proteins such as collagen and form advanced glycation end-products that make those proteins stiff and dysfunctional. By slowing that reaction in laboratory models, carnosine is thought to help skin keep the appearance of suppleness. These are study findings; the benefit in finished cosmetics is described in appearance terms, such as supporting the look of firmness and a brighter, more even tone. | Most of the evidence is from laboratory and ex-vivo skin experiments rather than large human trials. According to PubMed, an ex-vivo human skin study found that topical carnosine lowered UV-induced reactive oxygen species and glycation markers. Independent, well-controlled trials of carnosine alone measuring wrinkle or firmness outcomes in people are lacking, and several studies that include carnosine test it inside multi-ingredient formulas, so its individual contribution is hard to isolate. | 0 | 0 | 0 | Carnosine is generally considered well tolerated on the skin, with a low potential for irritation at cosmetic use levels. As with any new skincare ingredient, people with sensitive or reactive skin may want to patch test first, since individual reactions vary. | 1 | https://doi.org/10.1111/php.13850 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
24 | Cerebrolysin | https://superpower.com/guides/peptides/cerebrolysin | Brain & sleep | Wellness and performance | Neuropeptide preparation (porcine brain) | Non-FDA-approved peptide preparation; approved in some other countries | Low research | Although it has many human trials and systematic reviews, those show no clear benefit on stroke survival or function and only a weak, low-quality, possibly non-meaningful signal in vascular dementia. | Mixture of neuropeptides and amino acids from porcine brain, not a single defined peptide | Substantial human trials, but reviews show no clear stroke benefit and only a weak dementia signal | Cerebrolysin is a preparation of small peptides and amino acids derived from pig brain, used in some countries for stroke and dementia and sold elsewhere for cognition. It has been tested in many human trials, but systematic reviews found no clear benefit on survival or function after stroke and only a weak, low-quality signal in vascular dementia. As of 2026 it is not FDA-approved in the United States. | Cerebrolysin is proposed to act like the brain's own neurotrophic factors, the signals that support the survival and function of nerve cells. In laboratory and animal models it has shown these effects: - Neuroprotective - Anti-apoptotic - Anti-excitotoxic Because the preparation is a complex mixture, its precise active components and mechanism are not fully characterized. This describes the proposed mechanism, separate from whether it improves outcomes in people. | It has genuine human trials, and the pooled results are largely unfavorable. The main reviews reached these conclusions: Review | Finding | Certainty Cochrane systematic review of acute ischemic stroke, according to PubMed | No beneficial effect on death, with a possible increase in non-fatal serious adverse events; many trials were manufacturer-supported | Moderate-certainty evidence Separate Cochrane review in vascular dementia | A cognition and global-function signal, but any effect may be too small to be clinically meaningful | Very low quality evidence Independent analysis of brain-derived nootropics | Similar modest conclusions | Low certainty So despite extensive testing, the human evidence does not establish a clear benefit. | 3 | 0 | 0 | 11 | 33515100; 33620612; 28430363 | https://doi.org/10.1016/j.kjms.2014.02.009 ; https://doi.org/10.1007/s00401-006-0166-5 ; https://doi.org/10.1007/978-3-7091-6781-6_29 ; https://doi.org/10.1007/s10072-021-05089-2 ; https://doi.org/10.1002/14651858.CD007026.pub7 ; https://doi.org/10.1002/14651858.CD008900.pub3 ; https://doi.org/10.1016/j.cccb.2021.100012 ; https://pubmed.ncbi.nlm.nih.gov/33515100/ ; https://pmc.ncbi.nlm.nih.gov/articles/PMC4689177/ ; https://pubmed.ncbi.nlm.nih.gov/33620612/ ; https://pubmed.ncbi.nlm.nih.gov/28430363/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
25 | Cetrorelix | https://superpower.com/guides/peptides/cetrorelix | Sexual & reproductive | FDA-approved | GnRH antagonist | FDA-approved peptide, sold as Cetrotide, given as a subcutaneous injection during fertility treatment | FDA approved | It is approved by the FDA for preventing premature LH surges during controlled ovarian stimulation, supported by randomized controlled trials and meta-analyses showing it reliably blocks the LH surge and lowers the risk of severe ovarian hyperstimulation syndrome. | Cetrorelix is a synthetic ten-amino acid peptide that blocks the GnRH receptor in the pituitary gland, shutting down the hormone signals that would otherwise trigger early ovulation. It is FDA-approved as Cetrotide, a subcutaneous injection used during IVF to stop a premature LH surge so that eggs can mature and be collected on schedule. It remains a standard part of modern IVF stimulation, valued for acting quickly and for lowering the risk of ovarian hyperstimulation compared with older protocols. | Cetrorelix works by blocking the pituitary receptor that normally triggers ovulation. Gonadotropin-releasing hormone is released in pulses from the hypothalamus and tells the pituitary to secrete luteinizing hormone (LH) and follicle-stimulating hormone (FSH). During IVF, as stimulated follicles grow and estrogen climbs, the body can launch a premature LH surge that makes the ovaries release their eggs too early and ruins the cycle. Cetrorelix is a decapeptide that competes with natural GnRH for its receptor and occupies it, which rapidly suppresses LH and FSH release. The key difference from GnRH agonists is timing: Feature | GnRH agonists | Cetrorelix (GnRH antagonist) First effect on the pituitary | Stimulate it, causing a temporary surge | No initial flare Suppression | Downregulate it over a couple of weeks | Immediate, dose-dependent, and reversible That is why cetrorelix can be started later in the stimulation cycle and used for only a few days. It is given as a 0.25 mg dose in… | 0 | 0 | 0 | It is given as a 0.25 mg dose injected daily. || A single 3 mg dose was also studied, but only the 0.25 mg product is sold in the U. || According to PubMed, in a multicenter randomized trial a single 3 mg dose of cetrorelix prevented an LH surge in every patient studied, with shorter stimulation and fewer gonadotropin ampules than the long agonist protocol. | The most common effects are mild and local. They include: - Injection-site reactions such as redness, itching, or swelling - Nausea - Headache Serious effects are uncommon but worth knowing: - Ovarian hyperstimulation syndrome (OHSS), a risk of the overall IVF stimulation; according to PubMed, a Cochrane review found that antagonist protocols reduced OHSS compared with the long agonist protocol, with no conclusive difference in live birth rate - Allergic or hypersensitivity reactions, which can rarely be severe | 4 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/021197s017s022lbl.pdf ; https://go.drugbank.com/drugs/DB00050 ; https://doi.org/10.1016/s0015-0282(99)00524-5 ; https://doi.org/10.1002/14651858.CD001750.pub4 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
26 | CJC-1295 | https://superpower.com/guides/peptides/cjc-1295 | Bones & muscles | Wellness and performance | GHRH analog (secretagogue) | Non-FDA-approved peptide sold in the wellness/gray market, not an approved medicine | Low research | Human data are limited to short studies of hormone levels, with no controlled trials showing a benefit for the marketed muscle, fat-loss, recovery, or anti-aging uses. | GHRH analog ("growth hormone secretagogue"); a longer-acting "DAC" version and a short-acting "no-DAC" (modified GRF 1-29) version are both sold | Human data limited to short studies of hormone levels; benefit for muscle, fat, or anti-aging is unproven | CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone (GHRH). In two placebo-controlled trials of healthy adults aged 21 to 61 (Teichman, 2006), a single injection raised mean growth hormone 2- to 10-fold for 6 days or more. Mean IGF-1 rose 1.5- to 3-fold, but no controlled human trial shows benefit for muscle, fat loss, recovery, or anti-aging. CJC-1295 is not FDA-approved, it is not eligible for routine pharmacy compounding, and it is banned in sport. | The proposed mechanism is indirect. GHRH is the hypothalamic signal that tells the pituitary gland to release growth hormone in pulses. As a GHRH-receptor agonist, CJC-1295 is intended to amplify those pulses, raising growth hormone and, downstream, IGF-1. The marketed effects on body composition and recovery are inferred from that hormone rise rather than demonstrated directly. This describes the proposed pharmacology; whether it produces the claimed results in people is a separate question that controlled trials have not answered. The best-characterized human data come from two randomized, placebo-controlled trials in healthy adults aged 21 to 61 (Teichman, 2006) and a follow-up analysis of healthy men aged 20 to 40. Measure | Study group | Finding Mean growth hormone after one injection | Healthy adults aged 21 to 61 | Rose 2- to 10-fold for 6 days or more Mean IGF-1 after one injection | Healthy adults aged 21 to 61 | Rose 1.5- to 3-fold IGF-1 after repeat injections | Healthy adu… | The human evidence is limited to short pharmacology studies of hormone levels, not outcomes. According to PubMed, a Phase 1 study found CJC-1295 produced sustained, dose-dependent increases in growth hormone and IGF-1 and was described as well tolerated over the short term. A related long-acting GHRH study reported similar hormone rises along with some impairment of glucose tolerance in older adults. These measure hormone levels, not muscle, fat, or recovery, and the short-acting "no-DAC" product sold online is largely uncharacterized in controlled human trials. There is no sound human evidence that it delivers the marketed wellness benefits. CJC-1295 is often paired with ipamorelin, which acts at a separate receptor that growth hormone-releasing peptides (GHRPs) engage. No published human randomized controlled trial tests that combination as of September 2026. | 5 | 5 | 0 | What are the side effects of CJC-1295? In short human studies, CJC-1295 was generally well tolerated, with mild local and systemic effects, and no serious adverse reactions were reported. FDA has separately identified serious adverse events, including increased heart rate and a systemic vasodilatory reaction. A related long-acting GHRH study reported some impairment of glucose tolerance in older adults. No long-term safety data are available. | 8 | 16352683; 17018654; 15817669; 42395176; 7962295 | https://pubmed.ncbi.nlm.nih.gov/16352683/ ; https://pubmed.ncbi.nlm.nih.gov/17018654/ ; https://doi.org/10.1210/jc.2005-1536 ; https://doi.org/10.1530/eje.1.01965 ; https://pubmed.ncbi.nlm.nih.gov/15817669/ ; https://pubmed.ncbi.nlm.nih.gov/42395176/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://pubmed.ncbi.nlm.nih.gov/7962295/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
27 | Gonadorelin | https://superpower.com/guides/peptides/compounded-gonadorelin | Sexual & reproductive | Wellness and performance | GnRH (native) | Synthetic native GnRH; no current FDA-approved product for the TRT-adjunct use | Low research | The hormone mechanism is well established, but there is sparse direct human evidence for the marketed testosterone-therapy add-on use, and there is no approved product for it. | Hormone mechanism is well established, but direct evidence for the TRT-adjunct use is limited | Gonadorelin is a synthetic form of the natural reproductive hormone GnRH, used in wellness and men's-health settings as an add-on to testosterone therapy to help preserve fertility and testicular size. The strongest human data come from a different setting. In a 2021 meta-analysis of 420 men with congenital hypogonadotropic hypogonadism across seven studies, pulsatile GnRH began sperm production 5.3 months earlier than gonadotropin therapy (p = 0.004), with no significant difference in sperm concentration (p = 0.37) or pregnancy rate (p = 0.11). Direct evidence for the testosterone add-on use is limited, and there is no FDA-approved gonadorelin product for it. | Given in pulses, GnRH stimulates the pituitary to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which drive the testes to produce testosterone and sperm. This pulsatile mechanism is textbook physiology. A key nuance is that continuous, non-pulsatile exposure instead shuts the system down, so the fertility-preserving rationale depends on intermittent delivery and gonadorelin's very short duration of action. This describes the mechanism, separate from how well the specific add-on use is supported. | The hormone mechanism is well established, but the specific use is thinly supported. Pulsatile GnRH has a recognized role in treating certain fertility and hormone-deficiency conditions. However, there is limited direct published human evidence for the specific "add-on to testosterone therapy to preserve fertility and testicular size" use; this application is largely practice-based and extrapolated rather than supported by dedicated controlled trials, and gonadorelin's short duration makes its effect delivery-dependent. The best human data come from congenital hypogonadotropic hypogonadism, in which GnRH secretion or action fails from birth. A 2021 meta-analysis of 420 men across seven studies compared pulsatile GnRH with gonadotropin therapy: Outcome | Pulsatile GnRH vs gonadotropin therapy | p value Start of sperm production | 5.3 months earlier | 0.004 Sperm concentration | No significant difference | 0.37 Pregnancy rates | No significant difference | 0.11 None of these men were on testosterone therapy, so the results do not show whether gonadorelin works as an add-on. | 0 | 0 | 0 | 2 | 32777865 | https://pubmed.ncbi.nlm.nih.gov/32777865/ ; https://doi.org/10.1159/000057944 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
28 | Tesamorelin | https://superpower.com/guides/peptides/compounded-tesamorelin | Hormones & metabolism | Wellness and performance | GHRH analog | FDA-approved as Egrifta, but only for HIV-associated lipodystrophy | Moderate research | The approved HIV-lipodystrophy use has strong randomized-trial support, but the off-label wellness and anti-aging use in people without HIV is not established by dedicated trials and reverses off treatment. | Tesamorelin is an FDA-approved growth-hormone-releasing peptide, sold as Egrifta, for excess abdominal fat in HIV-associated lipodystrophy. In a randomized trial of 404 people with HIV (Falutz 2010), visceral fat fell 10.9% on tesamorelin versus 0.6% on placebo over 6 months. Its off-label use for body composition and anti-aging in people without HIV is not an approved indication and lacks dedicated trials. It is banned in sport. | Tesamorelin binds pituitary GHRH receptors and stimulates the body's own growth hormone release, which raises IGF-1 and, in its approved population, reduces visceral fat. This mechanism is well established and underlies the approved use. This describes how it works, separate from whether the off-label wellness use is supported. The label describes growth hormone released this way as both anabolic and lipolytic, meaning it also drives fat breakdown, and visceral fat is the depot the HIV trials measured. Visceral fat changed as follows in the largest trial: Group | Time point | Visceral fat change Tesamorelin | 6-month phase | Fell 10.9% Placebo | 6-month phase | Fell 0.6% Tesamorelin, continued | 12 months | Fell by about 18% | For the approved use, the evidence is strong; for the wellness use, it is extrapolated. According to PubMed, a randomized, placebo-controlled trial of 404 people with HIV-associated fat accumulation found tesamorelin significantly reduced visceral fat and raised IGF-1, with no change in glucose parameters. A 52-week extension found it generally well tolerated, and the lost visceral fat returned once treatment stopped. However, there are no dedicated controlled trials of the off-label body-composition or anti-aging use in people without HIV; that use is an extrapolation from the HIV population, and growth hormone-axis stimulation carries class considerations such as IGF-1 elevation and effects on glucose. | 0 | 0 | 0 | 4 | https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=3d783378-b02d-4f19-99dd-0fc91a042224 ; https://doi.org/10.1097/QAI.0b013e3181cbdaff ; https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=839334d3-8c1d-4c26-9036-2ab524a6ea75 ; https://doi.org/10.1097/QAD.0b013e32830a5058 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||||
29 | Copper tripeptide-1 | GHK-Cu | https://superpower.com/guides/peptides/copper-tripeptide-1 | Skin & aging | Cosmetic and topical | Carrier/copper peptide | Cosmetic ingredient rather than a drug, so does not require FDA approval | Moderate research | It has a large body of laboratory and animal data plus manufacturer-associated human studies pointing to appearance benefits, but the one independent controlled human trial found no clear objective effect, so the human evidence remains limited. | Cosmetic ingredient (GHK-Cu), a copper-bound peptide used in "anti-aging" and repair products | Deep laboratory and wound-healing support; independent human appearance evidence is mixed | Copper tripeptide-1, often called GHK-Cu, is a three-amino acid peptide (glycine-histidine-lysine) bound to a copper ion and used in skincare for its proposed role in skin renewal. Laboratory and animal studies show it can signal cells to make collagen and other matrix components. Independent human evidence is thin. In a randomized trial of 13 patients after CO2 laser resurfacing, GHK-Cu skincare showed no significant difference in redness or skin quality in blinded evaluations, though patients rated their overall skin quality higher (p = 0.04). As of 2026 it is a cosmetic ingredient, not an FDA-approved drug. | Laboratory studies suggest copper tripeptide-1 acts as a signal that tells skin cells to rebuild the supporting matrix. In cell and animal studies, GHK-Cu: - Stimulates fibroblasts to produce collagen, elastin, and glycosaminoglycans, the molecules that give skin its structure and cushioning - Helps regulate the enzymes that break that matrix down - Delivers copper, a mineral involved in tissue repair - Has been shown to act as an antioxidant and to support wound healing in animal models Reviews of laboratory work describe further activity, mostly studied in cells and animals rather than in skin products. In gene-expression analyses, the GHK peptide shows anti-inflammatory activity, increased blood-vessel formation, and changes in many genes tied to repair. These are systemic, preclinical findings, separate from the topical cosmetic use this page covers. Because of this activity, it is used in cosmetics with the aim of improving the appearance of firm, smooth, and evenly textured skin… | The research is deep on mechanism but thinner on independent human appearance outcomes. According to PubMed, review articles summarize extensive laboratory and animal evidence that GHK-Cu promotes matrix synthesis and wound healing, though many of those studies are associated with the ingredient's commercial developers. An independent randomized trial of 13 patients used GHK-Cu skincare after CO2 laser resurfacing. Blinded evaluators found no statistically significant difference in redness or skin quality, although patients rated their overall skin quality higher (p = 0.04). In short, the mechanism is well characterized, but strong independent proof of a cosmetic appearance benefit is still limited. Separately, a small set of animal studies tested GHK-Cu given by injection, and these findings are systemic and preclinical: Model | Finding Rats after knee ligament reconstruction | Weekly joint injections for 4 weeks led to a smaller knee laxity difference than saline at 6 weeks (p = 0.009), but the difference was not significant at 12 weeks Mice with lipopolysaccharide-induced acute lung injury | GHK-Cu lowered TNF-alpha and IL-6 through NF-κB p65 and p38 MAPK suppression Because both studies are in animals, they do not show an effect of systemic use in people. | 2 | 0 | 2 | Copper tripeptide-1 is generally well tolerated on the skin. Potential concerns are mostly practical: very high copper concentrations could be irritating, and the ingredient can be destabilized when layered with strong acids such as high-strength vitamin C or certain exfoliants, which is a formulation consideration rather than a safety hazard. Sensitive skin may react to any new product, so a patch test is reasonable. | 6 | https://doi.org/10.1155/2015/648108 ; https://doi.org/10.3390/brainsci7020020 ; https://doi.org/10.1163/156856208784909435 ; https://doi.org/10.1001/archfaci.8.4.252 ; https://doi.org/10.1002/jor.22831 ; https://doi.org/10.18632/oncotarget.11168 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
30 | Corticotropin | ACTH | https://superpower.com/guides/peptides/corticotropin | Hormones & metabolism | FDA-approved | Melanocortin / ACTH | Yes. Corticotropin (Acthar Gel) has been FDA-approved since 1952, and its infantile spasms indication was formally approved in 2010. Its label covers a broad set of conditions, reflecting both its age and its steroid-like breadth of effect. | FDA approved | Corticotropin is FDA-approved across several inflammatory and hormonal conditions, with controlled evidence in infantile spasms and long clinical use elsewhere. | A 39-amino-acid adrenocorticotropic hormone (ACTH) preparation in a long-acting gel | Corticotropin (adrenocorticotropic hormone, or ACTH; sold as Acthar Gel and Purified Cortrophin Gel) is a hormone preparation that stimulates the adrenal glands to make their own steroids and also acts directly on immune cells. It is one of the oldest biologic medicines, used today for conditions ranging from infantile spasms to multiple sclerosis relapses. It has been FDA-approved in the U.S. since 1952 and is given as a long-acting injection. | Corticotropin acts in two ways, summarized in the table below. Action | Where it binds | Effect Classic action | Melanocortin-2 receptor on the adrenal cortex | Stimulates the adrenal glands to synthesize and release cortisol, corticosterone, and other steroids, so much of its anti-inflammatory benefit comes indirectly, through the body's own steroid production Direct action | Melanocortin receptors on immune and other cells | Anti-inflammatory and immune-modulating effects that are independent of steroids This dual action is part of why it is still used in specific settings rather than being entirely replaced by synthetic steroids. In infantile spasms, a severe infant seizure disorder, a controlled study found high-dose ACTH more effective than prednisone for stopping the spasms. Because its downstream effects resemble those of corticosteroids, its side-effect profile does too. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Injection-site reactions - Fatigue - Fluid retention and swelling - Trouble sleeping and headache - High blood sugar In infants treated for infantile spasms, common side effects include: - Infections - Convulsions - High blood pressure - Irritability - Fever More serious considerations include: - Increased susceptibility to infection from immune suppression - Adrenal suppression when treatment is stopped - Growth suppression in children and gastrointestinal bleeding | 2 | 8604274 | https://pubmed.ncbi.nlm.nih.gov/8604274/ ; https://www.acthar.com/Static/pdf/Acthar-PI.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
31 | Cosyntropin | https://superpower.com/guides/peptides/cosyntropin | Hormones & metabolism | FDA-approved | ACTH(1-24) analog | Yes. Cosyntropin (Cortrosyn) has long been FDA-approved as a diagnostic agent for screening adrenocortical insufficiency. It is given as a single injection, with cortisol measured before and after. | FDA approved | Cosyntropin is FDA-approved as a diagnostic agent for adrenal insufficiency, with its ACTH stimulation test well established in clinical practice and studied across dosing protocols. | Synthetic ACTH 1-24, the active portion of adrenocorticotropic hormone | Cosyntropin (sold as Cortrosyn) is a synthetic fragment of adrenocorticotropic hormone used as a diagnostic agent to test whether the adrenal glands are working. A dose is given and the resulting rise in cortisol shows how well the adrenals respond. It has long been FDA-approved in the U.S. and is given as a single injection during the test. | Cosyntropin binds the melanocortin-2 receptor on the adrenal cortex, the same receptor as natural ACTH, and stimulates the adrenal glands to release cortisol. In the diagnostic test, a baseline cortisol level is measured, a dose of cosyntropin is given, and cortisol is measured again after a set interval. A healthy adrenal gland responds with a clear rise in cortisol; a blunted or absent rise points to adrenal insufficiency. Because the value of the test lies in the measured response, cosyntropin is given as a single dose under controlled conditions. Studies comparing test protocols have examined lower and standard doses; a meta-analysis found the low-dose test was better than the standard dose at detecting chronic adrenal insufficiency caused by the pituitary or hypothalamus. The test helps distinguish primary adrenal failure from other causes of low cortisol. | 0 | 0 | 0 | According to the prescribing information, reported side effects include: - Slow or fast heart rate - High blood pressure - Swelling in the hands or feet - Rash More serious considerations include: - Allergic reactions, including anaphylaxis | 2 | https://doi.org/10.1210/jc.2008-0710 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/016750s033lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
32 | Cyclosporine | https://superpower.com/guides/peptides/cyclosporine | Immune & defense | FDA-approved | Cyclic peptide immunosuppressant | Yes. The FDA approved cyclosporine and two later formulations on this timeline: Year | FDA approval 1983 | Cyclosporine, for transplant rejection 1995 | Neoral microemulsion 2002 | Restasis eye drop The systemic formulations carry boxed warnings, including for kidney toxicity and for the increased risk of serious infections and malignancies (especially lymphoma and skin cancer) that comes with im… | FDA approved | Cyclosporine is FDA-approved for transplant rejection, certain autoimmune diseases, and dry eye, supported by landmark transplant trials and controlled studies in its other uses. | A calcineurin-inhibitor immunosuppressant, a cyclic 11-amino-acid peptide of fungal origin | Cyclosporine (also spelled ciclosporin; brands include Sandimmune, Neoral, and the eye drop Restasis) is a cyclic peptide from a fungus that suppresses the immune system, and it transformed organ transplantation when it arrived in the 1980s. It works by blocking the activation of T cells. It has been FDA-approved in the U.S. since 1983, is available in oral, intravenous, and eye-drop forms, and carries boxed warnings for the systemic versions. | Cyclosporine enters T cells and binds a protein called cyclophilin, and the resulting complex blocks an enzyme called calcineurin. Calcineurin normally activates a transcription factor (NFAT) that switches on the gene for interleukin-2 and other signals T cells need to multiply and mount an immune response. By inhibiting calcineurin, cyclosporine prevents that activation, so the immune attack on a transplanted organ, or the overactive immune response in autoimmune disease, is suppressed. That targeted suppression of T-cell activation is what made it so valuable in transplantation. In the landmark Canadian multicenter trial, cyclosporine improved one-year kidney graft survival compared with the older azathioprine-based regimen. The same mechanism underlies its use in autoimmune conditions and, at low local doses in Restasis, in reducing the inflammation of chronic dry eye. | 0 | 0 | 0 | According to the prescribing information, common side effects of systemic use include: - High blood pressure - Kidney impairment with rising creatinine - Tremor - Excess hair growth and gum overgrowth More serious considerations include: - Boxed warnings for kidney toxicity and for increased risk of serious infections and cancers, including lymphoma and skin cancer - The need for blood-level monitoring and attention to many drug interactions - Restasis, acting locally, mainly causes eye burning or stinging and does not carry these systemic warnings | 1 | https://doi.org/10.1056/NEJM198310063091401 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
33 | Dalbavancin / Oritavancin / Telavancin | https://superpower.com/guides/peptides/dalbavancin-oritavancin-telavancin | Skin & aging | FDA-approved | Lipoglycopeptide antibiotics | Yes. All three are approved for acute bacterial skin and skin-structure infections. The table shows when each was approved and for what: Drug | FDA approval | Approved for Telavancin | 2009 | Acute bacterial skin and skin-structure infections; also hospital-acquired and ventilator-associated bacterial pneumonia due to susceptible S. aureus when alternatives are unsuitable Dalbavancin | 2014; exte… | FDA approved | Dalbavancin, oritavancin, and telavancin are FDA-approved for acute bacterial skin infections (and telavancin for some pneumonia), supported by randomized non-inferiority trials. | Lipoglycopeptide antibiotics derived from the glycopeptide class, active against Gram-positive bacteria including MRSA | Dalbavancin, oritavancin, and telavancin (sold as Dalvance, Orbactiv, and Vibativ) are lipoglycopeptide antibiotics, semi-synthetic relatives of vancomycin that treat Gram-positive infections, including MRSA. Dalbavancin's half-life of roughly two weeks and oritavancin's single-infusion course allow very infrequent dosing for a skin infection, while telavancin is dosed daily. All three are FDA-approved in the U.S., and they are given intravenously. | Like vancomycin, these drugs block bacterial cell-wall synthesis by binding the D-alanyl-D-alanine end of the wall's building blocks, preventing the cross-linking that gives the wall strength. The lipid tail anchors them in the bacterial membrane, which both prolongs their activity and, in the case of oritavancin and telavancin, lets them also disrupt the membrane itself, a second bactericidal mechanism. All are bactericidal against Gram-positive bacteria including MRSA. The standout practical feature is duration. Dalbavancin's half-life of roughly two weeks allows a once-weekly or even single-dose regimen, and oritavancin treats a skin infection with a single infusion. In its pivotal program, once-weekly dalbavancin was non-inferior to a conventional vancomycin-to-linezolid course for skin infections. Telavancin is dosed daily and has a broader approved role that includes some pneumonia. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Nausea, headache, and diarrhea - Rises in liver enzymes (dalbavancin) - Taste disturbance and foamy urine (telavancin) More serious considerations include: - Telavancin's boxed warnings for kidney toxicity (with higher mortality in pneumonia patients who already have moderate-to-severe kidney impairment) and for fetal harm - Oritavancin interferes with some blood-clotting tests and should not be used with intravenous unfractionated heparin for a period after dosing - Infusion-related reactions | 1 | https://doi.org/10.1056/NEJMoa1310480 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
34 | Daptomycin | https://superpower.com/guides/peptides/daptomycin | Skin & aging | FDA-approved | Cyclic lipopeptide antibiotic | Yes. Daptomycin was approved by the FDA in 2003 for complicated skin and skin-structure infections, with the S. aureus bloodstream infection indication (including right-sided endocarditis) added afterward. It is given once daily intravenously. | FDA approved | Daptomycin is FDA-approved for complicated skin infections and S. aureus bacteremia, supported by randomized non-inferiority trials. | A cyclic lipopeptide antibiotic active against Gram-positive bacteria | Daptomycin (sold as Cubicin) is a cyclic lipopeptide antibiotic that kills Gram-positive bacteria, including MRSA, by puncturing their cell membrane. It is used for serious skin infections and for Staphylococcus aureus bloodstream infections, but notably not for pneumonia. It has been FDA-approved in the U.S. since 2003 and is given intravenously. | Daptomycin works at the bacterial cell membrane rather than the cell wall. In the presence of calcium, its lipid tail inserts into the Gram-positive membrane, where multiple molecules cluster to form channels. These channels let potassium and other ions leak out, rapidly collapsing the membrane's electrical charge. Without that charge the bacterium cannot sustain DNA, RNA, and protein synthesis, and it dies quickly, without bursting open. That membrane mechanism gives concentration-dependent, rapid killing. One important limitation follows from its chemistry: daptomycin is inactivated by lung surfactant, so it does not work for pneumonia and is not used there. In the pivotal trial for bloodstream infection, daptomycin was non-inferior to standard therapy for S. aureus bacteremia and right-sided endocarditis, with less kidney dysfunction. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Diarrhea, headache, and dizziness - Rash - Abnormal liver tests and rises in the muscle enzyme CPK - Urinary tract infections - Low blood pressure and shortness of breath More serious considerations include: - Muscle injury (myopathy and rarely rhabdomyolysis), so CPK is monitored and statins may be paused - Eosinophilic pneumonia, an uncommon lung reaction - Peripheral neuropathy - Serious allergic reactions, including a severe drug reaction called DRESS - Kidney inflammation (tubulointerstitial nephritis) | 2 | https://doi.org/10.1056/NEJMoa053783 ; https://www.merck.com/product/usa/pi_circulars/c/cubicin/cubicin_pi.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
35 | Dasiglucagon | https://superpower.com/guides/peptides/dasiglucagon | Digestive & weight | FDA-approved | Glucagon analog | Yes. Dasiglucagon (Zegalogue) is FDA-approved, and its label has changed since approval: Date | FDA action | Who it covers 2021 | Approved for severe hypoglycemia in people with diabetes | Ages 6 and up June 2026 | Label replaced the age limit with a weight limit | Adults and children who weigh at least 20 kg (about 44 pounds) It is available as an autoinjector and a prefilled syringe. | FDA approved | Dasiglucagon is FDA-approved for severe hypoglycemia, supported by phase 3 trials showing rapid blood-sugar recovery versus placebo. | A glucagon analog peptide engineered for stability in a ready-to-use liquid | Dasiglucagon (sold as Zegalogue) is a stable glucagon analog formulated as a ready-to-use injection for the emergency treatment of severe low blood sugar. Because it stays stable in solution, it comes premixed in an autoinjector or prefilled syringe, with no reconstitution needed. It has been FDA-approved in the U.S. since 2021 and is now approved for adults and children with diabetes who weigh at least 20 kg. | Dasiglucagon activates the same liver glucagon receptor as native glucagon, triggering glycogenolysis and gluconeogenesis so the liver releases glucose and blood sugar rises quickly. Its structural changes do not alter what it does at the receptor; they make the molecule stable enough to be stored as a ready-to-use liquid, which matters in an emergency where every step of mixing and preparation costs time. That practical advantage is the point of the drug. In its phase 3 trial in adults with type 1 diabetes, dasiglucagon produced a median time to plasma-glucose recovery of 10 minutes versus 40 minutes with placebo, with nearly all patients recovering within 15 minutes. A separate pediatric trial supported its use in children. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Nausea and vomiting - Headache - Diarrhea (in adults) - Injection-site pain More serious considerations include: - A rise in blood pressure in people with pheochromocytoma - Low blood sugar rebound in people with insulinoma - Serious allergic reactions | 2 | https://doi.org/10.2337/dc20-2995 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/214231s004lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
36 | Davunetide | https://superpower.com/guides/peptides/davunetide | Brain & sleep | In clinical trials | Neuroprotective peptide | Investigational peptide, not approved by the FDA | Low research | The large, well-powered pivotal trial was clearly negative on both primary endpoints, and earlier signals in other conditions were small and never confirmed. | Intranasal neuroprotective treatment, studied chiefly for progressive supranuclear palsy | Davunetide is an investigational neuroprotective peptide derived from a brain protein, studied as an intranasal treatment for the rare neurodegenerative disease progressive supranuclear palsy. Its large pivotal trial clearly failed, showing no benefit over placebo, and earlier signals in other conditions were small and never confirmed. As of 2026 it is not approved. | Davunetide is proposed to stabilize microtubules, the internal scaffolding of nerve cells, and to reduce abnormal phosphorylation of tau, a protein that forms damaging tangles in several neurodegenerative diseases. It is derived from a neuroprotective protein and showed protective effects in laboratory models. This describes the proposed mechanism; as the pivotal trial below shows, it did not translate into clinical benefit. | The pivotal evidence is clearly negative, and earlier signals in other conditions were never confirmed. Condition | Evidence | Result Progressive supranuclear palsy | Phase 2/3 trial indexed on PubMed, over 300 patients enrolled | No difference from placebo on either co-primary endpoint Conditions such as mild cognitive impairment and schizophrenia | Earlier, smaller exploratory signals, summarized in a review | Never confirmed in larger trials The authors of the pivotal trial concluded that davunetide is not an effective treatment for progressive supranuclear palsy. The human evidence does not support a benefit. | 2 | 1 | 0 | 2 | https://doi.org/10.2174/138161211795589373 ; https://doi.org/10.1016/S1474-4422(14)70088-2 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
37 | Degarelix | https://superpower.com/guides/peptides/degarelix | Sexual & reproductive | FDA-approved | GnRH antagonist | Yes. Degarelix was approved by the FDA in 2008 for advanced prostate cancer. It is given as a subcutaneous injection, starting with a loading dose followed by a maintenance dose every 28 days. | FDA approved | Degarelix is FDA-approved for advanced prostate cancer, supported by a phase 3 trial showing castrate testosterone suppression non-inferior to leuprolide with faster onset. | A GnRH receptor antagonist peptide that suppresses testosterone without a flare | Degarelix (sold as Firmagon) is a synthetic decapeptide that blocks the gonadotropin-releasing hormone receptor, dropping testosterone to castrate levels within a few days and without the initial surge seen with older hormone drugs. It is used to treat advanced prostate cancer and lowers testosterone to castrate levels faster than the agonist leuprolide. It has been FDA-approved in the U.S. since 2008 and is given as a monthly subcutaneous injection. | Degarelix binds reversibly and competitively to GnRH receptors on the pituitary, immediately blocking the hormone signal that normally drives release of luteinizing hormone and follicle-stimulating hormone. Those gonadotropins fall within hours, and testosterone drops to castrate levels within a few days. Because it is an antagonist rather than an agonist, it causes no initial testosterone surge, so there is no need for the anti-androgen cover used to blunt the "flare" with agonist drugs. In advanced prostate cancer, removing testosterone deprives hormone-sensitive tumor cells of the signal they depend on. In the phase 3 CS21 trial, degarelix was non-inferior to leuprolide for keeping testosterone at or below castrate levels over 12 months, and it suppressed testosterone and PSA more quickly in the first weeks. That rapid onset without a flare is the main clinical distinction of the drug. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Injection-site reactions such as pain, redness, and swelling (common with the loading dose) - Hot flashes - Weight gain and fatigue - Increased liver enzymes More serious considerations include: - QT-interval prolongation, so caution is advised with other QT-prolonging drugs or electrolyte abnormalities - Hypersensitivity reactions - Reduced bone density with long-term androgen deprivation | 2 | https://doi.org/10.1111/j.1464-410X.2008.08183.x ; https://ferringusa.com/PI/Firmagon | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
38 | Desirudin | https://superpower.com/guides/peptides/desirudin | Heart & blood | FDA-approved | Direct thrombin inhibitor | Desirudin was approved by the FDA in 2003 for the prevention of deep vein thrombosis in patients undergoing elective hip replacement surgery. The only brand, Iprivask, has since been discontinued in the U.S., and no generic is sold. | FDA approved | Desirudin is FDA-approved for preventing deep vein thrombosis after hip replacement, supported by randomized trials showing lower clot rates than heparin. | A recombinant hirudin analog that directly inhibits thrombin | Desirudin (formerly sold as Iprivask) is a recombinant form of hirudin, the natural anticoagulant from the medicinal leech, that was used to prevent blood clots after hip replacement surgery. It directly and specifically blocks thrombin, the central enzyme of the clotting cascade. It was FDA-approved in the U.S. in 2003, but Iprivask has since been discontinued and no desirudin product is currently sold in the U.S. | Desirudin is a direct thrombin inhibitor. Thrombin is the key enzyme at the end of the clotting cascade, responsible for converting fibrinogen into the fibrin that forms a clot and for further activating platelets. Desirudin binds thrombin tightly at two sites at once, both its active site and the region it uses to grip fibrinogen, essentially clamping the enzyme shut. Unlike heparin, it does not need the body's antithrombin to work and it can inhibit thrombin that is already bound within a clot. That direct, antithrombin-independent action is useful for preventing the venous clots that can form after hip replacement, when immobility and surgical injury raise the risk. In its pivotal trial in elective hip replacement, desirudin reduced confirmed deep vein thrombosis compared with unfractionated heparin, without an increase in bleeding. It is given as a subcutaneous injection around the time of surgery. | 0 | 0 | 0 | Common side effects include: - Bleeding - Injection-site reactions - Anemia and nausea More serious considerations include: - Hemorrhage, the principal risk - A warning that spinal or epidural anesthesia carries a risk of spinal bleeding and paralysis, a caution shared across anticoagulants - Caution in kidney impairment, and the possible formation of antibodies to hirudin | 2 | https://doi.org/10.2106/00004623-199703000-00002 ; https://www.drugs.com/mtm/iprivask.html | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
39 | Desmopressin | https://superpower.com/guides/peptides/desmopressin | Heart & blood | FDA-approved | Vasopressin V2 analog | Yes. Desmopressin was first approved by the FDA in 1978, with later products including the Noctiva nasal spray (2017) and the Nocdurna sublingual tablet (2018) for nocturia. Noctiva and the Stimate nasal spray have since been discontinued in the U.S. Nocdurna carries a boxed warning about the risk of low blood sodium (hyponatremia), as Noctiva did. | FDA approved | Desmopressin is FDA-approved for diabetes insipidus, enuresis, nocturia, and certain bleeding disorders, supported by decades of clinical use and registration trials. | A synthetic vasopressin analog that selectively activates the V2 (antidiuretic) receptor | Desmopressin (desmopressin acetate; brands include DDAVP and Nocdurna) is a synthetic version of the antidiuretic hormone vasopressin, engineered to concentrate urine without raising blood pressure. It treats central diabetes insipidus, bedwetting, nighttime urination, and certain bleeding disorders. It has been FDA-approved in the U.S. since 1978 and comes as tablets, a sublingual form, nasal spray, and injection. | Desmopressin selectively activates the V2 vasopressin receptor in the kidney's collecting ducts, where it increases the number of water channels (aquaporin-2) that reabsorb water back into the body. The result is more concentrated urine and less urine volume. Because the chemical changes that give desmopressin this selectivity also remove its activity at the V1 receptors on blood vessels, it does not cause the vasoconstriction that vasopressin does. This makes it useful across several conditions. Desmopressin also has a second action unrelated to the kidney: it prompts the release of clotting factor VIII and von Willebrand factor from storage sites in blood-vessel walls. The table shows which action each use draws on: Condition | What desmopressin does Central diabetes insipidus, where the body lacks vasopressin | Restores normal water conservation Bedwetting and nighttime urination | Reduces overnight urine production Mild hemophilia A and type 1 von Willebrand disease | Releases sto… | 0 | 0 | 0 | Common side effects include: - Headache - Nausea - Nasal discomfort with the spray - Flushing More serious considerations include: - Low blood sodium (hyponatremia), which can cause seizures if severe, the reason fluid intake is restricted and the basis of the Nocdurna boxed warning - Caution in people at risk of fluid overload or with heart or kidney disease | 1 | https://drugs.com/cons/noctiva.html | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
40 | Difelikefalin | https://superpower.com/guides/peptides/difelikefalin | Skin & aging | FDA-approved | Kappa-opioid agonist peptide | Yes. Difelikefalin was approved by the FDA in 2021 for moderate-to-severe pruritus associated with chronic kidney disease in adults on hemodialysis. It is given as an intravenous bolus into the venous line of the dialysis circuit at the end of each session, three times a week. | FDA approved | Difelikefalin is FDA-approved for dialysis-associated itch, supported by randomized trials (KALM-1 and KALM-2) showing reduced itch intensity. | A peripherally restricted kappa-opioid receptor agonist peptide | Difelikefalin (sold as Korsuva) is a peptide that activates kappa-opioid receptors to relieve the intense itching that affects many people on dialysis. Because it barely enters the brain, it eases itch without the typical opioid effects on mood or breathing. It has been FDA-approved in the U.S. since 2021 and is given intravenously during hemodialysis. | Difelikefalin selectively activates kappa-opioid receptors, which are found on peripheral sensory nerves and on immune cells. The table below shows what activating each set of receptors does. Where the kappa receptors sit | Effect of activating them Itch-sensing peripheral sensory nerves | Dampens the transmission of itch signals Immune cells | May reduce the release of itch-promoting and inflammatory mediators The net effect is reduced itch. Its design is central to its profile: as a peripherally restricted peptide, it reaches these peripheral kappa receptors but has minimal entry into the brain, so it avoids the euphoria, dependence, and respiratory depression associated with classic opioids that act on mu receptors. In the KALM-1 trial, a significantly larger share of patients on difelikefalin than on placebo achieved a meaningful improvement in itch intensity over 12 weeks, with better itch-related quality of life. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Diarrhea - Dizziness and nausea - High potassium - Headache More serious considerations include: - Dizziness, drowsiness, and changes in mental status or gait, which can raise the risk of falls, especially with sedating medicines - Caution when combined with other central nervous system depressants | 2 | https://doi.org/10.1056/NEJMoa1912770 ; https://www.drugs.com/pro/korsuva.html | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
41 | Dihexa | https://superpower.com/guides/peptides/dihexa | Brain & sleep | Wellness and performance | Angiotensin IV-derived peptide | Non-FDA-approved peptide sold as a research chemical | Low research | There are no human data at all, and the key paper underlying its proposed mechanism has been retracted, so even the preclinical rationale carries an added reliability concern. | Angiotensin IV-derived peptide studied for cognition in animals | Preclinical only; no human trials, and a key mechanism paper was retracted | Dihexa is an experimental cognition peptide derived from angiotensin IV, sold on the "research peptide" market for brain function. Its evidence is entirely preclinical, with no human trials, and a key paper describing its proposed mechanism has been retracted. As of 2026 it is not FDA-approved or approved anywhere. | Dihexa has been proposed to promote the formation of new connections between nerve cells by enhancing a growth-factor pathway in the brain (hepatocyte growth factor and its receptor, c-Met). An important caveat belongs here: the primary research paper describing this mechanism has since been retracted, which weakens even the preclinical rationale. The remaining supporting data are from cell and rodent experiments. This describes a proposed mechanism, separate from any demonstrated benefit in people. | The evidence is preclinical, and partly compromised. Animal experiments (such as maze-based memory tests) have been reported, but the foundational mechanism paper has been retracted, and there are no completed human efficacy trials. There is no sound human evidence that dihexa improves cognition. | 0 | 0 | 0 | Is dihexa safe? No human safety data exist for dihexa as of September 2026, and no human exposure data on dihexa products have been identified. No human Phase 1 dose-escalation study, pharmacokinetic profile, or systematic adverse-event characterization has been published. The compound's proposed c-Met agonist mechanism raises a specific theoretical oncogenic concern, because c-Met signaling is linked to tumor proliferation, invasion, and metastasis in several cancer types. This is not a minor caveat. It is a major safety unknown for a compound being circulated in consumer nootropic markets with no clinical oversight. | 11 | 40312092; 40312093; 23055539; 30352967; 34827486 | https://doi.org/10.1124/jpet.112.199497 ; https://doi.org/10.1124/jpet.114.218735 ; https://doi.org/10.5435/JAAOSGlobal-D-25-00236 ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://pmc.ncbi.nlm.nih.gov/articles/PMC3533412/ ; https://pubmed.ncbi.nlm.nih.gov/40312092/ ; https://pubmed.ncbi.nlm.nih.gov/40312093/ ; https://pubmed.ncbi.nlm.nih.gov/23055539/ ; https://pubmed.ncbi.nlm.nih.gov/30352967/ ; https://clinicaltrials.gov/search?term=dihexa ; https://pubmed.ncbi.nlm.nih.gov/34827486/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
42 | Dipeptide diaminobutyroyl benzylamide diacetate | https://superpower.com/guides/peptides/dipeptide-diaminobutyroyl-benzylamide-diacetate | Skin & aging | Cosmetic and topical | Neuromuscular-relaxing peptide | Cosmetic ingredient rather than a drug, so does not require FDA approval | Low research | The mechanism is supported by laboratory work, but there is no sound human trial of the isolated peptide showing an appearance benefit; the available human study tested it only within a multi-ingredient formula. | Cosmetic ingredient (SYN-AKE), a synthetic venom-mimic peptide | Mechanism based on laboratory work; human evidence comes from combination formulas, not the isolated peptide | Dipeptide diaminobutyroyl benzylamide diacetate, sold under the trade name SYN-AKE, is a synthetic peptide modeled on a component of temple viper venom, used in skincare as a "needle-free" alternative aimed at expression lines. Laboratory work suggests it mimics a venom peptide that blocks the muscle receptor for acetylcholine, which is the rationale for marketing it to soften the look of dynamic wrinkles. As of 2026, the evidence is mainly laboratory and manufacturer data, with human testing done inside multi-ingredient formulas rather than on the peptide alone. | Laboratory studies suggest the peptide works by quieting the signal that makes facial muscles contract. Normally the neurotransmitter acetylcholine binds to receptors on muscle, called nicotinic acetylcholine receptors, to trigger contraction. The venom peptide it is modeled on reversibly blocks that receptor, and the synthetic version is proposed to do the same, so the small muscles that create "expression lines" contract less and the overlying skin looks smoother. This is the same general idea marketed for other "expression line" peptides, and it is why SYN-AKE is sometimes described as a topical alternative to muscle-relaxing injections. It is important to frame this accurately: The mechanism is demonstrated in laboratory settings, and a topical cosmetic does not reach or paralyze muscle the way an injection does. In finished products the goal is described in appearance terms, the look of fewer or softer dynamic lines. | The direct evidence for the isolated peptide is limited. According to PubMed, a 2026 ex-vivo and clinical study tested a serum that contained dipeptide diaminobutyroyl benzylamide diacetate together with acetyl hexapeptide-8, niacinamide, and other actives, and reported improvements in the appearance of wrinkles and skin quality. That evidence has three limits: - Because the peptide was one of several active ingredients, that result cannot be attributed to it alone. - No independent trial of SYN-AKE by itself measuring appearance outcomes was found. - Much of the supporting data is laboratory or manufacturer-based. | 0 | 0 | 0 | The peptide is generally reported as well tolerated on the skin, with low irritation potential at cosmetic use levels, and topical application is not known to produce a systemic muscle effect. As with any new skincare product, people with sensitive skin may want to patch test, since individual reactions vary. | 3 | https://www.happi.com/contents/view_suppliers-corner/2005-12-09/pentapharm-introduces-anti-wrinkle-active/ ; https://cosmeticsdesign-europe.com/Article/2007/12/14/snake-venom-based-anti-ageing-cream-launched-in-uk ; https://doi.org/10.1111/ics.70087 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
43 | DSIP | https://superpower.com/guides/peptides/dsip | Brain & sleep | Wellness and performance | Neuromodulatory nonapeptide | Non-FDA-approved peptide sold in the wellness/gray market | Low research | The human data are limited to sparse, dated, low-quality studies without reproducible efficacy, and no mechanism has been validated. | Naturally occurring nine-amino acid peptide linked in early research to sleep | Human evidence is sparse, old, and inconsistent; no mechanism is validated | DSIP (delta sleep-inducing peptide) is a naturally occurring peptide sold on the "research peptide" market for sleep and stress. Its human evidence is limited to a few small, dated, inconsistent studies, and no validated mechanism or reproducible benefit has been established. As of 2026 it is not FDA-approved and not approved as a drug anywhere. | DSIP has been proposed to play roles in: - Regulating sleep - Modulating the body's stress (HPA-axis) responses - Acting as an antioxidant It has no validated receptor or defined mechanism. The sleep association that gave it its name comes from early animal work that has not resolved into a clear understanding of how, or whether, it influences human sleep. This describes a proposed mechanism, separate from any demonstrated benefit. | The human evidence is thin and old. A small number of studies from the 1980s and 1990s examined DSIP in insomnia, chronic pain, and withdrawal states and reported inconsistent findings; most were small and uncontrolled, and no modern, well-conducted trials have established a reproducible benefit. There is no sound human evidence that DSIP improves sleep or stress. | 0 | 0 | 0 | 5 | 862769 | https://pubmed.ncbi.nlm.nih.gov/862769/ ; https://doi.org/10.1007/BF01971753 ; https://doi.org/10.1159/000115716 ; https://doi.org/10.1159/000115715 ; https://doi.org/10.5435/JAAOSGlobal-D-25-00236 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
44 | Dulaglutide | https://superpower.com/guides/peptides/dulaglutide | Hormones & metabolism | FDA-approved | GLP-1 receptor agonist | FDA-approved GLP-1 peptide, sold as Trulicity for type 2 diabetes | FDA approved | Dulaglutide is approved by the FDA for type 2 diabetes and for cardiovascular risk reduction, backed by the AWARD trial program and the REWIND cardiovascular outcomes trial. | In trials, lowered blood sugar and reduced major cardiovascular events by about 12% | Dulaglutide is a once-weekly GLP-1 receptor agonist built by fusing two GLP-1 analog chains to an antibody fragment, which extends its action to about five days. It was approved for type 2 diabetes in 2014 and gained a cardiovascular indication in 2020 after the REWIND trial showed a roughly 12% reduction in major cardiovascular events. It remains on the market as Trulicity. | Dulaglutide lowers blood sugar and curbs appetite by activating the GLP-1 receptor, mimicking a gut hormone the body releases after eating. Through that receptor it prompts the pancreas to release insulin when blood sugar is high. Because this effect is glucose-dependent, meaning it works mainly when blood sugar is already elevated, dulaglutide on its own carries a low risk of hypoglycemia. It also lowers glucagon (a hormone that raises blood sugar), slows the rate at which the stomach empties, and acts on appetite centers to reduce food intake. The antibody fragment it is attached to keeps it in the blood for about five days, which is what allows once-weekly dosing. In its trials, it typically lowered A1c by around 1.5%. In the REWIND cardiovascular outcomes trial, it reduced major cardiovascular events by about 12% in people with type 2 diabetes. | 0 | 0 | 0 | The most common side effects are gastrointestinal, and they are usually strongest when the dose is increased: - Nausea - Diarrhea - Vomiting - Abdominal pain - Decreased appetite - Fatigue Less common but more serious risks include: - Thyroid C-cell tumors: dulaglutide carries a boxed warning based on rodent studies. It is not known whether this happens in humans. - Pancreatitis, or inflammation of the pancreas - Gallbladder problems, including gallstones - Acute kidney injury, usually from dehydration caused by vomiting or diarrhea - Low blood sugar, especially when combined with insulin or a sulfonylurea - Worsening of diabetic retinopathy - Serious allergic reactions - Severe stomach and bowel side effects - Food or liquid entering the lungs during anesthesia | 3 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/125469s065lbl.pdf ; https://diabetesjournals.org/care/article/37/8/2159/29765/Efficacy-and-Safety-of-Dulaglutide-Added-Onto ; https://doi.org/10.1016/S0140-6736(19)31149-3 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
45 | Ecallantide | https://superpower.com/guides/peptides/ecallantide | Skin & aging | FDA-approved | Plasma kallikrein inhibitor | Yes. Ecallantide is FDA-approved, and its age range has widened since approval: Year | FDA action | Who it covers 2009 | Approved for acute attacks of hereditary angioedema | Patients 16 and older 2014 | Age lowered | Patients 12 and older It carries a boxed warning for anaphylaxis and must be administered by a healthcare professional equipped to manage anaphylaxis; it is not for self-injection. | FDA approved | Ecallantide is FDA-approved for acute hereditary angioedema attacks, supported by randomized trials including EDEMA3 showing improved symptom scores. | A plasma kallikrein inhibitor (a recombinant Kunitz-domain protein) | Ecallantide (sold as Kalbitor) is a protein that blocks plasma kallikrein, used to treat acute attacks of hereditary angioedema. By stopping kallikrein, it reduces production of the bradykinin that drives the swelling. It has been FDA-approved in the U.S. since 2009, is given by a healthcare professional, and carries a boxed warning for anaphylaxis. | Ecallantide blocks plasma kallikrein, an enzyme that cleaves a protein called high-molecular-weight kininogen to release bradykinin. Bradykinin is the mediator that causes the blood vessels to leak and the tissues to swell in hereditary angioedema. By inhibiting kallikrein, ecallantide reduces the generation of bradykinin and thereby controls the acute attack. This upstream action distinguishes it from drugs that block the bradykinin receptor directly. In the EDEMA3 trial, ecallantide significantly improved both symptom-severity and treatment-outcome scores compared with placebo. Because the molecule can provoke severe allergic reactions that may resemble an HAE attack, administration in a supervised setting is required. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Headache - Nausea and diarrhea - Fever - Injection-site reactions and nasopharyngitis More serious considerations include: - A boxed warning for anaphylaxis, which is why it is administered by a healthcare professional - Allergic reactions that can be hard to distinguish from an HAE attack | 2 | https://doi.org/10.1056/NEJMoa0905079 ; https://www.drugs.com/pro/kalbitor.html | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
46 | Echinocandins | https://superpower.com/guides/peptides/echinocandins | Heart & blood | FDA-approved | Lipopeptide antifungals | Yes. Caspofungin, micafungin, and anidulafungin are all FDA-approved, as is rezafungin; the table shows each one's approval year and approved uses. Drug | FDA approval | Approved uses include Caspofungin | 2001 | Candidemia, invasive candidiasis, and esophageal candidiasis; additionally, empiric therapy in febrile neutropenia and invasive aspergillosis refractory to or intolerant of other therapy… | FDA approved | The echinocandins are FDA-approved for invasive Candida infections and related indications, supported by randomized trials against amphotericin B and fluconazole. | Echinocandin antifungal lipopeptides that block fungal cell-wall synthesis | The echinocandins (caspofungin, micafungin, and anidulafungin; sold as Cancidas, Mycamine, and Eraxis) are antifungal lipopeptides that attack the fungal cell wall, a structure human cells lack. They are a preferred option for invasive Candida infections and are generally well tolerated. All three have been FDA-approved in the U.S. since the 2000s, a fourth (rezafungin, sold as Rezzayo) was approved in 2023, and all are given intravenously. | Echinocandins target the fungal cell wall, specifically the enzyme 1,3-beta-D-glucan synthase. This enzyme builds 1,3-beta-D-glucan, a structural sugar polymer that gives the fungal wall its integrity. By blocking it, echinocandins weaken the wall until the fungal cell can no longer withstand internal pressure and ruptures. They are fungicidal against most Candida species and fungistatic against Aspergillus. A key advantage is selectivity: human cells have no cell wall and no equivalent of this enzyme, so echinocandins cause relatively little direct toxicity to the patient. Caspofungin, micafungin, and anidulafungin are given intravenously once daily, and rezafungin once weekly. In its pivotal trial, caspofungin was at least as effective as amphotericin B for invasive candidiasis while causing fewer adverse effects, and anidulafungin outperformed fluconazole on the primary measure in its own trial. | 0 | 0 | 0 | Common side effects include: - Fever - Infusion-related reactions such as flushing, rash, or itching - Nausea and headache - Low potassium and raised liver enzymes More serious considerations include: - Liver effects and, rarely, more significant liver dysfunction - Rare severe allergic reactions - Dose adjustment for caspofungin in liver impairment and some drug interactions | 2 | https://doi.org/10.1056/NEJMoa021585 ; https://doi.org/10.1056/NEJMoa066906 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
47 | Efpeglenatide | https://superpower.com/guides/peptides/efpeglenatide | Hormones & metabolism | In clinical trials | Long-acting GLP-1 agonist | Investigational peptide, not approved by the FDA or EMA | Deep research | It has a large, positive, peer-reviewed Phase 3 cardiovascular outcomes trial plus supportive glycemic data, though it is not approved in major markets. | Long-acting GLP-1 receptor agonist given as a once-weekly injection | A large Phase 3 cardiovascular outcomes trial (AMPLITUDE-O) reported positive results | Efpeglenatide is an investigational long-acting GLP-1 receptor agonist, originally developed by Hanmi Pharmaceutical, given as a once-weekly injection for type 2 diabetes and cardiovascular risk. In a large Phase 3 outcomes trial it reduced major cardiovascular events in people with type 2 diabetes. As of 2026, it has not reached approval in major markets. | Efpeglenatide activates the GLP-1 receptor, the same incretin target as drugs such as semaglutide and dulaglutide. Activation of the receptor: - Enhances glucose-dependent insulin secretion - Suppresses glucagon - Slows gastric emptying - Reduces appetite In people with type 2 diabetes these effects lower blood sugar and body weight, and GLP-1 agonists as a class have also shown cardiovascular benefits. This describes the mechanism, separate from the trial outcomes below. | The key evidence is a large cardiovascular outcomes trial. According to PubMed, the Phase 3 AMPLITUDE-O trial enrolled over 4,000 adults with type 2 diabetes who had cardiovascular or kidney disease. The table summarizes what it and a follow-up analysis reported: Endpoint | Finding Major adverse cardiovascular events | Occurred less often with efpeglenatide than placebo (hazard ratio 0.73) Composite kidney outcome | Reduced with efpeglenatide Benefit by SGLT2 inhibitor use | A prespecified analysis found the benefit was consistent regardless of whether participants were already taking an SGLT2 inhibitor These are positive, peer-reviewed Phase 3 results, although the program has not reached approval. | 3 | 1 | 0 | 3 | https://www.ncbi.nlm.nih.gov/books/NBK551568/ ; https://doi.org/10.1056/NEJMoa2108269 ; https://doi.org/10.1161/CIRCULATIONAHA.121.057934 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
48 | Elamipretide | https://superpower.com/guides/peptides/elamipretide | Hormones & metabolism | In clinical trials | Mitochondria-targeting tetrapeptide | Yes, for one use, through the accelerated pathway. The FDA granted elamipretide accelerated approval on September 19, 2025, as Forzinity, to improve muscle strength in adults and children with Barth syndrome who weigh at least 30 kg. It is the first approved treatment for the condition. The regulatory path was contentious: - An earlier submission was turned down after the drug missed a walking-di… | FDA approved | It is approved (accelerated approval) for Barth syndrome, though that approval rests on a muscle-strength surrogate and small open-label data, with the randomized trial having missed its primary endpoints and a confirmatory trial still pending; its non-Barth uses remain unproven. | A mitochondria-targeting tetrapeptide, sold as Forzinity | Elamipretide is a mitochondria-targeting peptide that binds cardiolipin, a key molecule in the energy-producing inner membrane of mitochondria, developed by Stealth BioTherapeutics. It received FDA accelerated approval in 2025 as Forzinity for Barth syndrome, a rare genetic disorder of cardiolipin, making it the first approved treatment for that condition. Its approval rests on a muscle-strength surrogate measure with a confirmatory trial still required, and its other studied uses remain investigational. | Elamipretide binds cardiolipin in the inner mitochondrial membrane and helps stabilize the folded structure (cristae) where energy production takes place. By supporting that architecture, it is intended to improve the efficiency of the electron transport chain that generates ATP and to reduce harmful reactive oxygen species. In Barth syndrome, which is caused by mutations in the TAFAZZIN gene that disrupt cardiolipin remodeling, this mechanism is the rationale for treatment. Mechanism describes how the drug is thought to act, separate from the clinical outcomes that trials measure. | 0 | 0 | 0 | According to the prescribing information, the most common side effects are: - Injection-site reactions such as redness, pain, hardening, itching, bruising, and hives More serious considerations include: - Serious allergic reactions - A benzyl alcohol preservative, so it is not approved for newborns | 3 | https://doi.org/10.1016/j.gim.2024.101138 ; https://www.drugs.com/pro/forzinity.html ; https://doi.org/10.1186/s13023-025-03693-5 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
49 | Enfuvirtide | https://superpower.com/guides/peptides/enfuvirtide | Immune & defense | FDA-approved | HIV fusion inhibitor peptide | Enfuvirtide was approved by the FDA in 2003 for HIV-1 infection in treatment-experienced patients with ongoing viral replication despite antiretroviral therapy. Its maker discontinued Fuzeon in the U.S. on February 28, 2025, citing reduced need as newer treatments became available. | FDA approved | Enfuvirtide is FDA-approved for treatment-experienced HIV-1 infection, supported by the randomized TORO trials showing greater viral-load reduction. | An HIV-1 fusion (entry) inhibitor, a 36-amino-acid peptide | Enfuvirtide (formerly sold as Fuzeon) is a peptide HIV drug that blocks the virus from entering CD4 immune cells, the first of the so-called fusion inhibitors. It was used in treatment-experienced patients whose virus is no longer controlled by other antiretrovirals. It was FDA-approved in the U.S. in 2003, but Fuzeon was discontinued there in February 2025. | Enfuvirtide blocks the step where HIV fuses its envelope with the membrane of a CD4 immune cell to get inside. The viral surface protein gp41 must fold on itself, forming a hairpin-like structure, to pull the two membranes together. Enfuvirtide mimics a segment of gp41 and binds the region the protein needs to grip, preventing that folding. Without it, the virus cannot complete fusion and cannot enter the cell. Because it works outside the cell at the point of entry, its mechanism is entirely different from the drugs that act inside the cell on reverse transcriptase, protease, or integrase, which is why it retains activity against virus resistant to those classes. In the TORO trials, adding enfuvirtide to an optimized background regimen produced a significantly greater reduction in HIV-1 RNA than the background regimen alone. It must be injected twice daily, which, with frequent injection-site reactions, limits its use to situations where other options are exhausted. | 0 | 0 | 0 | Common side effects include: - Injection-site reactions such as pain, hardened lumps, redness, and cysts, which occur in nearly all patients - Diarrhea and nausea - Fatigue More serious considerations include: - An increased rate of bacterial pneumonia - Hypersensitivity reactions, which can recur if the drug is restarted | 2 | https://doi.org/10.1056/NEJMoa035026 ; https://gene.com/media/statements/ps_081924 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
50 | Enlicitide | https://superpower.com/guides/peptides/enlicitide | Digestive & weight | In clinical trials | Oral macrocyclic PCSK9 inhibitor peptide | FDA-approved oral PCSK9 inhibitor, sold as Lipfendra, taken as a once-daily tablet | FDA approved | It is approved by the FDA to lower LDL cholesterol, supported by multiple large, positive Phase 3 trials showing LDL reductions comparable to injectable PCSK9 antibodies. | Macrocyclic peptide that blocks PCSK9, the first oral drug in a class previously limited to injections | In Phase 3 trials, lowered LDL cholesterol by about 60% | Enlicitide is an oral PCSK9 inhibitor, the first in its class that can be taken as a once-daily tablet rather than an injection, developed by Merck to lower LDL ("bad") cholesterol. In large Phase 3 trials it lowered LDL cholesterol by roughly 60%, comparable to injectable PCSK9 antibodies. It was approved by the FDA in 2026 under the brand name Lipfendra. | Enlicitide binds circulating PCSK9 and stops it from attaching to the LDL receptor on liver cells. Normally PCSK9 marks those receptors for destruction, so blocking it lets more LDL receptors return to the cell surface and recycle. With more receptors available, the liver pulls more LDL cholesterol out of the blood, lowering LDL levels. Achieving this with a peptide small and stable enough to survive oral dosing is what distinguishes enlicitide from the injectable drugs in its class. | 0 | 0 | 0 | In the larger Phase 3 trial, CORALreef Lipids, side effects occurred at similar rates with enlicitide and placebo. In the trial of adults with HeFH, the most common side effects reported more often than with placebo were: - Dizziness (9% with enlicitide, 4% with placebo) - Diarrhea (7% with enlicitide, 2% with placebo) In both trials, similar proportions of people in the enlicitide and placebo groups stopped treatment because of a side effect. The prescribing information advises stopping enlicitide when pregnancy is recognized unless the benefits of treatment outweigh the potential risks to the fetus. It has the full safety details, and people should review their individual risks and other medications with their prescriber. | 4 | https://doi.org/10.1056/NEJMoa2511002 ; https://www.merck.com/product/usa/pi_circulars/l/lipfendra/lipfendra_pi.pdf ; https://www.merck.com/news/mercks-lipfendra-enlicitide-is-the-first-and-only-once-daily-oral-pcsk9-inhibitor-approved-by-the-u-s-fda-to-reduce-ldl-c-in-adults-with-hypercholesterolemia/ ; https://doi.org/10.1016/j.jacc.2026.03.036 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
51 | Epitalon | https://superpower.com/guides/peptides/epitalon | Brain & sleep | Wellness and performance | Pineal tetrapeptide (Ala-Glu-Asp-Gly) | Non-FDA-approved peptide sold in the wellness/gray market | Low research | The human data are sparse, dated, single-source, and not independently replicated, so any longevity or wellness benefit is unestablished. | Synthetic pineal tetrapeptide (Ala-Glu-Asp-Gly) marketed for longevity | Human evidence is sparse, dated, and from a single non-independent source | Epitalon is a synthetic four-amino acid peptide based on a pineal-gland extract, sold on the "research peptide" market for anti-aging and sleep. Its human evidence is limited to older studies from a single Russian research group, not independently replicated. As of 2026 it is not FDA-approved, though a 2026 FDA advisory committee gave a non-binding favorable vote toward allowing it to be compounded. | Epitalon is proposed to: - Help restore the body's melatonin rhythm - Act as an antioxidant - Influence gene expression, including claims of activating telomerase (an enzyme linked to cellular aging) These mechanistic claims rest on cell-culture and animal work, with the telomerase findings coming from laboratory systems. This describes the proposed mechanism, separate from demonstrated benefit in people. | The human evidence is limited and single-source. The main human reports come from one Russian research group and include older studies on melatonin rhythm and age-related conditions; these are generally small, largely non-English, and not independently replicated with modern randomization and blinding. No independent, large, modern trial establishes a longevity or wellness benefit. The telomerase and lifespan claims rest mainly on laboratory and animal work. | 0 | 0 | 0 | Are there side effects associated with Epitalon? No clinical safety studies of Epitalon in humans have been identified in the published literature. The Russian observational cohort studies and animal studies do not document significant adverse events at the doses studied. The absence of reported harms does not establish safety; it reflects the absence of adequately controlled human safety data. The long-term effects of Epitalon administration in humans, including effects on cell proliferation and oncogenesis given its telomerase-activating mechanism, have not been systematically studied. | 11 | 12374906; 40908429; 14523363; 38160808 | https://pubmed.ncbi.nlm.nih.gov/12374906/ ; https://doi.org/10.1023/a:1025493705728 ; https://doi.org/10.1023/a:1021104819170 ; https://www.ajmc.com/view/fda-panel-backs-6-peptides-for-compounding ; https://pubmed.ncbi.nlm.nih.gov/40908429/ ; https://www.fda.gov/media/193345/download ; https://pubmed.ncbi.nlm.nih.gov/14523363/ ; https://www.deadiversion.usdoj.gov/schedules/orangebook/c_cs_alpha.pdf ; https://www.fda.gov/media/94155/download ; https://www.statnews.com/2026/07/24/fda-peptide-compounding-panel-backs-epitalon-rejects-emideltide/ ; https://pubmed.ncbi.nlm.nih.gov/38160808/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
52 | Eptifibatide | https://superpower.com/guides/peptides/eptifibatide | Heart & blood | FDA-approved | GPIIb/IIIa inhibitor | Yes. Eptifibatide was approved by the FDA in 1998 for acute coronary syndrome, including patients managed medically and those undergoing percutaneous coronary intervention. It is given intravenously as a bolus followed by an infusion. | FDA approved | Eptifibatide is FDA-approved for acute coronary syndrome and PCI, supported by large randomized trials including PURSUIT showing reduced death or heart attack. | A platelet glycoprotein IIb/IIIa receptor antagonist, a cyclic heptapeptide antiplatelet drug | Eptifibatide (sold as Integrilin) is a small cyclic peptide, modeled on a molecule from rattlesnake venom, that blocks the final step of platelet clumping to prevent dangerous clots during heart attacks and stenting. It is given intravenously in acute coronary syndrome and during coronary procedures. It has been FDA-approved in the U.S. since 1998, and its main risk is bleeding. | Eptifibatide blocks the glycoprotein IIb/IIIa receptor on platelets, the receptor that represents the final common step in platelet aggregation. Normally, when platelets are activated, this receptor binds fibrinogen and links platelets together into a clot. Eptifibatide occupies the receptor and prevents that cross-linking, so platelets cannot aggregate even if they have been activated. The effect is potent but rapidly reversible once the infusion stops, because the drug binds the receptor reversibly. That makes it useful in the acute setting of a heart attack or a coronary stent procedure, where fresh clot formation on a disrupted plaque or a new stent is the danger. In the PURSUIT trial, eptifibatide reduced the combined rate of death or nonfatal heart attack at 30 days in acute coronary syndrome, at the cost of more bleeding. It is cleared by the kidneys, so dosing is reduced in kidney impairment. | 0 | 0 | 0 | Common side effects include: - Bleeding, especially at the vascular access site - Low blood pressure More serious considerations include: - Major hemorrhage, the principal risk - Low platelet count (thrombocytopenia) The prescribing information lists these effects and also contraindicates eptifibatide in people with active or recent serious bleeding, severe uncontrolled high blood pressure, or dialysis-dependent kidney failure, among other conditions. | 3 | 2033037 | https://pubmed.ncbi.nlm.nih.gov/2033037/ ; https://doi.org/10.1056/NEJM199808133390704 ; https://www.merck.com/product/usa/pi_circulars/i/integrilin/integrilin_pi.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
53 | Etelcalcetide | https://superpower.com/guides/peptides/etelcalcetide | Bones & muscles | FDA-approved | Calcimimetic peptide | Yes. Etelcalcetide was approved by the FDA in 2017 for secondary hyperparathyroidism in adults on hemodialysis. It is administered as an intravenous bolus at the end of each dialysis session, three times a week. | FDA approved | Etelcalcetide is FDA-approved for secondary hyperparathyroidism in dialysis patients, supported by randomized trials including a head-to-head comparison with cinacalcet. | A peptide calcimimetic that activates the calcium-sensing receptor | Etelcalcetide (sold as Parsabiv) is a peptide that activates the calcium-sensing receptor to lower parathyroid hormone, used for secondary hyperparathyroidism in people on dialysis for kidney disease. Unlike parathyroid hormone replacement, it suppresses an overactive parathyroid signal, and it is given intravenously at the end of each dialysis session. It has been FDA-approved in the U.S. since 2017. | Etelcalcetide binds and activates the calcium-sensing receptor on the parathyroid glands, increasing the receptor's sensitivity to calcium. The glands interpret this as a signal that calcium is adequate and reduce their secretion of parathyroid hormone, which in turn lowers the high calcium and phosphate turnover that drives bone and cardiovascular problems in dialysis patients. This is the opposite approach to parathyroid hormone replacement: etelcalcetide turns the hormone down rather than supplying it. Because it is a peptide given intravenously into the dialysis circuit, it does not depend on a patient taking a daily pill, which can improve adherence. In a head-to-head randomized trial, intravenous etelcalcetide lowered parathyroid hormone at least as effectively as oral cinacalcet, with a greater proportion of patients achieving large reductions. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Low blood calcium - Muscle spasms - Nausea, vomiting, and diarrhea - Headache More serious considerations include: - Serious low calcium, which can cause seizures or heart-rhythm changes, so calcium is monitored - Worsening heart failure in some patients - Upper gastrointestinal bleeding | 2 | https://doi.org/10.1001/jama.2016.19468 ; https://www.pi.amgen.com/united_states/parsabiv/parsabiv_pi.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
54 | Exenatide | https://superpower.com/guides/peptides/exenatide | Hormones & metabolism | FDA-approved | GLP-1 receptor agonist | FDA-approved GLP-1 peptide, formerly sold as Byetta (twice-daily) and Bydureon (once-weekly) for type 2 diabetes | FDA approved | It is approved by the FDA for type 2 diabetes and was the first medicine in the GLP-1 class, supported by its randomized controlled trial program. | Exenatide is the first GLP-1 receptor agonist ever approved, a synthetic copy of exendin-4 originally found in Gila monster venom, dosed twice daily as Byetta or once weekly as Bydureon. Approved in 2005, it launched the entire GLP-1 class and delivered modest reductions in blood sugar and weight. AstraZeneca discontinued both U.S. brands in 2024, and a generic of the twice-daily form has been sold since 2025. | Exenatide lowers blood sugar by activating the GLP-1 receptor, mimicking a gut hormone the body releases after meals. Through that receptor it triggers glucose-dependent insulin release, which keeps the risk of hypoglycemia low on its own, while lowering glucagon, slowing the rate at which the stomach empties, and reducing appetite. Because it is based on the lizard peptide exendin-4 rather than human GLP-1, it resists the enzyme that rapidly breaks down natural GLP-1, so it lasts long enough to be dosed twice daily. The extended-release Bydureon formulation encases the peptide in tiny microspheres that release it slowly, allowing once-weekly dosing. In its trials it produced moderate reductions in A1c along with some weight loss. Exenatide is the original GLP-1 drug, and the medicines that followed have largely surpassed it on both effectiveness and convenience. The clearest difference is potency, especially for weight. Exenatide produces relatively modest reductions in blood sugar a… | 0 | 0 | 0 | The most common side effects are gastrointestinal, with nausea especially common: - Nausea - Vomiting - Diarrhea - Feeling jittery - Dizziness - Headache - Decreased appetite Less common but more serious risks include: - Pancreatitis, or inflammation of the pancreas - Low blood sugar, especially when combined with a sulfonylurea - Acute kidney injury, usually from dehydration caused by vomiting or diarrhea - Gallbladder problems, including gallstones - Injection-site lumps with the extended-release form - For the extended-release Bydureon form, a boxed warning for thyroid C-cell tumors based on rodent studies, which is not carried by the twice-daily Byetta | 7 | 21194543 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/209210s024lbl.pdf ; https://pubmed.ncbi.nlm.nih.gov/21194543/ ; https://www.uhcprovider.com/en/resource-library/news/2024/discontinuation-bydureon-bcise-byetta.html ; https://doi.org/10.1056/NEJMoa1411892 ; https://doi.org/10.1056/NEJMoa2032183 ; https://doi.org/10.1056/NEJMoa2206038 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/215866s031lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
55 | Follistatin-344 | https://superpower.com/guides/peptides/follistatin-344 | Bones & muscles | Wellness and performance | Myostatin-inhibiting peptide | Non-FDA-approved peptide sold as a research chemical/performance drug | Low research | The myostatin-inhibition rationale is strong in animals, but there is no human efficacy evidence for the injectable peptide; the only human data come from small gene-therapy disease trials that do not transfer to the wellness use. | Myostatin-binding protein, marketed to remove a natural brake on muscle growth | Human data come only from small gene-therapy disease trials, not the injectable peptide | Follistatin-344 is a form of the natural protein follistatin that blocks myostatin, a brake on muscle growth, sold as a "research chemical" in the performance market for muscle gain. The strongest human data come from gene therapy, not the injectable peptide. In a small 2017 trial, six patients with sporadic inclusion body myositis gained a median 56.0 m per year on the 6-minute walk test after follistatin gene therapy, versus a 25.8 m decline in eight matched untreated controls (p = 0.01). It is not FDA-approved and is banned in sport. | Myostatin normally limits how much muscle the body builds. By binding and neutralizing myostatin, follistatin is proposed to release that brake and allow greater muscle growth. This pathway is well supported in animal models, where disrupting myostatin signaling produces pronounced muscle growth. This describes the proposed mechanism, which comes from animal work, separate from proven outcomes in people using the injectable peptide. | The human evidence belongs to gene therapy, not the peptide. According to PubMed, a small Phase 1/2a trial used a gene therapy delivering the follistatin (FS344) gene in six patients with Becker muscular dystrophy, reporting some walking improvements and muscle changes; follow-up reported ambulation data. This is a disease population and a gene-therapy delivery, not the injectable follistatin peptide sold for wellness, and it does not establish efficacy or safety of that peptide in healthy people. There are no controlled human trials of the injectable peptide. Two small studies of this gene therapy report walking results: Study | Patients | Design | Result Phase 1/2a trial in Becker muscular dystrophy | 6 treated | No placebo group | 4 of the 6 walked farther on the 6-minute walk test, by 29 m to 125 m; muscle biopsies showed less fibrosis Study in sporadic inclusion body myositis, an inflammatory muscle disease, published in 2017 | 6 treated, versus 8 matched, untreated controls | Same gene therapy alongside an exercise regimen; controls not randomized | Treated patients gained a median 56.0 m per year on the 6-minute walk test, versus a 25.8 m decline in controls (p = 0.01), with individual changes of 5 to 153 m The 2017 sample was tiny and the controls were not randomized, so that result is hypothesis-generating. | 2 | 2 | 0 | 5 | 25322757; 28279643 | https://doi.org/10.1038/387083a0 ; https://doi.org/10.1038/mt.2014.200 ; https://doi.org/10.3233/jnd-150083 ; https://pubmed.ncbi.nlm.nih.gov/25322757/ ; https://pubmed.ncbi.nlm.nih.gov/28279643/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
56 | Fragment 176-191 | https://superpower.com/guides/peptides/fragment-176-191 | Digestive & weight | Wellness and performance | GH C-terminal fragment | Non-FDA-approved peptide sold in the wellness/gray market | Low research | The fat-metabolism rationale is supported only by animal and laboratory work, there is no human efficacy evidence for the fragment itself, and its optimized cousin failed in human trials. | C-terminal fragment of the growth hormone molecule, marketed for fat loss | Evidence is animal and laboratory only; its optimized cousin AOD-9604 failed human trials | Fragment 176-191 is the unmodified tail piece of human growth hormone, sold on the wellness market as a fat-loss "research peptide." Its evidence is limited to animal and laboratory work. In rat fat-pad experiments, a close relative (hGH 177-191) matched whole growth hormone's antilipogenic activity but showed no significant lipolytic effect (Wu and Ng, 1993). Its modified cousin, AOD-9604, failed in human obesity trials. As of 2026 the fragment is not FDA-approved and is banned in sport. | The proposed theory is that the fat-related activity of growth hormone is concentrated in this tail fragment, so the fragment alone might reduce fat storage without the hormone's growth or glucose effects. In rat studies, the fragment was shown to carry the anti-fat-storage activity of the parent hormone, localizing that function to the C-terminal region. The tested peptide was hGH 177-191, a close relative of this fragment, and it showed no significant lipolytic effect in rat fat pads. These are animal and cell findings. This describes the proposed mechanism, separate from proven outcomes. The more detailed mechanism data belong to AOD-9604, the modified version, and not to the bare fragment. In obese Zucker rats, AOD-9604 cut weight gain over 50% in 19 days and raised lipolytic activity in adipose tissue, without the insulin-sensitivity harm seen with intact growth hormone. In obese mice, AOD-9604 increased fat oxidation and plasma glycerol, a marker of fat breakdown, and it did not… | The evidence is preclinical. Animal work localized the anti-lipogenic activity of growth hormone to this C-terminal fragment, and the closest human data belong to its modified version, AOD-9604, whose obesity trials failed to beat placebo. There are no controlled human trials of the bare fragment for fat loss, so its marketed benefit is unproven. The human data belong to AOD-9604, as reported in a review of obesity drug development. AOD-9604 trial | Result 12-week trial | AOD-9604 recipients lost 2.6 kg against 0.8 kg on placebo 24-week trial of 536 people | Failed to produce significant weight loss, which ended the obesity program Those results do not describe the bare fragment, which has not been tested in controlled human trials. | 2 | 2 | 0 | 5 | 8358331; 11146367; 11673763; 23092275 | https://pubmed.ncbi.nlm.nih.gov/8358331/ ; https://pubmed.ncbi.nlm.nih.gov/11146367/ ; https://pubmed.ncbi.nlm.nih.gov/11673763/ ; https://pubmed.ncbi.nlm.nih.gov/23092275/ ; https://doi.org/10.1159/000053183 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
57 | Ga-68 dotatate | https://superpower.com/guides/peptides/ga-68-dotatate | Digestive & weight | FDA-approved | SSTR imaging radiopeptide | Yes. Gallium Ga-68 dotatate (NETSPOT) was approved by the FDA in 2016 for the localization of somatostatin-receptor-positive neuroendocrine tumors by PET in adult and pediatric patients. It is given as a single intravenous injection before the scan. | FDA approved | Gallium Ga-68 dotatate is FDA-approved for PET imaging of neuroendocrine tumors, supported by studies showing high detection sensitivity and impact on management. | A gallium-68-labeled somatostatin analog used as a PET imaging agent | Gallium Ga-68 dotatate (sold as NETSPOT) is a radioactive imaging agent that attaches a tracer to a somatostatin analog to light up neuroendocrine tumors on a PET scan. It finds tumors that carry somatostatin receptors, helping doctors locate and stage them. It has been FDA-approved in the U.S. since 2016 and is given as a single intravenous injection before imaging. | The dotatate portion of the molecule binds with high affinity to somatostatin receptor subtype 2, which is overexpressed on well-differentiated neuroendocrine tumor cells. When injected, the tracer concentrates wherever those receptors are abundant, and the attached gallium-68 emits positrons that produce a signal on a PET scan. The result is a map that highlights tumor sites throughout the body, including small lesions that other imaging can miss. This receptor-targeted approach is more sensitive than the older somatostatin imaging agents. In a prospective study, gallium-68 dotatate PET/CT performed at least as well as, and often better than, the earlier indium-111 agent and changed management in about a third of patients. It is a diagnostic tool and is not itself a treatment, though its target is the same one used by the companion therapy lutetium Lu-177 dotatate. | 0 | 0 | 0 | No serious adverse reactions were identified in its clinical studies, according to the prescribing information. Side effects reported since approval include: - Pain or a burning sensation at the injection site - Nausea and vomiting More serious considerations include: - Radiation exposure, inherent to any radiopharmaceutical, kept as low as reasonably achievable - Hypersensitivity reactions, mostly rash and itching, and less often swelling or anaphylaxis-like reactions | 2 | https://doi.org/10.2967/jnumed.115.163865 ; https://www.novartis.com/us-en/sites/novartis_us/files/netspot.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
58 | Ganirelix | https://superpower.com/guides/peptides/ganirelix | Sexual & reproductive | FDA-approved | GnRH antagonist | Yes. Ganirelix, developed by Organon, was approved by the FDA in 1999. It is approved as a 0.25 mg once-daily subcutaneous injection for use during controlled ovarian stimulation. The Antagon brand name is no longer used in the U.S., where the product is now sold as ganirelix acetate injection and as Fyremadel. | FDA approved | Ganirelix is FDA-approved for preventing premature luteinizing hormone surges during IVF, supported by phase 3 trials showing pregnancy rates comparable to agonist protocols. | A GnRH receptor antagonist peptide used in assisted reproduction | Ganirelix (originally approved as Antagon) is a synthetic decapeptide that blocks the gonadotropin-releasing hormone receptor, used during fertility treatment to stop an egg from being released too early. Given once daily during ovarian stimulation, it prevents the premature luteinizing hormone surge that could otherwise disrupt an IVF cycle. It has been FDA-approved in the U.S. since 1999 and is given as a small daily subcutaneous injection. | Ganirelix competitively blocks GnRH receptors on the pituitary, rapidly suppressing the release of luteinizing hormone and follicle-stimulating hormone. During an IVF cycle, the ovaries are stimulated with injectable hormones to grow multiple follicles; if the body's own luteinizing hormone surges before those follicles are ready, ovulation can happen too early and the cycle can be lost. Giving ganirelix during stimulation holds that surge in check so eggs can be retrieved at the planned time. Because it is an antagonist, its effect is immediate and reversible, which allows a shorter, more flexible protocol than the older agonist-based approach that first had to suppress the pituitary over days. In a North American phase 3 trial, ganirelix compared with a long leuprolide protocol as follows: Outcome | Ganirelix vs long leuprolide protocol Ongoing pregnancy rates | Comparable Number of injections | Fewer Injection-site reactions | Fewer | 0 | 0 | 0 | It is approved as a 0.25 mg once-daily subcutaneous injection for use during controlled ovarian stimulation. | According to the prescribing information, common side effects include: - Injection-site reactions - Headache - Nausea - Abdominal or pelvic discomfort More serious considerations include: - Ovarian hyperstimulation syndrome, a risk of the overall stimulation cycle rather than of ganirelix specifically - Hypersensitivity reactions Ganirelix is contraindicated in pregnancy. | 4 | https://www.drugs.com/pro/fyremadel.html ; https://doi.org/10.1016/s0015-0282(00)01638-1 ; https://organonpro.com/en-us/product/ganirelix-acetate-injection/ ; https://www.organon.com/product/usa/pi_circulars/g/ganirelix/ganirelix_pi.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
59 | GHK-Cu | https://superpower.com/guides/peptides/ghk-cu | Skin & aging | Wellness and performance | Copper-binding tripeptide | Not FDA-approved (systemic/injectable use) | Low research | Systemic efficacy rests on animal and laboratory signaling data, with no controlled human trials for the injectable wellness use. | Copper-binding tripeptide involved in matrix remodeling and repair | For systemic use, evidence is animal and laboratory only; human data relate mostly to topical use | GHK-Cu is a copper-binding tripeptide involved in tissue repair, sold on the wellness market as an injectable for skin, hair, and tissue repair. For this systemic use the evidence is preclinical, with no controlled human trials; its better-studied role is topical. As of 2026 the injectable/systemic use is not FDA-approved. | In laboratory and animal models, GHK-Cu is described as a signal for tissue remodeling. It is reported to: - Influence the extracellular matrix - Deliver copper - Act as an antioxidant and anti-inflammatory - Support new blood-vessel formation - Switch on gene programs linked to repair These are cell and animal findings. This describes the proposed mechanism, separate from demonstrated benefit from systemic use in people. | For systemic use, the evidence is preclinical. The table sets out what has been studied in each model, with both animal studies drawn from PubMed: Model | Finding Rat | Injected GHK-Cu transiently improved ligament-graft healing Mouse | GHK-Cu reduced acute lung injury Human | Data essentially limited to topical cosmetic and wound contexts; no robust human trials establish efficacy or safety of injected GHK-Cu for skin, hair, or tissue repair The systemic benefit is therefore an extrapolation from cell and animal work. | 3 | 1 | 2 | 17 | 26236730; 3169264; 8227353; 14648529; 8326148; 17703734; 1809108; 15773538; 7544967 | https://doi.org/10.3390/brainsci7020020 ; https://doi.org/10.1002/jor.22831 ; https://doi.org/10.18632/oncotarget.11168 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC6073405/ ; https://pubmed.ncbi.nlm.nih.gov/26236730/ ; https://pubmed.ncbi.nlm.nih.gov/3169264/ ; https://pubmed.ncbi.nlm.nih.gov/8227353/ ; https://pmc.ncbi.nlm.nih.gov/articles/PMC4508379/ ; https://pubmed.ncbi.nlm.nih.gov/14648529/ ; https://pubmed.ncbi.nlm.nih.gov/8326148/ ; https://pubmed.ncbi.nlm.nih.gov/17703734/ ; https://pubmed.ncbi.nlm.nih.gov/1809108/ ; https://pubmed.ncbi.nlm.nih.gov/15773538/ ; https://pubmed.ncbi.nlm.nih.gov/7544967/ ; https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=021108 ; https://pmc.ncbi.nlm.nih.gov/articles/PMC3359723/ ; https://pmc.ncbi.nlm.nih.gov/articles/PMC4180391/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
60 | GHRP-2 | Pralmorelin | https://superpower.com/guides/peptides/ghrp-2 | Bones & muscles | Wellness and performance | GHRP / ghrelin agonist | Non-FDA-approved peptide (also known as pralmorelin) sold in the wellness/gray market | Low research | It is validated only as a short-acting growth hormone diagnostic stimulus, with no controlled human evidence supporting the marketed muscle, recovery, or anti-aging uses. | Ghrelin-receptor agonist/growth hormone-releasing peptide | GHRP-2 (pralmorelin) is a synthetic ghrelin-mimic peptide that prompts the pituitary to release growth hormone, sold in the wellness market for muscle, recovery, and appetite. Its only genuine validated use is as a diagnostic test of growth hormone capacity (approved in Japan), not as a treatment, and there are no controlled trials supporting the marketed wellness benefits. As of 2026 it is not FDA-approved and is banned in sport. | GHRP-2 activates the growth hormone secretagogue receptor (the ghrelin receptor) on the pituitary. Activating it has three reported effects: - It triggers a pulse of growth hormone, and growth hormone pulses raise IGF-1 downstream. - It tends to modestly raise other hormones such as cortisol and prolactin. - Like other ghrelin mimics, it can stimulate appetite. The marketed muscle and recovery claims are extrapolated from this hormone effect rather than demonstrated. This describes the proposed mechanism, separate from proven outcomes. | The validated human data concern diagnosis, not treatment. According to PubMed, GHRP-2 is used to probe pituitary growth hormone reserve, as in a study of the growth hormone response, which is a diagnostic application rather than a wellness-outcome trial. There are no controlled human trials showing that GHRP-2 improves muscle, fat, recovery, or aging. The marketed uses rest on its ability to raise growth hormone, not on demonstrated benefit. | 0 | 0 | 0 | 2 | https://doi.org/10.1210/jc.2004-1719 ; https://doi.org/10.1016/j.ghir.2023.101545 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
61 | GHRP-6 | https://superpower.com/guides/peptides/ghrp-6 | Bones & muscles | Wellness and performance | GHRP / ghrelin agonist | Non-FDA-approved peptide sold in the wellness/gray market | Low research | Human data are limited to short studies of growth hormone release, with the marketed wellness benefits resting on animal and laboratory work. | Ghrelin-receptor agonist / growth hormone-releasing peptide that markedly increases appetite | Human data are limited to short pharmacology studies; the marketed benefits are unproven | GHRP-6 is one of the original synthetic ghrelin-mimic peptides, sold in the wellness market to raise the body's own growth hormone and stimulate appetite. Human data are limited to short studies of growth hormone release, with no controlled trials proving the marketed muscle, recovery, or anti-aging benefits. As of 2026 it is not FDA-approved and is banned in sport. | GHRP-6 activates the growth hormone secretagogue receptor (the ghrelin receptor), prompting the pituitary to release growth hormone, and it is proposed to act partly by blunting the body's growth-hormone "brake," somatostatin. Compared with newer peptides it is less selective, notably: - Increasing appetite - Modestly raising cortisol - Modestly raising prolactin Laboratory work also describes growth hormone secretagogue receptors in heart and blood-vessel tissue, which is the basis for preclinical interest in other effects. The marketed benefits are extrapolated from the growth hormone rise. This describes the proposed mechanism, separate from proven outcomes. | The human evidence is short pharmacology. According to PubMed, an infusion study in healthy men found GHRP-6 raised growth hormone and IGF-1 while the pituitary remained responsive, a hormone-level result rather than a clinical outcome. Cardiovascular and cell-protective effects are described mainly in preclinical work and reviews. No controlled human trials support the marketed muscle, fat, recovery, or anti-aging uses. | 0 | 0 | 0 | 3 | https://doi.org/10.1161/01.res.0000016164.02525.b4 ; https://doi.org/10.1210/jcem.77.6.7903313 ; https://doi.org/10.1016/j.tem.2005.11.004 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
62 | Glepaglutide | https://superpower.com/guides/peptides/glepaglutide | Digestive & weight | In clinical trials | GLP-2 analog | Investigational peptide, not approved by the FDA | Moderate research | Its pivotal Phase 3 was positive for the twice-weekly regimen only, the once-weekly arm was null, and the FDA issued a Complete Response Letter requiring further evidence. | Long-acting GLP-2 analog given by subcutaneous injection for short bowel syndrome | Glepaglutide is an investigational long-acting GLP-2 analog, developed by Zealand Pharma as a subcutaneous injection for short bowel syndrome. In its Phase 3 trial the twice-weekly regimen reduced the need for intravenous nutrition, but the once-weekly regimen did not, and the FDA issued a Complete Response Letter in 2024 asking for more evidence. As of 2026 it is not approved. | Glepaglutide activates the GLP-2 receptor in the intestine. This signaling promotes growth and adaptation of the intestinal lining and increases nutrient and fluid absorption, with the goal of reducing dependence on intravenous feeding in short bowel syndrome. This describes the mechanism, separate from the trial results below. | The main evidence is one Phase 3 trial with a mixed result. According to PubMed, the two studies found: Study | Design | Result EASE trial | Phase 3, testing glepaglutide twice weekly, once weekly, or placebo | The twice-weekly regimen met the primary endpoint, reducing weekly intravenous support volume versus placebo and improving key secondary measures, but the once-weekly regimen did not reach significance Smaller study | Phase 3b | Reported increased energy absorption and reduced parenteral support over a year The evidence rests on a single pivotal trial in which one of the two tested regimens was negative. | 2 | 2 | 0 | 2 | https://doi.org/10.1053/j.gastro.2024.11.023 ; https://doi.org/10.1016/j.clnesp.2025.08.006 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
63 | Glucagon | https://superpower.com/guides/peptides/glucagon | Digestive & weight | FDA-approved | Glucagon receptor agonist | Yes. Glucagon is approved for severe hypoglycemia and as a diagnostic aid for gastrointestinal imaging. The table shows when each product was approved: Product | Type | FDA approval Glucagon for injection, including the recombinant GlucaGen | Injection | Approved for decades Gvoke | Newer ready-to-use injector | 2019 Baqsimi | Newer ready-to-use nasal powder | 2019 | FDA approved | Glucagon is FDA-approved for severe hypoglycemia and as a diagnostic aid, supported by long clinical use and trials of its injectable and nasal forms. | A pancreatic peptide hormone that raises blood glucose (counter-regulatory to insulin) | Glucagon (brands include Gvoke and the nasal powder Baqsimi) is a pancreatic hormone that raises blood sugar fast, used as emergency treatment for severe low blood sugar in people with diabetes. It signals the liver to release stored glucose. Glucagon products have long been FDA-approved in the U.S., and modern forms include ready-to-use injectors and a needle-free nasal powder. | Glucagon binds glucagon receptors on liver cells and switches on the pathways that release glucose. It stimulates glycogenolysis, the breakdown of stored glycogen into glucose, and gluconeogenesis, the making of new glucose, so the liver pushes glucose into the bloodstream and blood sugar rises within minutes. This is why it works as a rescue treatment when someone with hypoglycemia is unable to eat or drink. Because the effect depends on the liver having glucose stores to release, glucagon can be less effective when those stores are depleted, such as in prolonged fasting or starvation. Glucagon also relaxes the smooth muscle of the gastrointestinal tract, which is the basis of its separate use as a diagnostic aid during certain imaging studies. In a trial in adults with type 1 diabetes, a nasal powder formulation raised blood glucose about as effectively as injected glucagon, with the practical advantage of needing no injection or mixing in an emergency. | 0 | 0 | 0 | According to the injectable and nasal powder labels, common side effects include: - Nausea and vomiting - Headache - Injection-site reactions, or nasal and eye symptoms with the nasal powder More serious considerations include: - A sharp rise in blood pressure in people with pheochromocytoma - Low blood sugar rebound in people with insulinoma - Rare allergic reactions | 4 | https://www.novomedlink.com/diabetes/products/treatments/glucagen-hypokit.html ; https://doi.org/10.2337/dc15-1498 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/212097s000lbl.pdf ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/210134s000lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
64 | Glutathione | https://superpower.com/guides/peptides/glutathione | Skin & aging | Wellness and performance | Antioxidant tripeptide | Not FDA-approved as a drug; oral forms are sold as supplements and IV/inhaled forms are compounded | Moderate research | Multiple small randomized trials exist for skin-lightening and neurological uses, but the results are modest, mixed, short-term, and limited by study quality and oral bioavailability, so no clear benefit is established. | Naturally occurring antioxidant tripeptide | Small human trials for skin-lightening and neurological uses show modest, mixed results | Glutathione is a major antioxidant tripeptide inside the body's cells, sold as a supplement and, in wellness clinics, as an IV, injectable, or inhaled product for skin-lightening and general antioxidant support. Human trials are small and mixed. In a 6-month randomized trial of 153 people with cystic fibrosis, inhaled glutathione did not improve lung function (FEV1) over placebo (p = 0.180). The FDA has warned about compounded injectable glutathione, and as of 2026 glutathione is not FDA-approved as a drug. | Glutathione's biochemical role as a major intracellular antioxidant and detoxifier is well established; it neutralizes reactive molecules through enzyme systems. For skin-lightening, the proposed mechanism is inhibition of the pigment enzyme tyrosinase and a shift in pigment production toward lighter melanin. This describes the mechanism; the human evidence below tests whether supplementation produces the marketed effects. | There are several small human trials, with modest and mixed results. The skin results below are as reported on PubMed: Study | Area | Result 4-week trial of oral glutathione | Skin | Small reductions in skin pigment versus placebo 12-week trial of an oral combination | Skin | Reported skin lightening Systematic review | Skin | Skin-whitening evidence is inconclusive due to study quality and bioavailability concerns Randomized pilot of IV glutathione | Parkinson's disease | No significant benefit over placebo Meta-analysis | Parkinson's disease | Only a small motor-score improvement 6-month trial of oral glutathione in 54 non-smoking adults | Glutathione levels | Red blood cell, plasma, and lymphocyte glutathione rose 30% to 35% at the higher amount; levels returned to baseline after a 1-month washout 6-month randomized trial of inhaled glutathione in 153 people with cystic fibrosis | Lung function | FEV1 did not differ from placebo (p = 0.180), and oxidation markers did not change Overall the human evidence is real but modest, short-term, and inconsistent. | 7 | 4 | 0 | 8 | 24791752; 23631796 | https://www.fda.gov/media/94155/download ; https://doi.org/10.3109/09546631003801619 ; https://doi.org/10.1111/jocd.14137 ; https://doi.org/10.1111/jocd.12910 ; https://doi.org/10.1002/mds.22401 ; https://doi.org/10.3892/etm.2020.9557 ; https://pubmed.ncbi.nlm.nih.gov/24791752/ ; https://pubmed.ncbi.nlm.nih.gov/23631796/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
65 | Goserelin | https://superpower.com/guides/peptides/goserelin | Sexual & reproductive | FDA-approved | GnRH agonist | Yes. Goserelin, originally developed by ICI Pharmaceuticals (later Zeneca, now AstraZeneca), was approved by the FDA in 1989. The implant is available in a 3.6 mg monthly strength and a 10.8 mg three-month strength, and the approved indications have broadened over time across oncology and gynecology. | FDA approved | Goserelin is FDA-approved for prostate cancer, breast cancer, and endometriosis, backed by large randomized trials including the ZEBRA comparison with chemotherapy. | A GnRH (LHRH) receptor agonist peptide delivered as a subcutaneous implant | Goserelin (goserelin acetate, sold as Zoladex) is a synthetic decapeptide agonist of gonadotropin-releasing hormone delivered as a small implant that suppresses the body's production of testosterone and estrogen. It is used across prostate cancer, breast cancer, and endometriosis, and in one long-term breast-cancer trial it matched standard chemotherapy for survival in certain premenopausal women. It has been FDA-approved in the U.S. since 1989 and is given as a monthly or three-month depot implant. | Goserelin binds the GnRH receptor on pituitary cells. A first dose briefly stimulates the pituitary, causing a transient rise in luteinizing hormone and sex hormones known as the flare. Because the implant then delivers drug continuously rather than in natural pulses, the receptors downregulate and desensitize, and within a few weeks luteinizing hormone and follicle-stimulating hormone fall. Testosterone in men, or estrogen in women, drops to castrate or postmenopausal levels. Lowering those hormones is the point of treatment: Condition | Hormone lowered | Why it matters Prostate cancer | Testosterone | Hormone-sensitive tumors depend on it Premenopausal breast cancer | Ovarian estrogen | It can fuel estrogen-receptor-positive disease Endometriosis | Estrogen, inducing a reversible low-estrogen state | The low-estrogen state shrinks lesions In the long-term ZEBRA trial, goserelin was equivalent to standard CMF chemotherapy for disease-free and overall survival in premenopausal women w… | 0 | 0 | 0 | The implant is available in a 3.6 mg monthly strength and a 10. || 8 mg three-month strength, and the approved indications have broadened over time across oncology and gynecology. | According to the prescribing information, common side effects reflect reduced sex-hormone levels: - Hot flashes and sweating - Sexual dysfunction and vaginal dryness - Headache - Injection-site reactions - Bone-density loss with long-term use More serious considerations include: - Disease "flare" early in prostate-cancer treatment, sometimes managed with an anti-androgen - Increased risk of hyperglycemia and cardiovascular events with long-term androgen deprivation - Rare pituitary apoplexy | 2 | https://doi.org/10.1016/s0959-8049(03)00392-7 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/019726s076lbl020515s013lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
66 | Hexapeptide-9 | https://superpower.com/guides/peptides/hexapeptide-9 | Skin & aging | Cosmetic and topical | Signal peptide | As a cosmetic ingredient rather than a drug, does not require FDA approval | Low research | The ingredient's rationale rests on laboratory and manufacturer data, and the only controlled human study tested a modified version rather than standard hexapeptide-9, so there is no sound human evidence for the ingredient itself. | Cosmetic ingredient, a collagen-inspired signal peptide | Activity supported mainly by laboratory and manufacturer data | Hexapeptide-9 is a synthetic six-amino acid "signal" peptide whose sequence mirrors a short motif found in human collagen. Laboratory work suggests it signals skin cells to build more supporting matrix, which is the basis for its use in products aimed at the appearance of firmness and fewer fine lines. As of 2026, independent human evidence for the standard ingredient is limited, with the one controlled human study testing a chemically modified version rather than hexapeptide-9 itself. | Laboratory studies describe hexapeptide-9 as a matrikine, a peptide fragment that acts as a signal to skin cells. The proposed mechanism is that it tells dermal fibroblasts and surface keratinocytes to increase production of extracellular matrix components such as collagen, as well as to strengthen the junction between the upper and lower layers of skin. The idea is that healthier-looking matrix supports the appearance of firmer, smoother skin. These are laboratory and manufacturer findings about how the peptide behaves in cell models. In finished cosmetics the benefit is described in appearance terms, such as the look of firmness and reduced fine lines, rather than as a claim to rebuild collagen. | The direct human evidence is limited: - According to PubMed, a randomized, controlled trial reported wrinkle improvements, but it tested a cyclized derivative of the molecule rather than standard hexapeptide-9, and it was industry-sponsored. - Other studies use the peptide inside delivery systems or combination products, so the ingredient's individual effect is hard to isolate. - There is no independent, well-controlled human trial of standard hexapeptide-9 on its own, and supplier efficacy claims are largely unpublished. | 0 | 0 | 0 | Hexapeptide-9 is generally considered well tolerated on the skin, with low irritation potential at cosmetic use levels. As with any new skincare ingredient, a patch test is sensible for sensitive or reactive skin, since individual responses vary. | 4 | https://ashland.com/industries/personal-and-home-care/skin-and-sun-care/collaxyl-ng-biofunctional ; https://www.specialchem.com/cosmetics/inci-ingredients/hexapeptide-9 ; https://doi.org/10.1111/jocd.70290 ; https://doi.org/10.1016/j.mtbio.2025.101527 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
67 | Hexarelin | https://superpower.com/guides/peptides/hexarelin | Bones & muscles | Wellness and performance | GHRP / ghrelin agonist | Non-FDA-approved peptide (also known as examorelin) sold in the wellness/gray market | Low research | Human data are limited to short studies of growth hormone release, with the marketed wellness benefits resting on animal and laboratory work. | Potent ghrelin-receptor agonist / growth hormone-releasing peptide | Human data are limited to short pharmacology studies; the marketed benefits are unproven | Hexarelin is a potent synthetic ghrelin-mimic peptide that prompts the body to release growth hormone, sold in the wellness market for recovery and body composition. Human data are limited to short studies of growth hormone release, with no controlled trials supporting the marketed benefits, and repeated use appears to blunt its own effect. As of 2026 it is not FDA-approved and is banned in sport. | Three features of its proposed mechanism stand out: - It activates the growth hormone secretagogue (ghrelin) receptor on the pituitary to drive growth hormone pulses. - It also binds a receptor called CD36 in cardiovascular tissue, which underlies preclinical interest in effects on the heart that may be separate from growth hormone. - Studies report partial desensitization, in which the growth hormone response can diminish with repeated exposure. The marketed benefits are extrapolated from the growth hormone rise. This describes the proposed mechanism, separate from proven outcomes. | The human evidence is short pharmacology. According to PubMed, a study in healthy men found hexarelin produced a larger growth hormone rise than GHRH and acted in synergy with it, a hormone-level result rather than a clinical outcome. Its cardiovascular effects are described mainly in experimental models and reviews. No controlled human trials support the marketed muscle, recovery, or anti-aging uses. | 0 | 0 | 0 | 3 | https://doi.org/10.1161/01.res.0000016164.02525.b4 ; https://doi.org/10.1159/000126827 ; https://doi.org/10.1016/j.tem.2005.11.004 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
68 | Histrelin | https://superpower.com/guides/peptides/histrelin | Sexual & reproductive | FDA-approved | GnRH agonist | Yes. Histrelin's U.S. approval and market history: Year | Event Early 1990s | An earlier daily-injection form of histrelin was approved 2004 | Vantas implant approved for advanced prostate cancer 2007 | Supprelin LA implant approved for central precocious puberty 2021 | Vantas discontinued by its manufacturer Supprelin LA is now the only histrelin implant sold in the U.S. Each implant is designed… | FDA approved | Histrelin is FDA-approved for central precocious puberty, supported by implant studies showing durable hormone suppression. Its prostate cancer implant was also FDA-approved before it was discontinued. | A GnRH (LHRH) receptor agonist peptide delivered as a 12-month subdermal implant | Histrelin (histrelin acetate, sold as Supprelin LA and formerly as Vantas) is a synthetic nonapeptide agonist of gonadotropin-releasing hormone delivered as a small implant that releases drug for about a year. It suppresses the pituitary and the sex hormones it controls, and is used for central precocious puberty in children; a second implant for advanced prostate cancer in adults was discontinued in 2021. The implant products have been FDA-approved in the U.S. since the mid-2000s, and one implant lasts roughly 12 months. | Histrelin binds the GnRH receptor on the pituitary. As with other agonists in its class, an initial dose briefly stimulates the gland, producing a short rise in luteinizing hormone and sex steroids, the flare. Because the implant then delivers the drug continuously, the receptors downregulate and desensitize, and gonadotropin output falls. Sex-hormone levels drop to prepubertal levels in children or castrate levels in men. In central precocious puberty, that suppression stops the premature pubertal cascade, pausing bone maturation and breast or testicular development until a more appropriate age; in advanced prostate cancer, it removes the testosterone that hormone-sensitive tumors rely on. In the pivotal pediatric study, a single subdermal implant lowered peak stimulated luteinizing hormone from about 28 to under 1 mIU/mL and maintained suppression of luteinizing hormone and sex steroids for a full year. | 0 | 0 | 0 | According to the Supprelin LA label, the most common side effect is a reaction at the implant site, reported in about half of children in clinical trials: - Pain, bruising, soreness, or swelling where the implant is placed More serious considerations include: - Implant breakage or difficult removal - A brief rise in sex hormones in the first week, which can temporarily worsen symptoms - Mood and behavior changes such as irritability, crying, anger, or aggression - Convulsions - Raised pressure around the brain (pseudotumor cerebri), with symptoms such as headache and vision changes - Severe skin reactions | 3 | https://doi.org/10.1210/jc.2006-2479 ; https://www.endodocuments.com/supprelin-la/pi ; https://mdedge.com/content/hormone-blocker-sticker-shock-again-patients-lose-cheaper-drug-option | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
69 | Human chorionic gonadotropin | https://superpower.com/guides/peptides/human-chorionic-gonadotropin | Sexual & reproductive | FDA-approved | Glycoprotein gonadotropin | Yes, for its hormonal indications. The injectable hCG products have been FDA-approved for decades for ovulation induction, male hypogonadism, and cryptorchidism. The agency has separately warned that over-the-counter "homeopathic" hCG weight-loss products are not approved and that prescription hCG is not approved for weight loss. | FDA approved | Human chorionic gonadotropin is FDA-approved for ovulation induction, male hypogonadism, and cryptorchidism, with established clinical use. It is not approved for weight loss, and the FDA says it has not been shown to be effective for that use. | A gonadotropin hormone that mimics luteinizing hormone at its receptor | Human chorionic gonadotropin (hCG; FDA-approved injectable brands include Pregnyl and Novarel) is a placental hormone that acts like luteinizing hormone, triggering ovulation in women and testosterone production in men. It is used in fertility treatment, in male hypogonadotropic hypogonadism, and for undescended testicles in boys, and it is not approved for weight loss. In a Cochrane review of seven trials with 1,136 women, recombinant and urinary hCG gave similar ongoing pregnancy or live-birth rates (odds ratio 1.15, 95% confidence interval 0.89 to 1.49). | hCG binds the same receptor as luteinizing hormone (the LH/CG receptor) and mimics the natural mid-cycle luteinizing hormone surge. In women undergoing fertility treatment, a dose of hCG triggers the final maturation and release of the egg after the follicles have been grown with other hormones. In men, hCG stimulates the Leydig cells of the testes to produce testosterone and supports sperm production, which is why it is used in hypogonadotropic hypogonadism. In boys with non-anatomical undescended testicles, the testosterone it stimulates can promote testicular descent. In a Cochrane review, urinary-derived and recombinant hCG gave similar ongoing pregnancy or live-birth rates for triggering final egg maturation (odds ratio 1.15, 95% CI 0.89 to 1.49; seven trials, 1,136 women). The FDA has specifically stated that hCG has not been shown to be effective for weight loss and is not approved for that use, despite its promotion in some commercial diet programs. | 2 | 2 | 0 | According to the prescribing information, common side effects include: - Injection-site pain - Headache - Fluid retention or edema - Breast tenderness or gynecomastia (in males) - Irritability, restlessness, and depression More serious considerations include: - Ovarian hyperstimulation syndrome and multiple pregnancy in fertility use - Signs of early puberty in boys treated for cryptorchidism - Rare arterial thromboembolism | 5 | 33933392; 29772111 | https://doi.org/10.1002/14651858.CD003719.pub4 ; https://www.fda.gov/drugs/medication-health-fraud/questions-and-answers-hcg-products-weight-loss ; https://www.organon.com/product/usa/pi_circulars/p/pregnyl/pregnyl_pi.pdf ; https://pubmed.ncbi.nlm.nih.gov/33933392/ ; https://pubmed.ncbi.nlm.nih.gov/29772111/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
70 | Humanin | https://superpower.com/guides/peptides/humanin | Hormones & metabolism | Wellness and performance | Mitochondrial-derived peptide | Non-FDA-approved peptide sold in the wellness/gray market | Low research | There is rich mechanistic, animal, and human biomarker data, but no interventional human trials, so efficacy for any wellness use is unestablished. | Naturally occurring mitochondrial-derived peptide studied in aging and neuroprotection | Evidence is animal and observational; there are no interventional human trials | Humanin is a small peptide encoded within the mitochondria, studied for longevity and brain protection, and sold on the "research peptide" market. Its evidence is preclinical and observational, with no trials testing it as a treatment in people. As of 2026 it is not FDA-approved. | Humanin is proposed to: - Protect cells - Support nerve-cell survival - Reduce programmed cell death - Improve insulin sensitivity and metabolic signaling Its levels are reported to decline with age in some studies and to rise in others, and are reported lower in some diseases. In laboratory and animal work it protected neurons and, in worms and mice, was associated with extended lifespan and healthspan. These are preclinical findings. This describes the proposed mechanism, separate from demonstrated benefit in people. | The evidence is preclinical and observational. The table below summarizes what each type of study, as indexed on PubMed, has found. Type of evidence | What it shows Laboratory work | Humanin is released by support cells in the brain and can prevent loss of connections between neurons (here) Animal studies | Report lifespan and healthspan effects (here) Human observational studies | Humanin can be measured in blood, and studies disagree on whether levels fall or rise with age, an observational association rather than a treatment effect Human interventional trials | None of humanin as a therapy, so its marketed benefit is unproven in people | 0 | 0 | 0 | 13 | 35499074; 29955888; 33131010; 30242290; 21510972 | https://doi.org/10.1371/journal.pone.0006334 ; https://doi.org/10.3389/fnagi.2019.00123 ; https://doi.org/10.18632/aging.103534 ; https://www.deadiversion.usdoj.gov/schedules/orangebook/c_cs_alpha.pdf ; https://pubmed.ncbi.nlm.nih.gov/35499074/ ; https://pubmed.ncbi.nlm.nih.gov/29955888/ ; https://pubmed.ncbi.nlm.nih.gov/33131010/ ; https://pubmed.ncbi.nlm.nih.gov/30242290/ ; https://pubmed.ncbi.nlm.nih.gov/21510972/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://www.fda.gov/media/94155/download ; https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=210557 ; https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=022505 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
71 | Icatibant | https://superpower.com/guides/peptides/icatibant | Skin & aging | FDA-approved | Bradykinin B2 antagonist | Yes. Icatibant was approved by the FDA in 2011 for acute attacks of hereditary angioedema in adults, and generic versions are also available. It is formulated for subcutaneous self-injection. | FDA approved | Icatibant is FDA-approved for acute hereditary angioedema attacks, supported by randomized trials including FAST-3 showing faster symptom relief. | A bradykinin B2 receptor antagonist peptide | Icatibant (sold as Firazyr) is a peptide that blocks the bradykinin B2 receptor, used to treat acute attacks of hereditary angioedema, a condition of sudden, severe swelling. By blocking the mediator that drives the swelling, it shortens attacks. It has been FDA-approved in the U.S. since 2011 and can be self-administered as a subcutaneous injection. | Icatibant targets bradykinin, the molecule responsible for the swelling in hereditary angioedema. In HAE, a deficiency or dysfunction of the C1 inhibitor protein leads to overproduction of bradykinin, which binds B2 receptors on blood vessels and makes them dilate and leak fluid into tissues, producing the characteristic swelling and pain. Icatibant is a selective competitive antagonist at the B2 receptor, so it blocks bradykinin from acting there and allows the attack to subside. Because it acts directly at the receptor regardless of the upstream cause, it works in HAE attacks driven by bradykinin and can be given by the patient at the first sign of an attack. In the FAST-3 trial, icatibant shortened the median time to meaningful symptom relief to about 2 hours, compared with roughly 20 hours on placebo. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Injection-site reactions such as redness, swelling, pain, and itching, which are nearly universal - Fever - Dizziness More serious considerations include: - Potential for delayed airway symptoms in laryngeal attacks, which should be monitored in a medical setting - Hives, reported after approval | 2 | https://doi.org/10.1016/j.anai.2011.08.015 ; https://ndclist.com/ndc/54092-702/label | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
72 | IGF-1 DES | https://superpower.com/guides/peptides/igf-1-des | Bones & muscles | Wellness and performance | IGF-1 analog | Non-FDA-approved IGF-1 analog sold as a research chemical / performance drug | Low research | There is no human efficacy evidence; the muscle-growth rationale rests entirely on animal and cell studies. | Truncated, more potent version of IGF-1 | Evidence is animal and cell-based only; there are no human efficacy trials | IGF-1 DES is a shortened, more potent laboratory analog of insulin-like growth factor-1 (IGF-1), sold on the "research peptide" and performance market for muscle growth. Its evidence is entirely animal and cell-based, with no human trials, and it is a known performance-enhancing drug. As of 2026 it is not FDA-approved and is banned in sport. | IGF-1 DES acts on the IGF-1 receptor, the pathway that drives muscle protein synthesis and tissue growth. Because it is less bound by carrier proteins, it is proposed to have higher local activity than natural IGF-1. In rodents it improved nitrogen balance and reduced muscle protein breakdown, and it is used in cell culture as a high-potency growth stimulus. These are animal and laboratory findings. This describes the proposed mechanism, separate from proven outcomes in people. (A different, full-length IGF-1 product, mecasermin, is an approved drug for a rare growth disorder; IGF-1 DES is a separate, unapproved analog.) | The evidence is preclinical. According to PubMed, an animal study reported improved nitrogen balance and reduced protein breakdown, and the peptide is a standard high-potency reagent in cell-growth assays. There are no human clinical trials supporting muscle or performance use, so its marketed benefit is unproven in people. | 0 | 0 | 0 | 3 | https://doi.org/10.1042/bj2580267 ; https://doi.org/10.1152/ajprenal.1991.261.4.F626 ; https://doi.org/10.3389/fendo.2026.1822475 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
73 | IGF-1 LR3 | https://superpower.com/guides/peptides/igf-1-lr3 | Bones & muscles | Wellness and performance | IGF-1 analog | Non-FDA-approved IGF-1 analog sold as a research chemical/performance drug | Low research | There is no human efficacy evidence; the anabolic rationale rests on animal and cell studies, which also include an explicit tumor-growth signal. | Long-acting, modified version of IGF-1 | Evidence is animal and cell-based only; no human efficacy trials exist | IGF-1 LR3 is a long-acting laboratory analog of insulin-like growth factor-1 (IGF-1), sold as a "research chemical" and performance drug for muscle growth. Its evidence is entirely animal and cell-based, with no human trials, and laboratory work has flagged a tumor-growth concern tied to IGF signaling. As of 2026 it is not FDA-approved and is banned in sport. | IGF-1 LR3 activates the IGF-1 receptor, driving the growth signaling that promotes muscle protein synthesis in cell and animal models. Its modifications are proposed to prolong its activity in the body. In laboratory work it increased muscle-cell differentiation, and in a mouse model of cancer-related muscle wasting it limited muscle loss, but at the cost of accelerated tumor growth, illustrating the mitogenic (growth-promoting) concern that comes with strong IGF signaling. These are animal and cell findings. This describes the proposed mechanism, separate from proven outcomes in people. | The evidence is preclinical. According to PubMed, a mouse study found IGF-1 LR3 limited muscle loss in cancer cachexia but accelerated tumor growth, and laboratory assays show it stimulates muscle-cell growth. There are no human clinical trials supporting muscle or performance use, and the tumor-growth signal is a specific preclinical concern. Its marketed benefit is unproven in people. | 0 | 0 | 0 | 3 | 29535161 | https://pubmed.ncbi.nlm.nih.gov/29535161/ ; https://doi.org/10.1038/s41598-019-46178-9 ; https://doi.org/10.3389/fendo.2026.1822475 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
74 | Insulin analogs | https://superpower.com/guides/peptides/insulin-analogs-multiple | Hormones & metabolism | FDA-approved | Insulin receptor agonist | Yes. Insulin analogs have been FDA-approved since 1996, starting with lispro, followed by glargine in 2000 and others including aspart, glulisine, detemir, and degludec. They are approved to improve blood-sugar control in adults and, for many products, children with diabetes. | FDA approved | Insulin analogs are FDA-approved for type 1 and type 2 diabetes, supported by extensive randomized evidence including trials such as Treat-to-Target. | Engineered insulin peptide hormones with altered onset and duration | Insulin analogs are laboratory-engineered versions of the hormone insulin, redesigned to act faster or last longer than natural insulin, and they are prescribed for type 1 diabetes and for type 2 diabetes when other treatments are not enough. Rapid-acting analogs cover meals and long-acting (basal) analogs provide steady background coverage. Insulin analogs have been FDA-approved in the U.S. since the 1990s and are given by subcutaneous injection or pump. | Insulin analogs bind the insulin receptor on muscle, fat, and liver cells, just as natural insulin does. Activating the receptor prompts cells to take up glucose from the blood (through the GLUT4 transporter), stimulates storage of glucose, fat, and protein, and suppresses the liver's production of glucose, all of which lower blood sugar. The amino-acid changes in the analogs do not alter this core action; they change the pharmacokinetics, how fast the insulin is absorbed and how long it lingers. Rapid-acting analogs are engineered so their molecules separate and absorb quickly after injection, matching the glucose rise from a meal, while basal analogs are designed to precipitate or to bind albumin so they release slowly and provide flat, all-day coverage. Combining the two reproduces the body's natural pattern more closely than older insulins. In the Treat-to-Target trial, adding a basal analog to oral drugs let a larger share of patients reach their HbA1c goal without documented nig… | 0 | 0 | 0 | According to product labels such as the Humalog prescribing information, the most common and important side effect is: - Low blood sugar (hypoglycemia), which can be severe Other effects include: - Weight gain - Injection-site reactions or fatty lumps (lipodystrophy) - Low potassium More serious considerations include: - Severe hypoglycemia, which can cause seizures or loss of consciousness - Fluid retention and heart failure when combined with certain diabetes pills (thiazolidinediones) Insulin pens must never be shared between people, even if the needle is changed. | 3 | https://www.novocare.com/levemir.html ; https://doi.org/10.2337/diacare.26.11.3080 ; https://uspl.lilly.com/humalog/humalog.html | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
75 | Ipamorelin | https://superpower.com/guides/peptides/ipamorelin | Bones & muscles | Wellness and performance | GHRP / ghrelin receptor agonist | Non-FDA-approved peptide sold in the wellness/gray market | Low research | Human data are limited to short studies of growth hormone release and one phase 2 ileus trial that missed its endpoint, and the marketed recovery and body-composition claims rest on animal and laboratory work. | Selective ghrelin-receptor agonist ("growth hormone secretagogue") | Human data are limited to short pharmacology studies; benefit for recovery or body composition is unproven | Ipamorelin is a synthetic peptide that mimics ghrelin to prompt the body to release more of its own growth hormone, and it is sold on the wellness and "research peptide" market. In a phase 2 trial of 114 bowel-resection patients (Beck, 2014), intravenous ipamorelin brought a median first tolerated meal at 25.3 hours versus 32.6 hours on placebo, a difference that was not significant (p = 0.15). Other human data show only that it raises growth hormone. As of 2026 it is not FDA-approved, it is not eligible for routine pharmacy compounding, and it is banned in sport. | Ipamorelin activates the growth hormone secretagogue receptor, the same receptor the hunger hormone ghrelin uses, which triggers the pituitary to release growth hormone in pulses. In laboratory work it is described as relatively "selective," raising growth hormone with comparatively little effect on other hormones such as cortisol and prolactin. In conscious swine, it released GH without raising ACTH or cortisol, while GHRP-6 and GHRP-2 raised both. Because growth hormone and GHRH signaling act together, ghrelin-mimic peptides are often combined with GHRH analogs. No published human randomized controlled trial tests ipamorelin with CJC-1295 as of September 2026. The marketed benefits are extrapolated from this growth-hormone effect. This describes the proposed mechanism, separate from proven outcomes. | The human evidence is short pharmacology, not outcomes, and the supporting bone and gut data come from animal models: Study | Subjects | Finding Dose-ranging study, according to PubMed | Healthy men | Ipamorelin induced growth hormone release, a hormone-level finding rather than a clinical result; the study estimated a terminal half-life of 2 hours Bone study | Rats with glucocorticoid-related bone changes | Supporting data on bone effects Gut transit model | Rodent model of post-operative gut transit | Supporting data on gut effects The one published phase 2 efficacy trial (Beck, 2014) | 114 patients analyzed, adults after bowel resection, given intravenous ipamorelin or placebo | Median time to first tolerated meal was 25.3 versus 32.6 hours, p = 0.15, so it missed its primary endpoint; its secondary efficacy analyses showed no significant differences either Clinical development for post-operative ileus did not produce an approved product, and there are no controlled human trials supporting the marketed recovery or body-composition uses. | 4 | 2 | 2 | 12 | 9849822; 10496658; 25331030; 9186261; 9285939; 22901302 | https://my.clevelandclinic.org/health/body/22804-ghrelin ; https://pubmed.ncbi.nlm.nih.gov/9849822/ ; https://doi.org/10.1023/a:1018955126402 ; https://pubmed.ncbi.nlm.nih.gov/10496658/ ; https://doi.org/10.1054/ghir.2001.0239 ; https://doi.org/10.1124/jpet.108.149211 ; https://pubmed.ncbi.nlm.nih.gov/25331030/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://pubmed.ncbi.nlm.nih.gov/9186261/ ; https://pubmed.ncbi.nlm.nih.gov/9285939/ ; https://www.fda.gov/media/94155/download ; https://pubmed.ncbi.nlm.nih.gov/22901302/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
76 | Kisspeptin-10 | https://superpower.com/guides/peptides/kisspeptin-10 | Sexual & reproductive | Wellness and performance | Reproductive peptide | Non-FDA-approved peptide; remains investigational | Moderate research | There is real, peer-reviewed, placebo-controlled human investigational data with a well-characterized reproductive-axis mechanism, but the trials are small, use surrogate endpoints, often used a longer form of the peptide, and no approved efficacy exists. | Fragment of kisspeptin, which triggers the reproductive hormone axis | Real, peer-reviewed human investigational studies, though small and often using a longer form (kisspeptin-54) | Kisspeptin-10 is a fragment of a natural reproductive hormone, sold on the "research peptide" market and not FDA-approved. The one human trial of kisspeptin-10 itself was small. In a 2013 proof-of-concept study by George and colleagues, five men with type 2 diabetes and low testosterone took part. An 11-hour infusion in four of them raised luteinizing hormone (LH) from 3.9 to 20.7 IU/L (p = 0.03) and testosterone from 8.5 to 11.4 nmol/L (p = 0.002) against their own baseline, with no placebo group. Much other human work used the longer kisspeptin-54, and the peptide remains investigational. | Kisspeptin acts on receptors on the brain's GnRH neurons, stimulating the release of GnRH, which in turn drives the pituitary hormones LH and FSH that regulate the gonads. This reproductive-axis role is well established in humans and animals. Additional effects on brain regions involved in sexual and emotional processing are an emerging, investigational area. This describes the mechanism, separate from any approved treatment use. | There is genuine, peer-reviewed human investigational data, with limits. According to PubMed, controlled studies from academic groups have reported that kisspeptin modulates brain processing of sexual and emotional cues in healthy men (here and here) and in women with low sexual desire (here), alongside its well-characterized stimulation of reproductive hormones (review). These studies have limits: - They are small, early-phase studies. - They often use brain-imaging rather than clinical endpoints. - Much of the sexual-behavior work used the longer kisspeptin-54. The work is investigational and does not amount to an approved, proven treatment. The only trial of kisspeptin-10 itself was small. In 2013, George and colleagues found that a single intravenous dose raised LH in five men with type 2 diabetes and low testosterone, plus seven healthy men. In four of the men with diabetes, an 11-hour infusion raised LH and testosterone. Hormone | Before infusion | After infusion | p-value LH | 3.9 IU/L | 20.7 IU/L | 0.03 Testosterone | 8.5 nmol/L | 11.4 nmol/L | 0.002 The trial had no placebo arm, so it shows feasibility rather than benefit. The women's trial enrolled 32 premenopausal women with hypoactive sexual desire disorder in a crossover design using kisspeptin-54. Brain scans showed deactivation of the left inferior frontal gyrus, an imaging finding rather than a clinical outcome. | 0 | 0 | 0 | LH | 3.9 IU/L | 20. || 7 IU/L | 0. | 6 | 23153270 | https://wada-ama.org/en/prohibited-list ; https://doi.org/10.1172/JCI89519 ; https://doi.org/10.1172/jci.insight.121958 ; https://doi.org/10.1001/jamanetworkopen.2022.36131 ; https://doi.org/10.1210/endrev/bnad023 ; https://pubmed.ncbi.nlm.nih.gov/23153270/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
77 | KPV | https://superpower.com/guides/peptides/kpv | Digestive & weight | Wellness and performance | Anti-inflammatory tripeptide | Non-FDA-approved peptide sold in the wellness/gray market | Low research | The anti-inflammatory rationale is supported by consistent animal and cell data, but there are no human efficacy trials, and the regulatory status is a non-binding advisory recommendation rather than approval. | Three-amino acid fragment of alpha-MSH with anti-inflammatory activity in lab models | Evidence is animal and cell-based only; there are no human efficacy trials | KPV is a small anti-inflammatory peptide derived from the tail of the hormone alpha-MSH, sold on the "research peptide" market for gut and skin inflammation. Its evidence is preclinical, with no human efficacy trials, though a 2026 FDA advisory committee gave a non-binding favorable vote toward allowing it to be compounded. As of 2026 it is not FDA-approved. | KPV retains much of alpha-MSH's anti-inflammatory activity. In laboratory models it is taken up into gut and immune cells, where it is proposed to reduce pro-inflammatory signaling, including the NF-kB pathway and downstream inflammatory messengers such as TNF-alpha. Notably, some of its anti-inflammatory activity appears independent of the MC1R receptor. These are cell and animal findings. This describes the proposed mechanism, separate from demonstrated benefit in people. | The evidence is preclinical. According to PubMed, two mouse studies of colitis reported these results: Form tested | Model | Finding KPV | Mouse models of colitis | Reduced inflammation, partly independent of MC1R (here) Nanoparticle-delivered KPV | Mice with colitis | Eased colitis, with mucosal healing and reduced TNF-alpha (here) Its anti-inflammatory basis is reviewed here. There are no controlled human trials establishing KPV for gut or skin use, so its marketed benefit is unproven in people. | 2 | 0 | 2 | 3 | https://doi.org/10.1002/ibd.20334 ; https://doi.org/10.1016/j.ymthe.2016.11.020 ; https://doi.org/10.1136/ard.2007.079780 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
78 | Lanreotide | https://superpower.com/guides/peptides/lanreotide | Digestive & weight | FDA-approved | Somatostatin analog | Yes. Lanreotide was approved by the FDA in 2007 for acromegaly, with the gastroenteropancreatic neuroendocrine tumor indication added in 2014 and a carcinoid syndrome indication following. It is marketed as the Somatuline Depot prefilled syringe. | FDA approved | Lanreotide is FDA-approved for acromegaly and neuroendocrine tumors, supported by randomized evidence including the CLARINET trial showing prolonged progression-free survival. | A long-acting somatostatin analog peptide | Lanreotide (sold as Somatuline Depot) is a long-acting somatostatin analog that suppresses growth hormone and gut hormones and slows the growth of certain neuroendocrine tumors. It is used for acromegaly and for gastroenteropancreatic neuroendocrine tumors, and in the CLARINET trial it significantly delayed tumor progression. It has been FDA-approved in the U.S. since 2007 and is given as a deep subcutaneous injection about once a month. | Lanreotide binds somatostatin receptors, primarily subtypes 2 and 5, on hormone-secreting and tumor cells. Activating those receptors suppresses growth hormone and insulin-like growth factor 1 and reduces the release of gut hormones. Beyond controlling hormone excess, somatostatin-receptor activation has an antiproliferative effect on well-differentiated neuroendocrine tumors, slowing their growth. In acromegaly, that suppression lowers growth hormone and IGF-1 and improves symptoms; in neuroendocrine tumors, it both controls hormone-related symptoms and delays progression. In the CLARINET trial, lanreotide significantly prolonged progression-free survival compared with placebo in people with metastatic enteropancreatic neuroendocrine tumors: Group | Median progression-free survival Lanreotide | Not reached Placebo | 18 months The depot formulation is injected deeply under the skin about once a month. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Diarrhea and abdominal pain - Nausea - Gallstones - Injection-site reactions - Slowed heart rate More serious considerations include: - Gallbladder disease with long-term use - Changes in blood glucose and thyroid function - Cardiac conduction effects | 2 | https://doi.org/10.1056/NEJMoa1316158 ; https://www.ipsen.com/websites/Ipsen_Online/wp-content/uploads/2023/03/23125252/Somatuline-Depot_USPI_Feb_2023.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
79 | Larazotide acetate | https://superpower.com/guides/peptides/larazotide-acetate | Digestive & weight | In clinical trials | Zonulin antagonist (tight-junction regulator) | Investigational peptide, not approved by the FDA | Low research | Its pivotal Phase 3 was stopped for futility and pooled trial data show no effect on the permeability endpoint, so there is no sound human evidence that it works. | Larazotide acetate is an investigational oral peptide that was studied as an add-on to the gluten-free diet for celiac disease, intended to tighten the junctions between intestinal cells. Its pivotal Phase 3 trial was stopped for futility, and pooled trial data did not show an effect on a key measure of intestinal permeability. As of 2026, it is not approved and its lead program has been halted. | Larazotide was designed to act as a "tight-junction regulator." The intestinal lining has junctions between cells that control what passes through; in celiac disease these are thought to loosen, letting gluten fragments cross and trigger inflammation. Larazotide was proposed to counter the hormone zonulin and promote closure of these junctions, reducing the leakage. This is the proposed mechanism; as the trials below show, it did not translate into a confirmed clinical benefit. | The decisive evidence is negative, as the two main human analyses show: Evidence | Design | Result Phase 3 CeDLara trial | Interim analysis in 2022 against a primary endpoint of reducing celiac symptom severity | Stopped for futility after the analysis indicated it would not meet that endpoint Meta-analysis indexed on PubMed | 4 randomized trials | No significant effect on the lactulose-to-mannitol permeability ratio, a biological measure of gut leakiness, with only inconsistent symptom signals in gluten-challenge subgroups A mechanistic review describes the intended tight-junction pathway. Overall, the human evidence does not support a benefit. | 2 | 1 | 0 | 3 | https://doi.org/10.1152/ajpgi.00386.2020 ; https://www.beyondceliac.org/research-news/phase-3-study-discontinued/ ; https://doi.org/10.1016/j.clinre.2021.101782 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||||
80 | Leuprolide | https://superpower.com/guides/peptides/leuprolide | Sexual & reproductive | FDA-approved | GnRH agonist | Yes. Leuprolide was first approved by the FDA in 1985 as a daily subcutaneous injection, with the long-acting Lupron Depot following in 1989. Over the following decades the FDA cleared additional depot strengths, new indications, and several brands, including Eligard, the Fensolvi pediatric depot, and the ready-to-use Camcevi. | FDA approved | Leuprolide is FDA-approved for prostate cancer, endometriosis, uterine fibroids, and central precocious puberty, supported by decades of controlled trials and depot registration studies. | A GnRH (LHRH) receptor agonist peptide that suppresses sex-hormone production | Leuprolide (leuprolide acetate; brands include Lupron, Eligard, and Fensolvi) is a synthetic nonapeptide agonist of gonadotropin-releasing hormone that, given continuously, suppresses the pituitary and shuts down testosterone and estrogen production. It is prescribed for prostate cancer, endometriosis, and precocious puberty, lowering testosterone to castrate levels within two to four weeks. It has been FDA-approved in the U.S. since 1985 and comes in depot formulations lasting from one to six months. | Leuprolide binds the GnRH receptor on the pituitary, and its effect depends on how it is delivered. A first dose actually stimulates the pituitary, producing a short-lived surge in LH, FSH, and testosterone known as the "flare." Because leuprolide then occupies the receptor continuously rather than in natural pulses, the pituitary gonadotrophs downregulate and desensitize. Within about two to four weeks LH and FSH fall, and testosterone in men, or estrogen in women, drops to castrate or postmenopausal levels. That sustained suppression is the therapeutic goal, and the table below shows what it does in each condition. Condition | What hormone suppression does Prostate cancer | Removing testosterone starves hormone-sensitive tumor cells Endometriosis and fibroids | Lowering estrogen shrinks hormone-driven tissue Central precocious puberty | Switching off the premature hormone signal halts early sexual development and helps preserve adult height The flare is why men with advanced prostat… | 0 | 0 | 0 | According to the prescribing information, common side effects reflect low sex-hormone levels and the injection itself: - Hot flashes and sweating - Injection-site pain or reactions - Decreased libido and erectile dysfunction - Fatigue and mood changes - Bone-density loss with long-term use More serious considerations include: - Transient tumor "flare" symptoms in the first weeks of prostate-cancer treatment - Increased risk of hyperglycemia, diabetes, and cardiovascular events with long-term androgen deprivation - Rare seizures - Severe skin reactions - In children treated for precocious puberty, mood and behavior changes and raised pressure around the brain (pseudotumor cerebri), per the pediatric label | 3 | https://doi.org/10.1210/jc.2011-2704 ; https://www.rxabbvie.com/pdf/lupronuro_pi.pdf ; https://www.rxabbvie.com/pdf/lupronpediatric.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
81 | Linaclotide | https://superpower.com/guides/peptides/linaclotide | Digestive & weight | FDA-approved | Guanylate cyclase-C agonist | Yes. Linaclotide was approved by the FDA in stages, starting with adults and later extending to children. Indication | Population | FDA approval IBS-C | Adults | 2012 Chronic idiopathic constipation | Adults | 2012 IBS-C | Children 7 and older | Later approval Functional constipation | Children 2 and older | Later approval It carries a boxed warning that it is contraindicated in children under 2 … | FDA approved | Linaclotide is FDA-approved for IBS-C and chronic constipation, supported by large randomized phase 3 trials showing improved stool frequency and abdominal symptoms. | A guanylate cyclase-C agonist peptide that acts locally in the gut | Linaclotide (sold as Linzess) is a minimally absorbed peptide that works inside the gut to draw in fluid and ease abdominal pain, used for constipation-predominant irritable bowel syndrome and chronic constipation. It activates a receptor on the intestinal lining that increases fluid secretion and speeds transit. It has been FDA-approved in the U.S. since 2012, is taken as a daily capsule, and carries a boxed warning against use in very young children. | Linaclotide activates guanylate cyclase-C, a receptor on the surface of the cells lining the intestine. Switching on this receptor raises cyclic GMP inside and around those cells, which opens chloride and bicarbonate channels and drives secretion of fluid into the intestinal lumen. The added fluid softens stool and speeds its passage, relieving constipation. The elevated cyclic GMP outside the cells is also thought to reduce the sensitivity of the pain-sensing nerves in the gut wall, which may explain the reduction in abdominal pain seen in IBS-C. Because linaclotide stays in the gut and is not meaningfully absorbed, its effects are local. In the phase 3 IBS-C program, roughly a third of patients met the FDA combined responder endpoint versus about 14 percent on placebo. | 4 | 4 | 0 | According to the prescribing information, common side effects include: - Diarrhea, which is the most common reason for stopping - Abdominal pain - Gas and bloating More serious considerations include: - Severe diarrhea leading to dehydration Linaclotide is contraindicated in children under 2 years of age, which is the subject of its boxed warning, and in people with a known or suspected bowel obstruction. | 2 | https://doi.org/10.1038/ajg.2012.254 ; https://www.rxabbvie.com/pdf/linzess_pi.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
82 | Liraglutide | https://superpower.com/guides/peptides/liraglutide | Digestive & weight | FDA-approved | GLP-1 receptor agonist | Yes. Victoza was first approved in 2010 for type 2 diabetes, and later to reduce cardiovascular risk in people with type 2 diabetes and heart disease. Saxenda was approved in 2014 for weight management, and both have since been approved for use in adolescents. | FDA approved | It is approved by the FDA for type 2 diabetes, chronic weight management, and cardiovascular risk reduction in type 2 diabetes, backed by the large LEAD, SCALE, and LEADER randomized controlled trial programs. | FDA-approved GLP-1 peptide, sold as Victoza for type 2 diabetes and Saxenda for weight management | Liraglutide is a once-daily GLP-1 receptor agonist and the first of its kind, engineered from human GLP-1 with a fatty-acid chain that binds albumin to extend its action. Sold as Victoza for type 2 diabetes and Saxenda for weight management, it produced about 8% average weight loss in the SCALE trial and became the first GLP-1 shown to reduce cardiovascular events in LEADER. Its albumin-binding design paved the way for once-weekly semaglutide. | Liraglutide activates the GLP-1 receptor, mimicking a natural gut hormone the body releases after eating. Through that receptor it prompts the pancreas to release insulin when blood sugar is high. Because this effect is glucose-dependent, meaning it works mainly when blood sugar is already elevated, liraglutide on its own carries a low risk of causing hypoglycemia. It also reduces the release of glucagon (a hormone that raises blood sugar) and slows the rate at which the stomach empties, which blunts the rise in blood sugar after a meal and helps a person feel full for longer. Beyond the gut and pancreas, liraglutide acts on appetite centers in the brain, where it increases feelings of fullness and reduces hunger and how much a person eats. This appetite effect is a large part of why it produces weight loss, not just better blood sugar control. Native GLP-1 breaks down within minutes, so liraglutide is engineered with a fatty-acid chain that binds to albumin in the blood. This extends… | 0 | 0 | 0 | In the SCALE weight-management trial, adults on the 3.0 mg dose lost about 8% of their body weight over 56 weeks, compared with about 2. | The most common side effects are gastrointestinal, and they are usually strongest when the dose is increased: - Nausea - Diarrhea - Vomiting - Constipation - Decreased appetite - Headache - Fatigue Less common but more serious risks include: - Thyroid C-cell tumors: liraglutide carries a boxed warning based on rodent studies. It is not known whether this happens in humans. - Pancreatitis, or inflammation of the pancreas - Gallbladder problems, including gallstones - Acute kidney injury, usually from dehydration caused by vomiting or diarrhea - Low blood sugar, especially when combined with insulin or a sulfonylurea - Increased heart rate | 6 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/022341s044lbl.pdf ; https://www.drugs.com/liraglutide.html ; https://www.sciencedirect.com/science/article/pii/S1043661825004700 ; https://doi.org/10.1056/NEJMoa1603827 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/206321s022lbl.pdf ; https://doi.org/10.1056/NEJMoa1411892 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
83 | Lixisenatide | https://superpower.com/guides/peptides/lixisenatide | Hormones & metabolism | FDA-approved | GLP-1 receptor agonist | Yes. Lixisenatide was approved in the U.S. in 2016 for type 2 diabetes. Sanofi discontinued the standalone Adlyxin product in the U.S. in 2023 for business reasons, though lixisenatide remains available in the combination product Soliqua. | FDA approved | It is approved by the FDA for type 2 diabetes, supported by the GetGoal trial program and the ELIXA cardiovascular outcomes trial. | FDA-approved GLP-1 peptide, formerly sold as Adlyxin for type 2 diabetes | Lixisenatide is a short-acting, once-daily GLP-1 receptor agonist derived from the lizard peptide exendin-4, taken before a meal to blunt the after-meal blood sugar spike in type 2 diabetes. It was FDA-approved in 2016 and shown to be cardiovascular-safe in the ELIXA trial in people who had recently had acute coronary syndrome. Its standalone product Adlyxin was discontinued in the U.S. in 2023, though lixisenatide remains available combined with insulin glargine in Soliqua. | Lixisenatide lowers blood sugar by activating the GLP-1 receptor. Through that receptor, it: - Drives glucose-dependent insulin release, which keeps the risk of hypoglycemia low on its own - Lowers glucagon - Markedly slows the rate at which the stomach empties Because it is short-acting, its strongest effect is blunting the post-meal blood sugar spike rather than providing round-the-clock coverage, which is why it is taken before a meal. In the ELIXA trial, in people who had recently had acute coronary syndrome, lixisenatide was shown to be cardiovascular-safe, one of the first cardiovascular outcome trials for a GLP-1 drug. | 0 | 0 | 0 | The most common side effects are gastrointestinal: - Nausea - Vomiting - Diarrhea - Headache - Dizziness Less common but more serious risks include: - Pancreatitis, or inflammation of the pancreas - Severe allergic reactions, including anaphylaxis - Acute kidney injury, usually from dehydration caused by vomiting or diarrhea - Low blood sugar, especially when combined with insulin or a sulfonylurea | 3 | https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/208471s009lbl.pdf ; https://doi.org/10.1056/NEJMoa1509225 ; https://www.rxless.com/resources/adlyxin-lixisenatide-will-no-longer-be-available-in-the-us | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
84 | LL-37 | https://superpower.com/guides/peptides/ll-37 | Immune & defense | Wellness and performance | Host-defense antimicrobial peptide | Non-FDA-approved peptide sold in the wellness/gray market | Low research | There is a rich endogenous and preclinical science base, but no approved product and no human efficacy data for the injected wellness use, and its biological effects are context-dependent. | The only human cathelicidin, a natural antimicrobial and immune-signaling peptide | Biology well studied, but no human efficacy evidence for the injected wellness use | LL-37 is the body's natural antimicrobial "host-defense" peptide, intensely studied as part of the immune system and sold on the "research peptide" market for antimicrobial and immune support. Its biology is well described, but there is no approved product and no human efficacy evidence for the injected wellness use, and its effects are context-dependent. As of 2026 it is not FDA-approved. | LL-37 has two broad actions. Its positively charged, membrane-active structure can directly disrupt the membranes of microbes, and it also modulates the immune system, influencing immune-cell recruitment, inflammation, and wound healing, and binding some microbial factors. These roles are documented in a large laboratory and animal literature. Importantly, its effects are context-dependent: it can be either pro- or anti-inflammatory and has been implicated in some inflammatory skin diseases. This describes its biology, separate from demonstrated benefit from giving it as a therapy. | The evidence is preclinical for any injected wellness use. LL-37's biology in innate immunity, wound healing, and skin disease is documented in humans and in extensive laboratory work, including studies of how it disrupts microbes and binds microbial factors (example). However, there are no controlled human trials establishing efficacy or safety of self-administered LL-37 for antimicrobial, immune, or healing wellness uses, and its context-dependent, sometimes pro-inflammatory, behavior argues against simple benefit claims. | 0 | 0 | 0 | 16 | 11015447; 11389039; 12603850; 23766266; 15985530; 16497887; 40270954; 17873860; 17676051; 16215847; 34687253; 37480520 | https://doi.org/10.1016/j.bbrc.2020.03.162 ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://www.fda.gov/media/94155/download ; https://www.fda.gov/advisory-committees/pharmacy-compounding-advisory-committee/meeting-pharmacy-compounding-advisory-committee ; https://pubmed.ncbi.nlm.nih.gov/11015447/ ; https://pubmed.ncbi.nlm.nih.gov/11389039/ ; https://pubmed.ncbi.nlm.nih.gov/12603850/ ; https://pubmed.ncbi.nlm.nih.gov/23766266/ ; https://pubmed.ncbi.nlm.nih.gov/15985530/ ; https://pubmed.ncbi.nlm.nih.gov/16497887/ ; https://pubmed.ncbi.nlm.nih.gov/40270954/ ; https://pubmed.ncbi.nlm.nih.gov/17873860/ ; https://pubmed.ncbi.nlm.nih.gov/17676051/ ; https://pubmed.ncbi.nlm.nih.gov/16215847/ ; https://pubmed.ncbi.nlm.nih.gov/34687253/ ; https://pubmed.ncbi.nlm.nih.gov/37480520/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
85 | LTX-315 | https://superpower.com/guides/peptides/ltx-315 | Skin & aging | In clinical trials | Oncolytic peptide | Investigational peptide, not approved by the FDA | Moderate research | There is real but limited positive human evidence from an early-phase, uncontrolled trial, with no randomized efficacy data and later results resting partly on company reports. | Oncolytic peptide injected directly into tumors (intratumorally) | Early-phase human data show injected-tumor shrinkage and immune activation | LTX-315 is an investigational "oncolytic" peptide that is injected directly into tumors to break tumor cells apart and provoke an immune response, developed by Lytix Biopharma. In an early-phase trial it shrank injected tumors and triggered immune cell infiltration, and the company has described plans toward a registrational trial in melanoma. As of 2026, it is not approved and its efficacy has not been tested in controlled trials. | LTX-315 inserts into and disrupts cell membranes, causing tumor cells to rupture in a way that releases tumor antigens and "danger signals." This form of cell death is intended to alert the immune system, drawing in cancer-fighting T-cells and potentially producing responses even in tumors that were not injected (an "abscopal" effect). The approach is being combined with immune-checkpoint drugs on the theory that releasing tumor antigens makes the immune response stronger. This describes the proposed mechanism, separate from the outcomes below. | The human evidence is early-phase and uncontrolled. According to PubMed, a Phase 1 dose-ranging trial in advanced solid tumors reported: - Tumor necrosis - Infiltration of cancer-fighting T-cells - At least 30% shrinkage of injected tumors in some patients - Signs of a systemic immune response However, standard objective responses to the drug alone were not seen. Later Phase 2 and combination data have been reported mainly via company releases. There are no controlled efficacy trials yet, so the benefit is suggested but not established. | 0 | 0 | 0 | 2 | https://doi.org/10.1158/1078-0432.CCR-20-3435 ; https://verrica.com/press_release/verrica-pharmaceuticals-announces-fda-acceptance-of-its-ind-application-for-ltx-315-a-potential-first-in-class-oncolytic-peptide-based-immunotherapy-for-the-treatment-of-basal-cell-carcinoma/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
86 | Lutetium Lu-177 dotatate | https://superpower.com/guides/peptides/lutetium-lu-177-dotatate | Digestive & weight | FDA-approved | SSTR-targeted radiopeptide | Yes. Lutetium Lu-177 dotatate (Lutathera) was approved by the FDA in 2018 for somatostatin-receptor-positive gastroenteropancreatic neuroendocrine tumors in adults, with later expansion to adolescents. It is given as four intravenous infusions about eight weeks apart. | FDA approved | Lutetium Lu-177 dotatate is FDA-approved for gastroenteropancreatic neuroendocrine tumors, supported by the NETTER-1 trial showing improved progression-free survival. | A lutetium-177-labeled somatostatin analog delivering targeted radiation (peptide receptor radionuclide therapy) | Lutetium Lu-177 dotatate (sold as Lutathera) is a targeted radiation therapy that attaches a radioactive isotope to a somatostatin analog to deliver radiation directly to neuroendocrine tumors. It was the first peptide receptor radionuclide therapy approved in the United States. It has been FDA-approved in the U.S. since 2018 and is given as a series of intravenous infusions. | The dotatate peptide binds somatostatin receptor subtype 2 on neuroendocrine tumor cells and is taken inside them. Attached to it is lutetium-177, which emits beta particles, a short-range form of radiation. Because the tracer concentrates in receptor-rich tumor cells, the radiation is delivered largely where it is needed, damaging the DNA of the tumor cells and the cells immediately around them while sparing much of the healthy tissue. This targeted delivery is the principle of PRRT, often described as a "theranostic" pairing with the gallium-68 imaging agent: the scan confirms the target before the therapy is given. In the NETTER-1 trial in advanced midgut neuroendocrine tumors, lutetium-177 dotatate markedly improved progression-free survival compared with high-dose octreotide. An amino-acid solution is infused alongside it to protect the kidneys. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Nausea and vomiting, partly from the protective amino-acid infusion - Fatigue - Low blood counts More serious considerations include: - Bone-marrow suppression and a risk of secondary myelodysplastic syndrome or leukemia - Kidney and liver toxicity - A temporary surge of tumor hormones (neuroendocrine hormonal crisis) - Allergic reactions, including swelling of the face or throat (angioedema) - Radiation exposure and effects on fertility | 2 | https://doi.org/10.1056/NEJMoa1607427 ; https://www.novartis.com/us-en/sites/novartis_us/files/lutathera.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
87 | Lutetium Lu-177 vipivotide tetraxetan | https://superpower.com/guides/peptides/lutetium-lu-177-vipivotide-tetraxetan | Sexual & reproductive | FDA-approved | PSMA-targeted radioligand | Yes. Lutetium Lu-177 vipivotide tetraxetan (Pluvicto) is FDA-approved, and its indication has widened in steps: Year | FDA action 2022 | Approved for PSMA-positive metastatic castration-resistant prostate cancer, initially after hormonal and taxane chemotherapy 2025 | Indication broadened to patients who have not yet had chemotherapy 2026 | Added use alongside a hormone-blocking drug for metastat… | FDA approved | Lutetium Lu-177 vipivotide tetraxetan is FDA-approved for PSMA-positive prostate cancer, supported by the VISION trial showing improved survival. | A PSMA-targeted radioligand therapy labeled with lutetium-177 | Lutetium Lu-177 vipivotide tetraxetan (sold as Pluvicto) is a targeted radiation therapy that homes in on a protein found on prostate cancer cells and delivers radiation directly to them. It is used for PSMA-positive metastatic prostate cancer, either after other treatments have stopped working or earlier alongside hormone therapy. It has been FDA-approved in the U.S. since 2022 and is given as a series of intravenous infusions. | Prostate cancer cells typically display large amounts of PSMA, a protein on their surface. The targeting part of this drug binds PSMA, and the attached lutetium-177 emits beta-particle radiation over a short range. Because the drug accumulates on PSMA-bearing cells, it delivers a concentrated dose of radiation to the cancer and its immediate surroundings while limiting exposure to more distant healthy tissue, causing lethal DNA damage in the targeted cells. Patients are selected using a PSMA PET scan to confirm the target is present before treatment. In the VISION trial, adding this radioligand therapy to standard care improved both imaging-based progression-free survival and overall survival compared with standard care alone, in men whose disease had progressed after hormonal and chemotherapy treatment. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Fatigue - Dry mouth - Nausea and decreased appetite - Anemia and constipation More serious considerations include: - Bone-marrow suppression - Kidney toxicity - Radiation exposure and precautions to protect others - Effects on fertility | 3 | https://doi.org/10.1056/NEJMoa2107322 ; https://www.novartis.com/us-en/sites/novartis_us/files/pluvicto.pdf ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/215833s037lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
88 | Mazdutide | https://superpower.com/guides/peptides/mazdutide | Digestive & weight | In clinical trials | GLP-1 / glucagon dual agonist | Approved in China (2025) but investigational and not FDA-approved in the United States | Deep research | It has multiple positive, replicated Phase 3 trials published in major journals, supporting a national approval in China, though it is not FDA-approved. | GLP-1 and glucagon receptor dual agonist given as a once-weekly injection | Multiple positive Phase 3 trials in Chinese adults with obesity | Mazdutide is a GLP-1 and glucagon dual-receptor agonist, developed by Innovent Biologics under license from Eli Lilly, given as a once-weekly injection for weight management and type 2 diabetes. In large Phase 3 trials it produced substantial weight loss, and it was approved in China in 2025, while remaining investigational in the United States. As of 2026 it is not FDA-approved. | Mazdutide combines two hormone actions. The GLP-1 receptor arm: - Enhances glucose-dependent insulin secretion - Slows gastric emptying - Reduces appetite The glucagon receptor arm is intended to increase energy expenditure and promote breakdown of fat in the liver. The rationale for adding glucagon action is to boost weight loss and reduce liver fat relative to a GLP-1 drug alone. This describes the proposed mechanism, separate from the outcomes measured in trials. | The evidence comes from large Phase 3 trials in Chinese adults. According to PubMed, the two GLORY trials reported these weight results: Trial | Population | Duration | Weight result GLORY-1 | Obesity or overweight | 48 weeks | Significant weight reduction versus placebo GLORY-2 | Moderate-to-severe obesity | 60 weeks | Mean weight change of about -17% with mazdutide versus about -2% with placebo In GLORY-2, gastrointestinal effects were the most common side effects. A systematic review summarized consistent results across studies in predominantly Chinese populations. These are positive, replicated Phase 3 results underpinning the China approval, though not an FDA approval. | 2 | 0 | 0 | GLORY-1 was a Phase 3 randomized controlled trial of once-weekly mazdutide 4 mg or 6 mg versus placebo over 48 weeks in Chinese adults with obesity or overweight with comorbidities. | What are the side effects of mazdutide? The safety profile reported in Phase 2 and Phase 3 trials is mainly gastrointestinal: vomiting, nausea, and diarrhea were the most common adverse events in the 60-week GLORY-2 trial in China, and most were mild to moderate. A 2024 meta-analysis of randomized trials in people with and without diabetes likewise found a higher risk of transient, mild or moderate gastrointestinal side effects. As of September 2026, published US safety data come only from Phase 1 and Phase 2 trials. | 11 | 42251595 | https://www.ncbi.nlm.nih.gov/books/NBK551568/ ; https://doi.org/10.1001/jama.2026.8142 ; https://doi.org/10.1007/s40265-025-02249-y ; https://doi.org/10.1056/NEJMoa2411528 ; https://doi.org/10.1111/dom.71058 ; https://clinicaltrials.gov/study/NCT06124807 ; https://doi.org/10.3390/ijms232314631 ; https://doi.org/10.1111/dom.15693 ; https://doi.org/10.1136/bmj-2026-372161 ; https://pubmed.ncbi.nlm.nih.gov/42251595/ ; https://doi.org/10.3389/fendo.2024.1309118 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||
89 | Mecasermin | https://superpower.com/guides/peptides/mecasermin | Hormones & metabolism | FDA-approved | IGF-1 (recombinant) | Yes. Mecasermin was approved by the FDA in 2005 for growth failure in children with severe primary IGF-1 deficiency, or with growth hormone gene deletion who have developed neutralizing antibodies to growth hormone. It is given as a twice-daily subcutaneous injection. | FDA approved | Mecasermin is FDA-approved for severe primary IGF-1 deficiency, supported by clinical studies showing increased growth velocity in affected children. | Recombinant human insulin-like growth factor 1 (IGF-1) | Mecasermin (sold as Increlex) is recombinant human insulin-like growth factor 1 (IGF-1), used to treat children who cannot make IGF-1 or cannot respond to growth hormone. It supplies the growth signal that growth hormone would normally produce, bypassing the missing step. It has been FDA-approved in the U.S. since 2005 and is given as a twice-daily injection timed around meals. | Mecasermin is identical to natural IGF-1 and binds the IGF-1 receptor on cells throughout the body, directly delivering the growth-promoting signal that would normally follow growth hormone action. In children with severe primary IGF-1 deficiency, growth hormone is present but the body cannot generate IGF-1 in response, so replacing IGF-1 restores growth that growth hormone therapy alone cannot achieve. Because IGF-1 shares actions with insulin, mecasermin can lower blood sugar, which is why it is dosed shortly before or after a meal. In the pivotal study of children with growth hormone insensitivity, IGF-1 raised average height velocity from about 2.8 cm per year at baseline to 8.0 cm per year in the first year of treatment. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Low blood sugar, which is why dosing is tied to meals - Injection-site changes such as fatty lumps - Enlargement of the tonsils or adenoids More serious considerations include: - Increased pressure around the brain (intracranial hypertension) - Slipped hip growth plate and worsening scoliosis - Cancers, which have been reported in children treated with mecasermin Mecasermin is contraindicated once the growth plates have closed and in children with cancer or a history of cancer. | 2 | https://doi.org/10.1210/jc.2006-1610 ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/021839s033lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
90 | Mechano growth factor | https://superpower.com/guides/peptides/mechano-growth-factor | Bones & muscles | Wellness and performance | IGF-1 splice variant | Non-FDA-approved peptide sold as a research chemical / performance drug | Low research | The muscle-repair rationale rests on laboratory and cell studies, there is no human efficacy evidence, and the pegylated form sold on the market is uncharacterized. | Muscle-produced splice variant of IGF-1; a pegylated form (PEG-MGF) is also sold | Laboratory and cell-based only; no human efficacy trials | Mechano growth factor (MGF) is a muscle-made splice variant of IGF-1, sold on the research-peptide market and often pegylated as PEG-MGF. Its strongest human evidence is observational. In a 2003 biopsy study, one bout of leg exercise raised MGF mRNA significantly in eight men aged 25 to 36 but not in seven men aged 70 to 82. There are no controlled human trials of MGF, and it is not FDA-approved and is banned in sport. | MGF is proposed to act on muscle stem cells (satellite cells), activating them and helping them multiply and delay aging, which would support muscle repair and growth. This is attributed to its unique tail region, thought to work somewhat differently from the classic IGF-1 growth signal. In human muscle-cell cultures, the MGF peptide enhanced satellite-cell activation and fusion, and laboratory versions promoted cell growth and migration. These are cell and laboratory findings. The pegylated form sold on the market is a modification that has not been characterized as a pharmaceutical. This describes the proposed mechanism, separate from proven outcomes in people. | The evidence is preclinical. The table below summarizes the studies indexed on PubMed, from cell work to the strongest human finding, which is observational. Study | Design | Finding A study | Human muscle-cell cultures | The MGF peptide enhanced satellite-cell activation and fusion, with age-dependent effects A related laboratory study | Laboratory | Reported effects on cell growth and migration Kandalla's cell study | Satellite cells from neonatal, young-adult, and old-adult donors | The MGF E peptide extended proliferative lifespan and delayed senescence in cells from neonatal and young-adult donors, but not from old-adult donors A 2003 biopsy study | Observational, 8 men aged 25 to 36 and 7 aged 70 to 82 | One bout of leg exercise raised MGF mRNA significantly in the young men but not the older men; the study measured the body's own MGF and did not give MGF itself There are no controlled human trials of MGF or PEG-MGF for muscle or recovery, and the pegylated form specifically is uncharacterized. The marketed benefit is unproven in people. | 4 | 3 | 1 | 4 | 18837392; 21354439; 12562960 | https://doi.org/10.1016/j.mad.2011.02.007 ; https://pubmed.ncbi.nlm.nih.gov/18837392/ ; https://pubmed.ncbi.nlm.nih.gov/21354439/ ; https://pubmed.ncbi.nlm.nih.gov/12562960/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
91 | Melanotan I | https://superpower.com/guides/peptides/melanotan-i | Skin & aging | Wellness and performance | MC1R agonist | As a tanning peptide, non-FDA-approved and unregulated | Low research | The receptor pharmacology is solid, but there is no controlled human evidence supporting unregulated self-injected tanning; the only rigorous human data belong to the approved drug for a different, medical use. | MC1R agonist that stimulates skin pigment production | No controlled evidence supporting unregulated self-injected tanning | Melanotan I is a synthetic peptide that darkens skin by activating a pigment receptor, sold on the gray market as an injectable "tanning peptide." The same molecule, as the approved drug afamelanotide (Scenesse), is used for a rare light-sensitivity disorder. In two placebo-controlled trials of the approved implant in 168 adults with EPP, U.S. patients logged a median 69.4 pain-free hours in direct sunlight versus 40.8 on placebo (P = 0.04). No controlled trial supports the gray-market tanning product, which is not FDA-approved as of 2026. | Melanotan I activates MC1R on pigment-producing skin cells, which raises production of the dark pigment eumelanin, darkening the skin independently of UV exposure. The receptor pharmacology is well characterized. This describes how it produces pigmentation, separate from whether unregulated self-injection for tanning is effective or safe. In a placebo-controlled study of 65 fair-skinned volunteers, epidermal melanin density rose an average of 41% in low-MED, burn-prone skin and 12% in high-MED skin. That result shows the molecule's pigment effect, not the quality or safety of gray-market vials. | The rigorous human data belong to the approved drug and a different use. Afamelanotide has clinical trial evidence for reducing phototoxicity in the rare disorder it treats, not for cosmetic tanning. There are no controlled human trials supporting unregulated self-injected Melanotan I for tanning, so its cosmetic benefit and safety as sold are unestablished. Two placebo-controlled trials of the approved implant, reported in 2015, enrolled 168 adults with EPP, split by trial as shown below. Trial | Adults with EPP | Median pain-free hours in direct sunlight, afamelanotide versus placebo | P value United States | 94 | 69.4 versus 40.8 | 0.04 European Union | 74 | 6.0 versus 0.8 | 0.005 In the EU trial, patients also had 77 phototoxic reactions versus 146 (P = 0.04). The most common adverse events were headache, nausea, nasopharyngitis, and back pain, with mild implant-site hyperpigmentation in about one third of treated patients. These figures come from a medical implant used for EPP, so they say nothing about tanning vials. | 2 | 0 | 0 | 3 | 16763547; 26132941 | https://pubmed.ncbi.nlm.nih.gov/16763547/ ; https://pubmed.ncbi.nlm.nih.gov/26132941/ ; https://doi.org/10.1016/j.jpba.2012.11.040 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
92 | Melanotan II | https://superpower.com/guides/peptides/melanotan-ii | Skin & aging | Wellness and performance | Melanocortin agonist (MC1R/MC3R/MC4R) | Non-FDA-approved, unregulated product sold in the gray market | Low research | There is no controlled human evidence for the marketed uses, and the published literature consists of case reports and clinician warnings, including concerns about changes in pigmented skin lesions. | Non-selective melanocortin receptor agonist, marketed for tanning and libido | No controlled human evidence for the marketed uses; case reports describe skin-lesion concerns | Melanotan II is a synthetic melanocortin peptide sold on the gray market for tanning and libido, and it is not FDA-approved. No controlled human trials support tanning or libido use. Its first human study, a 1996 pilot in three healthy men, found increased pigmentation in two of three and spontaneous erections lasting 1 to 5 hours. One of two men escalated to the highest dose had Grade II somnolence and fatigue. Published case reports add concerning skin changes. | Melanotan II is proposed to work through two receptor effects: activating MC1R on skin cells to drive pigmentation and tanning, and activating MC4R in the brain, which is linked to sexual arousal and appetite. The sexual and appetite effects come largely from animal and early pharmacology work. This describes the proposed mechanism, separate from whether unregulated use for these purposes is effective or safe. | There are no controlled human trials supporting tanning or libido use. The published clinical literature consists mainly of case reports and clinician warnings. Reports have described new or changing moles and darkening of pigmented lesions after use of melanocortin tanning injections (example and example), and poison-center and dermatology sources describe nausea, flushing, and other effects. These are reports and warnings, not controlled trials, and unregulated product quality adds further uncertainty. The first human data came from a 1996 pilot study in three healthy men, which reported: Finding | Result Increased pigmentation | 2 of the 3 men Spontaneous erections | Lasted 1 to 5 hours Mild nausea | Appeared at most dose levels Grade II somnolence and fatigue | 1 of 2 men escalated to the highest dose It was a small drug-development study, not evidence that gray-market use is safe. The most serious skin report followed later: in one case report, a 20-year-old woman with fair skin developed melanoma after using it with a tanning bed. | 4 | 2 | 0 | 5 | 8637402; 24355990 | https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://doi.org/10.1001/archdermatol.2008.623 ; https://doi.org/10.1111/j.1365-2133.2009.09362.x ; https://pubmed.ncbi.nlm.nih.gov/8637402/ ; https://pubmed.ncbi.nlm.nih.gov/24355990/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
93 | MK-677 (ibutamoren) | Ibutamoren | https://superpower.com/guides/peptides/mk-677-ibutamoren | Bones & muscles | Wellness and performance | Non-peptide ghrelin mimetic | Non-FDA-approved, investigational drug; a small molecule, not a peptide | Moderate research | It has genuine multi-year human trials showing it raises growth hormone, IGF-1, and lean mass, but efficacy for meaningful functional outcomes is unproven, there are negative trials and metabolic safety signals, and it is not approved. | Orally active ghrelin-mimic growth hormone secretagogue | Human trials show it raises growth hormone, IGF-1, and lean mass, but not strength or function, with metabolic signals | MK-677 (ibutamoren) is an orally active, non-peptide drug that mimics the hunger hormone ghrelin to raise the body's own growth hormone, sold on the wellness market for muscle, sleep, and appetite. In a randomized trial of 65 healthy adults aged 60 to 81 (Nass 2008), fat-free mass rose 1.1 kg on MK-677 versus a 0.5 kg loss on placebo over 12 months (P < 0.001), yet strength and function did not improve and fasting glucose rose. A large Alzheimer's trial failed. As of 2026 it is not FDA-approved and is banned in sport. | MK-677 activates the growth hormone secretagogue (ghrelin) receptor, prompting the pituitary to release growth hormone in pulses, which raises IGF-1. Its distinguishing feature is that it is orally bioavailable, unlike the injectable peptide secretagogues. This describes the mechanism; the human trials below show what it does and does not achieve. | It has real human trials with a mixed picture. According to PubMed, two trials define it: Trial | Participants | Duration | Main finding Nass 2008, randomized trial | 65 healthy adults aged 60 to 81 | 2 years | MK-677 raised growth hormone and IGF-1 Sevigny 2008, trial | 563 people with mild to moderate Alzheimer's disease | 12 months | Raised IGF-1 but found no significant difference from placebo on any of 4 clinical scales In the Nass trial's first year, fat-free mass rose 1.1 kg on MK-677 and fell 0.5 kg on placebo (P < 0.001), but strength and function did not improve. Body weight rose 2.7 kg versus 0.8 kg on placebo, and fasting glucose rose 5 mg/dL. MK-677 was also associated with: - Increased appetite - Weight gain - Mild fluid retention - Higher fasting glucose - Reduced insulin sensitivity So it reliably raises growth hormone and lean mass, but without demonstrated functional benefit, with metabolic concerns, and with negative results for disease. | 2 | 2 | 0 | 8 kg on placebo, and fasting glucose rose 5 mg/dL. | 5 | 19015485; 18981485 | https://www.fda.gov/media/94155/download ; https://doi.org/10.7326/0003-4819-149-9-200811040-00003 ; https://doi.org/10.1212/01.wnl.0000335163.88054.e7 ; https://pubmed.ncbi.nlm.nih.gov/19015485/ ; https://pubmed.ncbi.nlm.nih.gov/18981485/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||
94 | Motixafortide | Aphexda | https://superpower.com/guides/peptides/motixafortide | Heart & blood | FDA-approved | CXCR4 antagonist peptide | Yes. Motixafortide was approved by the FDA in 2023 for use in combination with filgrastim to mobilize stem cells for collection and subsequent autologous transplantation in patients with multiple myeloma. It is given as a subcutaneous injection, with premedication to reduce the risk of reactions. | FDA approved | Motixafortide is FDA-approved for stem-cell mobilization in multiple myeloma, supported by the phase 3 GENESIS trial showing higher collection yields. | A CXCR4 receptor antagonist peptide | Motixafortide (sold as Aphexda) is a peptide that blocks the CXCR4 receptor to pull stem cells out of the bone marrow into the blood, where they can be collected for a transplant in people with multiple myeloma. Used with a standard mobilizing drug, it raises the yield of stem cells collected. It has been FDA-approved in the U.S. since 2023 and is given as a subcutaneous injection. | Blood-forming stem cells are normally held in the bone marrow by the interaction between the CXCR4 receptor on the stem cells and a marrow signal called CXCL12 (also known as SDF-1). Motixafortide is a high-affinity, long-acting CXCR4 antagonist that interrupts this anchoring signal, releasing stem cells from the marrow into the bloodstream, where they can be collected by apheresis. It is used together with filgrastim, a growth factor that also mobilizes stem cells, and the two work synergistically to raise the yield. Collecting enough stem cells in as few sessions as possible matters for the success and efficiency of an autologous transplant. In the phase 3 GENESIS trial, far more patients reached the target collection of CD34-positive cells in up to two apheresis sessions with motixafortide plus filgrastim than with filgrastim alone. | 0 | 0 | 0 | According to the prescribing information, common side effects include: - Injection-site reactions such as pain, redness, and itching - Flushing - Back pain and nausea More serious considerations include: - Serious hypersensitivity or systemic reactions, so premedication and monitoring are used - The potential to mobilize tumor cells, which is why it is not used in leukemia - Embryo-fetal toxicity | 2 | https://doi.org/10.1038/s41591-023-02273-z ; https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/217159s009lbl.pdf | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
95 | MOTS-c | https://superpower.com/guides/peptides/mots-c | Hormones & metabolism | Wellness and performance | Mitochondrial-derived peptide | Non-FDA-approved peptide sold in the wellness/gray market | Low research | The mechanism is interesting but human data are observational only, with no trials of the administered peptide establishing a benefit. | Naturally occurring mitochondrial-derived peptide studied in metabolism and exercise | Animal and observational; no completed interventional human trials of the given peptide | MOTS-c is a small peptide encoded within the mitochondria, studied as an "exercise mimetic" for metabolic health, and sold on the "research peptide" market. Its evidence is preclinical and observational, with no completed trials testing the administered peptide in people. As of 2026 it is not FDA-approved, though a 2026 FDA advisory committee gave a non-binding favorable vote toward allowing it to be compounded. | MOTS-c is proposed to move into the cell nucleus under metabolic stress and influence genes that regulate metabolism, including the AMPK energy-sensing pathway, improving muscle glucose handling and insulin sensitivity. Its blood levels reportedly decline with age and rise after intense exercise. In mice, MOTS-c improved exercise capacity and metabolic markers. These are cell and animal findings. This describes the proposed mechanism, separate from demonstrated benefit in people. | The evidence is largely preclinical: Study type | What it shows Cell and rodent studies | The source of the metabolic and exercise effects, according to PubMed, summarized in reviews of its therapeutic potential and of mitochondrial peptides and exercise Human studies | Mostly observational rather than interventional, showing that circulating MOTS-c rises after exercise Trials of administered MOTS-c | None completed for any metabolic or performance use Its marketed benefit is therefore unproven in people. | 3 | 1 | 1 | What are the side effects of MOTS-c? No peer-reviewed human safety data exists, and FDA has identified no human exposure data for drug products containing MOTS-c. Long-term safety in humans is entirely unknown. | 7 | 25738459; 33473109; 35499074 | https://doi.org/10.3389/fendo.2023.1120533 ; https://doi.org/10.1016/j.bbagen.2021.130011 ; https://pubmed.ncbi.nlm.nih.gov/25738459/ ; https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks ; https://www.wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf ; https://pubmed.ncbi.nlm.nih.gov/33473109/ ; https://pubmed.ncbi.nlm.nih.gov/35499074/ | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||
96 | Murepavadin | https://superpower.com/guides/peptides/murepavadin | Immune & defense | In clinical trials | Antimicrobial 'protegrin' peptidomimetic | Investigational antimicrobial peptidomimetic, not approved by the FDA | Low research | The pivotal intravenous Phase 3 program was halted for kidney toxicity with no positive confirmatory efficacy data, and inhaled development did not mature. | Murepavadin is an investigational antimicrobial peptidomimetic that targets a protein unique to Pseudomonas aeruginosa, developed by Polyphor for serious lung infections. Its intravenous Phase 3 program was halted after an unexpected rate of kidney injury, and later inhaled development did not mature. As of 2026 it is not approved. | Murepavadin acts through a species-specific, non-lytic mechanism. It targets LptD, an outer-membrane protein that Pseudomonas aeruginosa needs to transport and assemble lipopolysaccharide, a building block of its outer membrane. Disrupting LptD impairs the bacterium's outer-membrane construction and kills it. In the laboratory, it was active against multidrug-resistant and even colistin-resistant strains. This describes the mechanism, separate from the safety outcome below. | The pivotal program was stopped for safety. Program | Population | Outcome Phase 1 study, indexed on PubMed | Healthy volunteers | Characterized the drug's intravenous pharmacokinetics and early safety Phase 3 PRISM program, which followed | Patients with pneumonia | Closed in 2019 after a higher-than-expected incidence of acute kidney injury in the murepavadin group; enrollment had already been suspended A review summarizes the drug's novel class and antibacterial profile. There is no positive confirmatory efficacy trial, and the IV program ended on a safety signal. | 2 | 2 | 0 | 2 | https://doi.org/10.1080/14787210.2018.1441024 ; https://doi.org/10.1128/AAC.02355-17 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||||
97 | Nafarelin | Synarel | https://superpower.com/guides/peptides/nafarelin | Sexual & reproductive | FDA-approved | GnRH agonist | Yes. Nafarelin was approved by the FDA in 1990 for endometriosis, with central precocious puberty added shortly afterward. It is marketed as a metered nasal spray delivering 200 micrograms per spray. | FDA approved | Nafarelin is FDA-approved for endometriosis and central precocious puberty, supported by controlled trials including head-to-head comparison with danazol. | A GnRH (LHRH) receptor agonist peptide given as a nasal spray | Nafarelin (nafarelin acetate, sold as Synarel) is a synthetic decapeptide agonist of gonadotropin-releasing hormone given as a nasal spray that suppresses the pituitary and the sex hormones it controls. It is used for endometriosis and central precocious puberty, and in a multicenter trial it reduced endometriosis lesions about as well as the older drug danazol with a different side-effect profile. It has been FDA-approved in the U.S. since 1990 and is unusual in its class for being delivered intranasally. | Nafarelin binds the GnRH receptor on the pituitary. Repeated dosing first stimulates the gland, then, through continuous rather than pulsatile exposure, downregulates and desensitizes the receptors so that luteinizing hormone and follicle-stimulating hormone output falls. In women this lowers ovarian estrogen to produce a reversible, menopause-like low-estrogen state. That hypoestrogenic state is what treats endometriosis: estrogen-dependent lesions regress and the associated pain eases while treatment continues. In central precocious puberty, higher divided daily dosing suppresses the premature hormone signal and halts early sexual development. In a multicenter double-blind trial, intranasal nafarelin reduced laparoscopic endometriosis scores about as effectively as oral danazol, with most patients improving, while avoiding danazol's unfavorable effects on blood lipids. Because the low-estrogen state causes bone loss, treatment for endometriosis is generally limited to about six mont… | 0 | 0 | 0 | It is marketed as a metered nasal spray delivering 200 micrograms per spray. | According to the prescribing information, common side effects reflect low estrogen and the nasal route: - Hot flashes and sweating - Vaginal dryness and decreased libido - Headache - Nasal irritation or rhinitis - Acne and emotional lability More serious considerations include: - Bone-density loss, which limits the duration of endometriosis treatment - Fetal exposure risk, so it must not be used in pregnancy - Mood and behavior changes such as irritability, crying, and depression - Convulsions - Raised pressure around the brain (pseudotumor cerebri) in children | 3 | https://doi.org/10.1056/NEJM198802253180805 ; https://www.pfizermedical.com/synarel ; https://www.pfizermedical.com/synarel/adverse-reactions | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||
98 | Nangibotide | https://superpower.com/guides/peptides/nangibotide | Immune & defense | In clinical trials | TREM-1 inhibitor peptide | Investigational peptide, not approved by the FDA | Low research | The controlled Phase 2b trial did not meet its primary endpoint, with a positive signal confined to a biomarker-defined subgroup that remains unconfirmed. | TREM-1 inhibitor given by intravenous infusion for septic shock | Phase 2b trial (ASTONISH) did not meet its primary endpoint | Nangibotide is an investigational peptide that inhibits the inflammatory receptor TREM-1, developed by Inotrem as an intravenous treatment for septic shock. Its Phase 2b trial did not meet its primary endpoint, though a signal appeared in a subgroup of patients with high levels of a related biomarker. As of 2026 it is not approved. | Nangibotide acts as a decoy that interferes with TREM-1 (Triggering Receptor Expressed on Myeloid cells-1). TREM-1 normally amplifies the immune system's inflammatory response, and in septic shock this amplification can become harmful. By blocking TREM-1 engagement, nangibotide is intended to dampen the excessive release of inflammatory signals. A related marker, soluble TREM-1, is used to identify patients whose TREM-1 pathway is most activated. This describes the mechanism, separate from the trial outcome below. | The controlled evidence did not meet its goal. According to PubMed, the Phase 2b ASTONISH trial in septic shock did not meet its primary endpoint, an improvement in organ-failure score: Patient group | Organ-failure score result Predefined high-biomarker group | Improvement not statistically significant Overall | Improvement not statistically significant Higher biomarker cutoffs only | Clinically relevant improvement, a subgroup finding that remains unconfirmed The company had earlier framed the result as positive, but the peer-reviewed publication states the primary outcome was not achieved. Efficacy is therefore not established. | 3 | 0 | 0 | 1 | https://doi.org/10.1016/S2213-2600(23)00158-3 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | ||||||
99 | Nesiritide | https://superpower.com/guides/peptides/nesiritide | Heart & blood | FDA-approved | Natriuretic peptide | Yes. Nesiritide was approved by the FDA in 2001 for acute decompensated heart failure in patients with shortness of breath at rest or with minimal activity. After the neutral ASCEND-HF results and shifting practice, the product was largely withdrawn from the U.S. market, so its approval is now mainly of historical interest. | FDA approved | Nesiritide is FDA-approved for acute decompensated heart failure on the basis of short-term symptom and hemodynamic improvement, though the large ASCEND-HF trial later found no benefit on survival or rehospitalization. | Recombinant human B-type natriuretic peptide (BNP), a vasodilator | Nesiritide (sold as Natrecor) is a laboratory-made copy of B-type natriuretic peptide, a hormone the heart releases when it is under strain, developed as an intravenous treatment for acute heart failure. It relaxes blood vessels and lowers heart-filling pressures, but a large trial later found it did not reduce death or rehospitalization. As of 2026 it has been FDA-approved in the U.S. since 2001, though it has largely been withdrawn from the market. | Nesiritide reproduces the 32-amino-acid sequence of human BNP and binds the natriuretic peptide receptor-A, raising the second messenger cyclic GMP in blood-vessel walls. This relaxes both arteries and veins, lowering the pressure the heart has to pump against and the pressure filling it (reflected as a lower pulmonary capillary wedge pressure). It also promotes sodium and water excretion by the kidney and dampens the renin-angiotensin-aldosterone system. Those effects improve the hemodynamics of acute heart failure, but the two key trials reached different results: Trial | Findings VMAC, the earlier trial | Nesiritide lowered filling pressure more than nitroglycerin or placebo and improved breathing at 3 hours ASCEND-HF, the larger later trial | Only a small, non-significant effect on dyspnea and no benefit on 30-day death or rehospitalization, while increasing episodes of low blood pressure That gap between short-term hemodynamics and hard outcomes is the central story of the drug. | 2 | 2 | 0 | Common side effects include: - Low blood pressure, which can be symptomatic or prolonged - Headache - Nausea More serious considerations include: - Significant hypotension, the main safety concern - Slowed heart rate - Earlier concerns about worsening kidney function, which were not confirmed in ASCEND-HF | 1 | https://doi.org/10.1056/NEJMoa1100171 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X | |||||||
100 | NNZ-2591 | https://superpower.com/guides/peptides/nnz-2591 | Brain & sleep | In clinical trials | IGF-1-related peptide | Investigational peptide, not approved by the FDA | Low research | The only peer-reviewed human efficacy data come from a small, open-label, uncontrolled Phase 2 with no placebo arm, so a benefit is not yet established; a controlled Phase 3 is ongoing. | Oral analog of cyclic glycine-proline, related to the IGF-1 system | Published human data from an open-label Phase 2; a placebo-controlled Phase 3 is ongoing | NNZ-2591 is an investigational oral peptide related to a natural fragment of IGF-1, developed by Neuren Pharmaceuticals for several rare genetic neurodevelopmental disorders including Phelan-McDermid, Rett, and Angelman syndromes. Its published human evidence is an open-label (uncontrolled) Phase 2 trial reporting broad improvement, and a placebo-controlled Phase 3 is under way. As of 2026 it is not approved. | As an analog of cyclic glycine-proline, NNZ-2591 is proposed to modulate the IGF-1 signaling system, including helping to normalize the availability of IGF-1, which supports the formation and function of connections between nerve cells. The rationale is that correcting IGF-1-related signaling could help the brain circuits affected in these developmental disorders. This describes the proposed mechanism; the human efficacy data so far are uncontrolled. | The published human evidence is open-label. According to PubMed, a single-group, open-label Phase 2 trial in children and adolescents with Phelan-McDermid syndrome reported that the drug was generally well tolerated and that most efficacy measures improved from baseline over 13 weeks. Because this study had no placebo group, improvement cannot be separated from natural variation or expectation effects. Results in Rett, Angelman, and Pitt-Hopkins syndromes have been reported mainly through company announcements. A placebo-controlled Phase 3 is intended to test efficacy properly; until then, the benefit is promising but unproven. | 0 | 0 | 0 | 2 | https://doi.org/10.1212/NXG.0000000000200338 ; https://doi.org/10.1212/NXG.0000000000200405 | William Maish, MD MBA MPH | October 5, 2026 | Taken from @MeesesRfriends on X |