Peptides

ARA-290, also called cibinetide, is an 11-amino-acid peptide carved from the three-dimensional structure of erythropoietin - specifically from the face of the molecule that activates tissue repair rather than the face that makes red blood cells. That separation is the whole idea: erythropoietin protects injured tissue in animal models, but raising hematocrit in patients who do not need it causes thrombosis and strokes. ARA-290 has been through several small randomized trials in small fiber neuropathy, where it improved symptoms and increased corneal nerve fiber density, and one in type 2 diabetes where it improved both neuropathic symptoms and HbA1c. The trials are genuinely positive and genuinely small - a few dozen patients each, mostly from one group - and nothing has progressed to a confirmatory phase 3.

BPC-157 is a synthetic 15-amino-acid peptide, a fragment of a protein found in human gastric juice. Clinicians and athletes increasingly use it for musculoskeletal injuries. In rats it consistently speeds healing of many tissues. Human data amount to three small, uncontrolled pilot reports, all by the same first author. It is not approved by the FDA and is banned in professional sport.

Fenbendazole is a veterinary dewormer. It is on this site because of a cancer claim that spread online from 2019 onward, and the honest summary of that claim is short: there is no clinical trial evidence that fenbendazole treats cancer in humans. It does have real anti-proliferative activity in cell and animal models, through the same tubulin mechanism that kills worms. It also has real documented harm in people who have taken it for cancer: multiple published cases of severe drug-induced liver injury, including in a patient on immunotherapy where the liver damage was initially mistaken for an immune-related adverse event. A 2025 case series reporting benefit in three self-administering patients has been retracted.

FOXO4-DRI is a senolytic - a compound designed to kill senescent cells, the damaged cells that stop dividing but refuse to die and pump out inflammatory signals. It works by a clever trick: senescent cells stay alive because FOXO4 sequesters p53 in the nucleus, so the peptide is a retro-inverso decoy that breaks that interaction, p53 leaves the nucleus, and the cell kills itself. In the 2017 Cell paper that introduced it, it restored fitness, fur density and kidney function in fast-aging and naturally aged mice. Nine years later there is still no human trial, no human pharmacokinetics and no human safety data of any kind. There is also a significant piece of counter-evidence: in pulmonary arterial hypertension models, eliminating senescent cells made the disease worse, not better.

KPV (lysine-proline-valine) is the last three amino acids of α-melanocyte-stimulating hormone (α-MSH). It keeps the hormone's anti-inflammatory action without its effect on skin pigment. In mice, KPV in the drinking water eased chemically induced colitis, and it cut colitis-associated tumors. It is taken up by PepT1, a peptide transporter that is switched on in the inflamed colon. No human study of KPV has been published.

Larazotide is an eight-amino-acid peptide that tightens the junctions between intestinal cells. The logic for celiac disease is specific: gluten peptides reach the lamina propria partly by passing between enterocytes through junctions that gluten itself loosens, so a drug that keeps those junctions shut should blunt the reaction. It is the most clinically advanced non-dietary celiac treatment there has been, and it has an unusual record: the trial that met its primary endpoint did so at the lowest of three doses, with 1 mg and 2 mg no different from placebo. Earlier gluten-challenge trials failed on permeability, their actual primary endpoint, while showing symptom benefit. A phase 3 program followed and has not delivered an approved drug.

LL-37 is the only cathelicidin humans make - a 37-residue antimicrobial peptide released from the precursor hCAP18 in skin, neutrophils and epithelia, which kills bacteria, recruits immune cells and drives re-epithelialization. It has been through three randomized trials in chronic wounds, and the results run in exactly the direction that should make anyone cautious. A 2014 trial in hard-to-heal venous leg ulcers found the peptide safe and reported a marked effect, with mean ulcer area down 68% at the lower concentration. A 2021 multicenter trial in 148 patients then found no significant improvement in healing across the whole cohort, with benefit only in a post-hoc subgroup with large ulcers. A separate randomized trial in diabetic foot ulcers reported benefit.

SNAP-8 (acetyl octapeptide-3) is a cosmetic peptide sold as a topical alternative to botulinum toxin. The idea is a mimic of the N-terminal end of SNAP-25, one of the SNARE proteins that lets a nerve terminal release acetylcholine; a decoy that competes for a place in the SNARE complex should weaken muscle contraction and so soften expression lines. That is the same mechanism claimed for its better-known and shorter predecessor Argireline (acetyl hexapeptide-8), which has been through at least one randomized placebo-controlled trial. SNAP-8 itself has essentially no independent clinical literature. It appears in studies of multi-peptide microneedle patches where it is one ingredient among several, from which nothing can be attributed to it specifically.

TB-500 is a product built on Ac-LKKTETQ, a synthetic, acetylated copy of the seven-amino-acid actin-binding region of thymosin beta-4. It began as a veterinary preparation and is marketed for wound healing and tissue repair. It has never been tested for efficacy in humans. In a lab study, the intact peptide did not speed wound closure; one of its breakdown products did.

Thymosin beta-4 (Tβ4) is a 43-amino-acid protein found in almost every cell, where it is the main store of unused actin, the building block of the cell skeleton. Animal studies report faster skin-wound healing, stronger repaired ligaments and improved recovery after heart or brain injury. Small human trials of topical treatment for venous ulcers and eye disease have encouraging but inconclusive findings. It is not approved as a medicine.

VIP - vasoactive intestinal peptide - is a 28-amino-acid neuropeptide the body makes, densely present in the lung, where it relaxes smooth muscle, dilates pulmonary vessels and restrains inflammation. As a drug it is called aviptadil, and it has been tried in three quite different settings with three different outcomes. Inhaled VIP in sarcoidosis was safe and produced measurable immunoregulatory effects in an open phase 2 study. Inhaled aviptadil in pulmonary hypertension gave modest hemodynamic changes in a 20-patient study. And in COVID-19 respiratory failure, one 196-patient randomized trial reported a survival benefit at 60 days while the larger, better-powered TESICO trial found nothing. That sequence - promising small trial, null large trial - is the most informative thing about it.

AOD-9604 is a synthetic copy of the last fifteen amino acids of growth hormone, with a tyrosine stuck on the front. The idea, worked out at Monash University in the 1990s, is that this is the part of growth hormone that burns fat, separated from the parts that raise IGF-1 and blood sugar. In obese mice it reduced weight gain and fat mass and raised fat oxidation and energy expenditure; none of these studies measured IGF-1, so the separation the molecule is named for has not actually been demonstrated. It was developed for obesity by Metabolic Pharmaceuticals and abandoned. No trial of AOD-9604 in humans for weight, fat or anything else appears in the published literature — the human evidence for it is adipose tissue in a dish.

Capromorelin is an orally active ghrelin-receptor agonist from the Pfizer pyrazolinone-piperidine series. It has the best human trial of any compound in this group after MK-677: 395 adults aged 65-84 with mild functional limitation, randomized to four dose schedules or placebo. At six months, lean body mass had risen 1.4 kg against 0.3 kg on placebo, and — unusually for this class — a physical performance measure improved, with tandem walk better by 0.9 seconds at 6 months and stair climb by 12 months. Fasting glucose, HbA1c and insulin resistance all rose, and fatigue and insomnia were reported. The human program was stopped; capromorelin is instead approved as a veterinary appetite stimulant for dogs and cats.

CJC-1295 is GHRH(1-29) with four amino acid substitutions and a maleimide group that makes it latch permanently onto albumin in the bloodstream, stretching a peptide with a four-minute half-life into one lasting almost a week. In the one published human trial, single subcutaneous doses raised growth hormone 2- to 10-fold for six days or more and IGF-1 1.5- to 3-fold for 9-11 days, with an estimated half-life of 5.8-8.1 days. That is the entire human efficacy literature: 28- and 49-day dose-ranging studies in healthy volunteers, with no measurement of muscle, fat, strength or anything else clinical. Confusingly, most of what is sold as "CJC-1295" is the version without the albumin-binding group, which is simply modified GHRH(1-29) and lasts hours, not days.

GHRP-2 (pralmorelin) is a synthetic hexapeptide that releases growth hormone through the ghrelin receptor, about as strongly as hexarelin and more strongly than GHRH. Japan licensed it as a single-dose diagnostic test for growth hormone deficiency, and that is essentially its whole clinical career. It is not selective: at growth hormone-releasing doses it also raises prolactin, and raises ACTH and cortisol about as much as CRH does. Repeated dosing over days to weeks produces complex changes in the growth hormone axis, including desensitization depending on dose and frequency. There is no controlled trial of GHRP-2 for muscle, fat or strength in healthy people.

GHRP-6 is the original growth hormone-releasing peptide, the compound whose receptor turned out to be the ghrelin receptor. In people it releases about three times as much growth hormone as GHRH, and combining the two is strongly synergistic. Unusually for a growth hormone stimulus, the response barely declines with age. Its pharmacokinetics are known: after an intravenous bolus the distribution half-life is about 7.6 minutes and elimination about 2.5 hours. What does not exist is any trial of what taking it for weeks or months does to IGF-1, muscle or fat in healthy people; it also raises ACTH and cortisol, and it makes people hungry.

Hexarelin is a synthetic hexapeptide that releases growth hormone through the ghrelin receptor, and it does so more strongly than GHRH itself: 1 ug/kg intravenously produced about twice the growth hormone response of the same dose of GHRH in healthy young men. It has been studied mainly as a diagnostic agent for growth hormone deficiency, where hexarelin plus GHRH matches the insulin tolerance test. The problem with taking it is tachyphylaxis: over 16 weeks of twice-daily subcutaneous dosing the growth hormone response fell by about half, IGF-1 did not change at all, and body composition and bone density did not move. Like GHRP-2, it also raises prolactin, ACTH and cortisol.

HGH fragment 176-191 is the C-terminal tail of human growth hormone, synthesized on its own. It is the peptide behind AOD-9604, which is this same fragment with a tyrosine added, and the two share a literature. In obese mice, chronic treatment cut cumulative weight gain and fat mass, and it suppressed fat synthesis as strongly as the intact hormone, and the AOD-coded analog raised lipolytic activity in fat tissue from obese rodents and from humans in a dish. No study in this literature measured IGF-1, and no trial has ever given the peptide to a person: everything known about it comes from mice, rats and isolated cells.

Ipamorelin is a synthetic pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) that releases growth hormone through the ghrelin receptor. Novo Nordisk designed it in the 1990s from the GHRP-1 series, and its selling point was selectivity: in pigs it released growth hormone as strongly as GHRP-6 but, unlike GHRP-6 and GHRP-2, did not raise ACTH or cortisol even at more than 200 times the effective dose. The catch is that almost nothing has been published about what it does in people. The one controlled human trial gave it intravenously for postoperative bowel paralysis, and found no benefit over placebo. No published human study has measured growth hormone, IGF-1 or body composition on ipamorelin.

MK-677 (ibutamoren) is an orally active drug that mimics ghrelin at the GHS-R1a receptor, making the pituitary release more of the body's own growth hormone in its normal pulses. It reliably raises growth hormone and IGF-1: 25 mg daily restored IGF-1 in older adults to young-adult levels within four weeks, and a two-year randomized trial found about 1.1 kg more fat-free mass at 12 months than placebo. What it has never shown is a benefit that people can feel: the same trial found no change in strength, walking, stair climbing or quality of life, and trials in hip-fracture recovery and Alzheimer's disease were negative. It consistently raises fasting glucose, HbA1c and appetite, and it was never approved for any human use.

Sermorelin is GHRH(1-29), the shortest fragment of growth hormone-releasing hormone that keeps full activity, and it is the parent of every GHRH analog including tesamorelin and CJC-1295. It was a licensed medicine: a diagnostic injection for pituitary function and, briefly, a treatment for short stature in children. It reliably releases growth hormone, but as a treatment it lost to recombinant growth hormone in head-to-head comparisons — children on daily growth hormone grew faster than children on GHRH(1-29), and in a randomized comparison only the growth hormone group gained height relative to bone age. Its half-life is about four minutes. It is no longer marketed in the US, and there is no trial of it in healthy adults for any purpose.

Somatropin is recombinant human growth hormone — the 191-amino-acid protein itself, which is what "HGH 191AA" on a vial means. It is a long-approved prescription medicine for growth hormone deficiency and several causes of short stature. Outside those uses, the evidence is much less flattering than its reputation. In healthy older adults, a meta-analysis of 18 study populations found about 2.1 kg more lean mass and 2.1 kg less fat, no weight change, no improvement in bone density, and significantly more soft-tissue swelling, joint pain, carpal tunnel syndrome, gynecomastia and new diabetes — concluding it cannot be recommended as an anti-aging therapy. In young athletes the pattern repeats: lean mass up 2.1 kg, strength and exercise capacity not improved, and more swelling and fatigue.

Tesamorelin (Egrifta) is a synthetic version of growth hormone-releasing hormone (GHRH). It makes the pituitary release more of the body's own growth hormone. It is approved to reduce excess abdominal fat in people with HIV. In two phase 3 trials, daily injections cut visceral (deep abdominal) fat by about 15% more than placebo over 26 weeks while leaving fat under the skin alone, and it also lowered liver fat. The fat returns once treatment stops. One trial in older adults reported better executive function, but a later trial in people with HIV found no clear cognitive benefit.

IGF-1 DES is IGF-1 with its first three amino acids — glycine, proline, glutamate — clipped off. Unlike most designer peptides it is a real thing that occurs in the body: it has been isolated from bovine colostrum, human brain and porcine uterus, and an acid protease in serum makes it from intact IGF-1. Losing the glutamate at position 3 costs it almost all of its affinity for the IGF binding proteins, so it is about ten times more potent than IGF-1 at growing cells in a dish. In rats it is cleared roughly four times faster than IGF-1 and distributes into tissue far more readily, and in catabolic models it improved nitrogen balance and slowed muscle protein breakdown. Thirty years on from the review that said its clinical opportunities had not yet been evaluated, they still have not been: there is no published human trial.

IGF-1 LR3 is a laboratory-engineered version of insulin-like growth factor-1: the natural protein with glutamate at position 3 swapped for arginine and a 13-amino-acid extension bolted onto the N terminus. Both changes weaken its grip on the IGF binding proteins that normally hold IGF-1 in circulation, so more of it reaches the IGF-1 receptor. It was designed as a cell-culture and livestock research reagent, never as a medicine, and it has never been given to a person in a published trial. The animal work is not the story the bodybuilding market tells: in pigs a four-day infusion reduced daily weight gain and food intake and suppressed growth hormone, and in guinea pigs it enlarged the gut, kidneys, adrenals and spleen without increasing overall growth. It is prohibited in sport, and detectable in serum by validated antidoping methods.

Mechano growth factor is a splice variant of the IGF-1 gene, IGF-1Ec in humans, switched on in muscle after mechanical loading or damage. Its distinctive part is the E domain, and what is sold as "MGF" is a synthetic 24-amino-acid peptide copied from the end of that domain. PEG-MGF adds polyethylene glycol to slow its disappearance. The E peptide has real preclinical credentials: it pushes human muscle satellite cells to proliferate and fuse, and it does so through a receptor that is not the IGF-1 receptor. It also has three problems. It did not work on satellite cells from old muscle, the age group the sarcopenia pitch targets; the same peptide drives growth in prostate cancer cells, and the IGF-1Ec transcript is overexpressed in prostate and colorectal tumors; and there is no published study of the PEGylated form in any species, let alone a human trial.

Cagrilintide is a long-acting analog of amylin, the pancreatic hormone co-secreted with insulin that signals meal-related satiety. It works on its own - the phase 2 trial gave up to 10.8% weight loss at 4.5 mg over 26 weeks, beating daily liraglutide 3.0 mg at 9.0% - but it is being developed primarily as half of CagriSema, a fixed combination with semaglutide. That combination gave 20.4% weight loss at 68 weeks against 3.0% on placebo in REDEFINE 1, and 13.7% against 3.4% in people with type 2 diabetes. The interest in amylin is that it suppresses appetite by a different route from GLP-1, so the two add up rather than overlap - and in eloralintide's phase 2 trial the amylin mechanism alone reached 20%.

Eloralintide is a selective amylin receptor agonist - selective being the operative word, since amylin signals through receptor complexes built on the calcitonin receptor and earlier analogs hit both. Its phase 2 trial is the reason the amylin class is now taken seriously on its own: 48 weeks of once-weekly dosing produced mean weight reductions of 18% at 6 mg and 20% at 9 mg, against 0.4% on placebo. That is semaglutide territory, reached without touching the GLP-1 receptor at all. The adverse-effect profile is also different rather than simply lighter: nausea peaked at 64% in one dose group, and fatigue - which is not a prominent incretin effect - reached 43-46% at the higher doses. There is no phase 3 data, and no cardiovascular or long-term evidence of any kind.

Exenatide is the original GLP-1 receptor agonist, and it came out of a lizard. Exendin-4 was isolated from the venom of the Gila monster, Heloderma suspectum, and turned out to be a full agonist at the human GLP-1 receptor that resists the enzyme which destroys the human hormone. It reached the market in 2005 as twice-daily Byetta and later as weekly Bydureon, and everything that followed - liraglutide, semaglutide, tirzepatide - descends from the idea it proved. By modern standards it is weak: roughly 1% of body weight lost, and its cardiovascular outcome trial, EXSCEL, missed superiority at a hazard ratio of 0.91 with a confidence interval touching 1.00. Its most interesting current life is outside diabetes, and that story ended badly too: a promising phase 2 result in Parkinson's disease was followed by a clean negative phase 3.

Mazdutide is a glucagon/GLP-1 dual agonist built on oxyntomodulin, a natural gut peptide that hits both receptors. It was licensed from Eli Lilly to Innovent Biologics and developed almost entirely in China, which makes its trial program unusual: every efficacy result comes from Chinese participants, who start from a lower mean body weight than the Western obesity trials. GLORY-1 gave 14.01% weight loss at 6 mg over 48 weeks against a 0.30% gain on placebo, and GLORY-2, at 9 mg over 60 weeks, gave 16.65% against a 1.50% loss. Those are tirzepatide-class numbers. The caveat is the population: whether they transfer to a heavier, more metabolically damaged Western cohort has not been tested, and a head-to-head against semaglutide is only now running.

Orforglipron is the first GLP-1 receptor agonist that is not a peptide. That matters for a practical reason: a small molecule can be made by ordinary chemical synthesis rather than fermentation, and swallowed as a normal tablet with no food or water restrictions - unlike oral semaglutide, which needs an absorption enhancer and an empty stomach. In ATTAIN-1, 72 weeks of 36 mg daily gave a mean 11.2% weight loss against 2.1% on placebo; in ATTAIN-2, in people with obesity and type 2 diabetes, 9.6% against 2.5%. That places it below injected semaglutide and well below tirzepatide on weight, and roughly where oral semaglutide sits - while being far easier to take and, in principle, far easier to manufacture at scale.

Retatrutide is an experimental once-weekly injected peptide from Eli Lilly that activates three hormone receptors: GIP, GLP-1 and glucagon. In a 48-week phase 2 trial in adults with obesity, the 12 mg dose lowered body weight by 24.2%, against 2.1% on placebo. The first phase 3 trial, in type 2 diabetes, confirmed large falls in HbA1c and weight. It is not approved; in the cited literature its phase 3 obesity trials are still under way.

Semaglutide is the GLP-1 receptor agonist that turned obesity into a treatable condition in mainstream medicine. In STEP 1, 68 weeks of 2.4 mg weekly produced a mean 14.9% weight loss against 2.4% on placebo, with half of participants losing 15% or more. In SELECT, 17,604 people with obesity and established cardiovascular disease but no diabetes had a 20% reduction in major cardiovascular events over the trial - the result that moved it from a weight drug to a cardiovascular one. The costs are real and well documented: gastrointestinal effects in most people, about 4.5% discontinuing for them in STEP 1, and weight regain when it stops. A year after withdrawal in the STEP 1 extension, participants had regained two-thirds of what they lost.

Survodutide activates the glucagon receptor as well as the GLP-1 receptor. Adding glucagon agonism to an incretin is counterintuitive - glucagon raises blood sugar - but it also raises energy expenditure and acts directly on the liver, and in a weight-losing context the GLP-1 arm covers the glycemic downside. The phase 2 obesity trial gave 14.9% weight loss at 4.8 mg over 46 weeks against 2.8% on placebo. The more striking result is hepatic: in a phase 2 trial in MASH, 48 weeks improved histological steatohepatitis without worsening fibrosis in 47-62% of participants against 14% on placebo, and a phase 3 trial in MASLD found 84.2% achieved a 30% or greater reduction in liver fat against 24.3%. The tolerability cost is high: vomiting in 41% against 4% on placebo in the MASH trial.

Tirzepatide is a once-weekly injected peptide that activates two gut-hormone receptors, GIP and GLP-1. It is approved for type 2 diabetes and, as Zepbound, for chronic weight management. In a 72-week trial in adults with obesity, the top dose lowered body weight by 20.9%, against 3.1% on placebo. In a head-to-head trial it caused more weight loss than semaglutide (20.2% vs 13.7%). Most side effects are gastrointestinal, and the weight comes back when treatment stops.

DSIP is a nine-amino-acid peptide pulled out of the cerebral venous blood of sleeping rabbits in Basel in 1977 and named for what its discoverers thought it did. Unusually for a peptide sold online, it was actually tested in people: several small controlled trials in insomniacs through the 1980s, all using intravenous doses of 25 nmol/kg. The early results were encouraging and the later, better-controlled ones were not — one concluded sleep improvement was "of little clinical significance" and a 1992 double-blind study found the effects weak, partly an artifact of the placebo group, and "not likely to be of major therapeutic benefit". Nearly fifty years on, no DSIP gene, precursor protein or receptor has been identified, and a 2006 review called the sleep hypothesis "extremely poorly documented and still weak". Its plasma half-life in dogs is four minutes.

Epitalon is a four-amino-acid peptide, Ala-Glu-Asp-Gly, designed in St Petersburg from the amino acid composition of Epithalamin — a bovine pineal gland extract — and later shown to be present in that extract. It is the peptide behind the claim that you can lengthen your telomeres, and that claim does rest on real experiments: Khavinson's group reported telomerase activation and telomere elongation in human fetal fibroblasts in 2003, and an independent laboratory reproduced dose-dependent telomere lengthening in human cell lines in 2025. What the marketing tends to blur is that the long-term human trials — the ones showing lower mortality in elderly cardiac patients — used Epithalamin, the extract, not the synthetic tetrapeptide, and that almost the entire literature on both comes from one research group.

GB-115 is a synthetic glycyl-tryptophan dipeptide analog of cholecystokinin studied as an anxiolytic. A Russian open-label pilot in 31 people with generalized anxiety disorder reported reduced anxiety and fatigue over 21 days, with 6 mg daily selected after a small dose-finding stage. Without a placebo group, efficacy remains uncertain.

Noopept is a Russian dipeptide designed to mimic the piracetam pharmacophore, reported active at doses about a thousandth of piracetam's. It is a prodrug: the parent is undetectable in rat brain an hour after dosing, and the active species is cycloprolylglycine, a peptide the brain already makes. Its clinical evidence is Russian, small and uncontrolled, and its primary molecular action appears to be stabilization of HIF-1.

Pinealon is a three-amino-acid peptide, Glu-Asp-Arg, from the same St Petersburg program that produced epitalon — designed for the brain rather than the pineal gland despite the name. The cell work is real: it cuts reactive oxygen species and necrotic death in cerebellar granule neurons, neutrophils and PC12 cells, and its labeled form reaches the nucleus and binds DNA sequence-selectively. The animal work is more mixed than the marketing suggests. In old rats given it before carotid occlusion, survival improved but position-finding, motivational behavior and motor performance all fell and brain caspase-3 rose. The one human study — 32 patients, open, Russian-language — found Pinealon less effective than its sister peptide Vesugen, with prooxidant activity on chemiluminescence and a fall in circulating CD34+ cells that the authors read as inhibition of hemopoiesis.

Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) described as an analog of tuftsin. It is studied as an anxiolytic. In Russian clinical studies of generalized anxiety and related disorders, it matched the benzodiazepine medazepam on anxiety, and adding it to phenazepam reduced phenazepam's side effects. Proposed mechanisms include slowing enkephalin breakdown and modulating GABA-A receptors.

Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro), an analog of the ACTH(4-10) fragment of the hormone ACTH, given as a nasal spray. It is used in acute stroke therapy. In rats it raises BDNF and its receptor in the brain. Almost all of its clinical research is published in Russian, and the human studies are small and mostly unblinded.

Bremelanotide (PT-141, Vyleesi) is a cyclic seven-amino-acid analog of α-MSH that activates melanocortin receptors in the brain, chiefly MC4R. It is approved in the US for low sexual desire (hypoactive sexual desire disorder) in premenopausal women, based on two phase 3 trials of 1,267 women in which an as-needed 1.75 mg injection modestly increased desire and reduced distress. It was first developed as a nasal spray for erectile dysfunction, where it produced erections in men who did not respond well to sildenafil. Nausea affects about 40% of users.

GHK-Cu is the copper complex of GHK (glycyl-histidyl-lysine), a tripeptide found in human plasma, saliva and urine whose levels fall with age. In lab studies it raises collagen and elastin production and supports skin cells, and it is a common ingredient in anti-wrinkle products. The best human evidence is one 1994 trial in which a GHK-Cu gel sped the healing of diabetic foot ulcers. The cosmetic studies are described mainly in reviews by the peptide's discoverer, and an independent review found few published clinical studies.

Kisspeptin-10 is the shortest natural form of kisspeptin, the hypothalamic hormone that switches on the reproductive axis. It is the ten amino acids at the end of the longer kisspeptins and keeps their full activity at the kisspeptin receptor. A single injection releases GnRH and so LH within minutes, and infusions raise testosterone in healthy men and in men with type 2 diabetes and low testosterone. It clears from the blood in about 4 minutes, so studies have used infusions, and its effects in women depend on the phase of the menstrual cycle. It is not approved for any use.

Oxytocin is a nine-amino-acid hormone made in the hypothalamus. It contracts the uterus in labor and releases milk, and in the brain it acts on social, sexual and stress behavior through a single receptor. Injected oxytocin is a standard drug for preventing bleeding after birth. As a nasal spray it raised oxytocin in the cerebrospinal fluid, but the large trials of intranasal oxytocin in autism and obesity were negative, a famous finding that it increases trust failed to replicate, and it did no better than placebo for women's sexual function.

B7-33 is a single-chain fragment of relaxin-2, the pregnancy hormone that softens connective tissue and dilates blood vessels. Full relaxin is a two-chain, three-disulfide protein that is expensive and awkward to make; serelaxin, the recombinant version, failed its phase 3 heart failure trial. B7-33 is an attempt to keep the anti-fibrotic and vasoprotective activity in a much simpler molecule, and the striking finding is that it is a functionally selective agonist at RXFP1 - it drives the anti-fibrotic pERK pathway without the cAMP signaling that relaxin also produces. In animals it replicates serelaxin's vasoprotective functions and reduced left ventricular fibrosis faster than perindopril in a cardiomyopathy model. No human study exists.

Bronchogen is the tetrapeptide Ala-Glu-Asp-Leu (AEDL), the lung member of the Khavinson family. Unusually for this group, some of its literature is actually about the organ it is named after: peptide therapy modulated the morphofunctional state of bronchial epithelium in rats with obstructive lung pathology, and a companion Russian-language paper reported anti-inflammatory and regenerative effects in the same model. Its most cited result is physical rather than biological - bronchogen raises the melting temperature of calf thymus and mouse liver DNA by 3.1 °C, measured by scanning microcalorimetry, over a narrow range of peptide-to-DNA ratios. That is direct evidence it binds DNA, and no evidence at all about lungs. There is no human trial.

Cardiogen is sold as the heart bioregulator of the Khavinson family, usually given the sequence Ala-Glu-Asp-Arg (AEDR). There is no published research on it. Searching the literature for cardiogen as a peptide returns nothing relevant - and it returns a great deal that is irrelevant, because CardioGen-82 is a completely different product: a rubidium-82 generator used for cardiac PET imaging. That collision means a casual search appears to find literature where none exists. Searching instead for the sequence, or for a heart-designated Khavinson tetrapeptide, returns nothing at all. This entry exists to record that absence and to flag the name collision.

Cartalax is the tripeptide Ala-Glu-Asp (AED), one of the short "peptide bioregulators" developed by Vladimir Khavinson's group in St Petersburg and promoted for cartilage. In cell cultures it switched on cartilage-forming genes in aging human stem cells and lowered markers of aging in chondrocytes. There are no published human trials, and almost every study comes from the developers' own group.

Cerebroprotein hydrolysate is a mixture of low-molecular-weight peptides and amino acids made by enzymatic digestion of pig brain - the same class of product as Cerebrolysin, with which it is used interchangeably in much of the literature. It is licensed and widely prescribed in parts of Asia, Eastern Europe and Latin America for stroke and dementia, and it has been assessed repeatedly by Cochrane. The conclusions are consistent and unflattering. For acute ischemic stroke: across seven RCTs and 1773 participants, no effect on death, and moderate-certainty evidence of an increase in non-fatal serious adverse events (RR 2.39, 95% CI 1.10-5.23). For vascular dementia: cognition and global function improved, but on very low-quality evidence throughout.

Chonluten is a tripeptide derived from bronchial epithelial cells, the second lung-designated member of the Khavinson family alongside bronchogen. Its literature is essentially one study, but it is a better one than most in this group: an Italian group at the University of Chieti, working with the St Petersburg institute, tested five Khavinson peptides on human THP-1 monocytes. Chonluten inhibited tumor necrosis factor production by monocytes stimulated with bacterial lipopolysaccharide, all five peptides reduced LPS-stimulated TNF and IL-6 expression in differentiated cells, and all reduced adhesion of treated monocytes to activated endothelium. That is a coherent anti-inflammatory result in human cells, from a partly independent group. There is no animal study specific to chonluten in the indexed literature, and no human trial.

Cortagen is the tetrapeptide Ala-Glu-Asp-Pro, the brain-cortex member of the Khavinson family. It has the most concrete animal result in the whole short-peptide program, and it is worth stating precisely: 10 µg/kg intramuscularly for ten days after the sciatic nerve was cut and sutured increased the growth rate of regenerating nerve fibers by 27% and their conduction velocity by 40%. That is a specific dose, a specific model, and two quantified outcomes - which is more than most compounds in this group offer. A follow-up examined delayed effects on injured nerve function, and a microarray study looked at gene expression in mouse heart. The human literature is a Russian-language report of Cortexin and Cortagen in chronic cerebral ischemia.

Crystagen is one of the immune-designated short peptides in the Khavinson family, and its indexed literature consists of a single Russian-language paper: a study of the molecular aspects of immunoprotective activity of Vilon, Timogen, Crystagen and R-1 in spleen during aging. That is the entire file. There is no animal efficacy study specific to it, no human study, no pharmacokinetics and no published sequence in the sources available here. Everything else asserted about it - the organ it regulates, what it does, how to take it - comes from sellers and from the general claims made for the family as a whole.

DNSP-11 is an 11-amino-acid peptide from the pro-domain of GDNF, the glial cell line-derived neurotrophic factor that has been the most persistent hope in Parkinson's disease research. GDNF itself protects and restores dopamine neurons in animals, but it is a large protein that does not cross the blood-brain barrier and has repeatedly disappointed in human trials requiring direct brain infusion. DNSP-11 is an attempt to get the effect from a fragment small enough to deliver differently, and in rats it does have dopamine-neuron-stimulating actions, increases ERK1/2 phosphorylation and works when given intranasally. There is no human study. Notably, it does not appear to act through GDNF's own receptor.

FGL is a synthetic peptide copying the fibroblast growth factor receptor binding site of NCAM, the neural cell adhesion molecule that governs how neurons connect and reconnect. The rodent literature is unusually consistent for a compound in this group: it prevented memory impairment and loss of newborn hippocampal cells after chronic stress in aging animals, rescued spatial learning after neonatal phencyclidine treatment, alleviated amyloid-beta-induced CA1 pyramidal cell loss in young adult rats, mobilized neural stem cells and has an anti-inflammatory action of its own. Those are five separate models pointing the same way. There is still no human trial, and the NCAM-targeting approach has been reviewed as a pharmacological strategy without reaching the clinic.

Livagen is the tetrapeptide Lys-Glu-Asp-Ala, designed in the Khavinson program as the liver bioregulator. Its literature is narrower than vilon's and almost entirely about chromatin. In lymphocytes taken from elderly donors it activated ribosomal genes, decondensed pericentromeric structural heterochromatin and released genes that had been repressed by age-related condensation. It also reduced chromosomal aberrations induced by cobalt ions in cells from old donors. Beyond that there is a rat study of digestive enzyme activity, and that is close to the whole file. No animal lifespan study, no liver disease model, no human trial.

Ovagen is sold as one of the Khavinson organ peptides, usually given the sequence Glu-Asp-Leu and assigned to the liver or the ovary depending on the seller. There is no published research on it under that identity. Searching the literature returns a substantial set of papers - and every one of them is about a completely different product: Ovagen is the trade name of a veterinary follicle-stimulating hormone preparation used to superovulate goats, sheep and cattle. That is a pituitary gonadotrophin extract, not a tripeptide, and it has no relationship to the compound sold under this name to humans. This entry exists to record the absence of evidence and to flag the collision.

P-21, more precisely written P021, is a tetrapeptide derived from an active region of ciliary neurotrophic factor, with an adamantane group attached to make it stable and brain-penetrant. It comes from Khalid Iqbal's laboratory, and the work is deliberate rather than opportunistic: the founding paper showed the adamantylated peptides improved learning and memory and promoted neurogenesis and synaptic plasticity in mice, and two later studies showed that early treatment prevented amyloid and tau pathology, neurodegeneration and cognitive deficit in mouse models, including when started in early postnatal development. That is a prevention result, which is rarer and harder than rescuing an already-damaged animal. There is no human trial.

PNC-27 is a chimeric peptide - a fragment of p53 that binds HDM-2, joined to penetratin, a sequence that carries cargo across membranes. Its proposed mechanism is unusual and specific: cancer cells display HDM-2 in their plasma membrane, normal cells do not, and PNC-27 binds that membrane-bound HDM-2 and forms pores, lysing the cell. In leukemia cells it induced necrosis while sparing normal hematopoietic cells, and later work describes additional disruption of mitochondrial membranes. It is a fifteen-year-old cell-culture program from a small group of investigators, with no human trial and no published clinical development.

Teriparatide is the first 34 amino acids of human parathyroid hormone, and it is the odd one out in this group: a licensed medicine with a fracture-outcome trial behind it. Parathyroid hormone continuously elevated - as in hyperparathyroidism - destroys bone. Given as a single daily injection it does the opposite and builds it, which is one of the more surprising dose-schedule effects in pharmacology. The pivotal trial randomized 1637 postmenopausal women with prior vertebral fractures: new vertebral fractures occurred in 14% on placebo against 5% and 4% on 20 µg and 40 µg. VERO later compared it head to head with risedronate in severe osteoporosis and found new vertebral fractures in 5.4% against 12.0%, a hazard ratio of 0.44. It is included here because it is a peptide bioregulator in the literal sense - and because it shows what the rest of this group's evidence would look like if it existed.

Testagen is the tetrapeptide Lys-Glu-Asp-Gly (KEDG), designated the reproductive bioregulator in the Khavinson family and sold on the implication that it supports testicular function. Its indexed biological literature is one study, and that study is not about the testes: testagen was one of several fluorescently labeled peptides shown to enter the nucleus of HeLa cells and to bind deoxyribooligonucleotides with a preference for CAG-containing sequences. There is no study of testosterone, spermatogenesis, fertility or any reproductive endpoint. The only other indexed paper using the name is a 2025 materials-science study of testagen as a corrosion inhibitor on copper surfaces in saline, which is a legitimate use of a peptide and tells you nothing about biology.

Thymalin is a polypeptide extract of calf thymus, made in St Petersburg from the 1970s and the thymic half of Vladimir Khavinson's bioregulator program - epitalon's parent extract Epithalamin being the pineal half. Its most striking claim is also its most-cited paper: a controlled study in elderly people reporting that mortality fell 2.0-2.1-fold in the Thymalin group, and 4.1-fold in those given Thymalin with Epithalamin annually for six years. That is an extraordinary result, published in a journal with limited reach, from the group that developed the compound, and never independently replicated. It is not a defined molecule: it is a tissue hydrolysate whose composition is set by a manufacturing process, and the dipeptides KE and EW have since been identified within it.

Thymosin alpha-1 is a 28-residue peptide from thymosin fraction 5, a thymus extract, and it is licensed in around thirty countries as an immunomodulator - mainly for chronic hepatitis B and as an adjunct in sepsis. It has a better evidence base than anything else in this group except teriparatide, and it has just had the reckoning that comes with proper trials. In 2013 ETASS reported 28-day mortality in severe sepsis of 26.0% against 35.0% on control, and a decade of meta-analyses built on that. Then TESTS, a 1106-patient double-blind placebo-controlled phase 3 trial published in the BMJ in 2025, found 28-day mortality of 23.4% against 24.1%, hazard ratio 0.99 - no benefit. A 2026 Cochrane review of hepatitis B rates all its evidence as very low certainty.

Vesugen is the tripeptide Lys-Glu-Asp (KED), designated the vascular bioregulator in the Khavinson program. It appears in the single small human study this family has - 32 patients aged 41-83 with chronic polymorbidity and organic brain syndrome, in which Vesugen and pinealon were reported to slow biological-age indicators, with Vesugen the more effective of the two. The same study reported prooxidant activity on chemiluminescence and a fall in circulating CD34+ hematopoietic cells that the authors themselves flagged as needing further work. Beyond that its literature is vascular endothelial cell proliferation in aging, atherosclerosis and restenosis, neurogenesis in Alzheimer's disease and antihypoxic activity in rodents.

Vilon is the dipeptide Lys-Glu (KE), the shortest compound in the Khavinson bioregulator program and the thymic counterpart to epitalon. Its mouse data are the most substantial in this group: subcutaneous vilon from the sixth month of life increased physical activity and endurance, lowered body temperature, prolonged lifespan and prevented spontaneous tumors, with no unfavorable effects on development. It also has a genuinely interesting mechanistic result - DNA microarray of 15,247 clones in mouse heart found vilon changed expression of 36, and epitalon of 98, which is a specific and modest effect rather than the sweeping one the marketing implies. As with the rest of the program, the human work is chromatin studies in lymphocytes from elderly donors, not clinical trials.

Elamipretide (SS-31) is a four-amino-acid peptide that concentrates in the inner mitochondrial membrane and binds cardiolipin, a membrane lipid that mitochondria need to form their inner folds (cristae). In September 2025 the US FDA gave it accelerated approval, as Forzinity, to improve muscle strength in Barth syndrome. Its randomized trials have mostly missed their primary endpoints, in Barth syndrome, mitochondrial myopathy, heart attack and macular degeneration. The positive signals come mainly from open-label extensions and secondary measures.

HDAP2 is a synthetic four-amino-acid peptide, biotin-D-Arg-Phe-Phe-D-Arg-amide, designed to bind cardiolipin, the signature lipid of the inner mitochondrial membrane, and hold it in its normal bilayer form. In mice it preserved retinal ganglion cells after optic nerve crush, and both the cells and their axons in an inherited glaucoma model, without lowering eye pressure. All of the evidence is from cells and mice, from the lab that invented and patented it. It has not been tested in people.

Humanin is a 24-amino-acid peptide encoded not in the nucleus but inside mitochondrial DNA, within the 16S rRNA gene. It was found in 2001 by screening a surviving region of an Alzheimer's brain for factors that protect neurons from amyloid-beta toxicity, which is an unusually direct origin story. It belongs to the same class as mots-c - mitochondria-derived peptides, or mitokines, which appear to signal cellular stress from mitochondria to the rest of the body. The preclinical literature is broad: cytoprotection against apoptosis, cardiovascular effects, roles in cancer and degenerative disease and in the testis. There is no human trial. Circulating humanin declines with age, which is interesting and is not the same as a reason to inject it.

MOTS-c is a 16-amino-acid peptide encoded in mitochondrial DNA, not in the cell nucleus. In mice, injections prevented diet-induced obesity and insulin resistance and improved running capacity at every age tested. In people, exercise raises the body's own MOTS-c, but no trial has given MOTS-c to humans, and measurements of it in blood disagree between methods.