Evidence table
Every study on this site, in one table
113 studies across 12 peptides, each one graded by how strong it is and linked to its PubMed record. This is the whole evidence base behind every page here. 40 human trial. 34 small human study. 17 review. 15 animals. 4 cells in a dish. 3 systematic review.
Sources checked 08-24-2026. Ordered by how often each peptide is searched, strongest study first within each one. Nothing on this page is a recommendation and no amounts appear anywhere on this site.
Count the rows before you read them. Most of what is sold as a peptide has been tested in mice, in cells, or in a dozen people with no comparison group. A long table is not a strong table, so we show you the grade in every row.
| Peptide | Who or what was studied | What was found, and the catch | Source | Where we use it |
|---|---|---|---|---|
| Tirzepatide | Human trial n = 670 people | After 36 weeks of open label treatment that produced about 21% weight loss, people switched to placebo gained back enough to end 14.0% heavier over the following 52 weeks, while those who kept taking the drug lost a further 5.5%. Limit: This is the trial that shows the benefit depends on staying on the drug indefinitely, and no trial has tested beyond 176 weeks. The first 36 weeks were open label, and only people who tolerated treatment reached randomization, so the randomized group is a filtered, tolerant population. It compares continuing with abrupt stopping, and says nothing about whether a gradual taper or a structured maintenance plan would land differently. Eli Lilly funded. | Aronne 2024 PMID 38078870 | Weight loss Tirzepatide |
| Tirzepatide | Human trial n = 751 people | Head to head against a once weekly GLP-1 only drug over 72 weeks in adults with obesity and no diabetes, weight fell 20.2% versus 13.7%, and waist circumference fell 18.4 cm versus 13.0 cm. Limit: Open label, and weight related outcomes plus side effect reporting are exactly the things knowing your assignment can shift. Phase 3b, designed and funded by the company that makes the winning drug. People with diabetes were excluded. 72 weeks, so nothing here speaks to durability. | Aronne 2025 PMID 40353578 | Weight loss Tirzepatide |
| Tirzepatide | Human trial n = 475 people | Added on top of daily basal insulin for 40 weeks, HbA1c fell 2.11 to 2.40 percentage points versus 0.86 on placebo, and weight fell 5.4 to 8.8 kg while the placebo group gained 1.6 kg. Limit: This is an add-on design, so the real comparison is insulin plus tirzepatide against insulin alone, not against another modern drug. Only 40 weeks. Because everyone stayed on insulin, low blood sugar episodes were common in every arm including placebo, so this trial cannot tell you the drug's own hypoglycemia risk. Eli Lilly funded. | Dahl 2022 PMID 35133415 | Tirzepatide |
| Tirzepatide | Human trial n = 2002 people | In people with type 2 diabetes who already had heart disease or were at high risk of it, HbA1c fell about 1 percentage point more than with titrated insulin glargine over 52 weeks, and adjudicated major heart events were fewer in number, hazard ratio 0.74. Limit: Open label. The heart event count was a safety readout, not the primary endpoint, and the trial was never powered to prove a heart benefit: the confidence interval, 0.51 to 1.08, includes no effect at all. Insulin comparator again. Treatment ran at least 52 weeks and up to 104. Eli Lilly funded. | Del Prato 2021 PMID 34672967 | Tirzepatide |
| Tirzepatide | Human trial n = 1879 people | Head to head against a once weekly GLP-1 only drug over 40 weeks, HbA1c fell further on tirzepatide at every dose level tested, and weight fell by an extra 1.9 to 5.5 kg. Limit: Open label: everyone knew which drug they were on, which can bend both side effect reporting and anything the participant reports. The comparator drug was used below the maximum now available for type 2 diabetes, so this is not maximum against maximum. Only 40 weeks. Run and funded by Eli Lilly, which makes the drug that won. | Frías 2021 PMID 34170647 | Tirzepatide |
| Tirzepatide | Human trial n = 938 people | In adults who had both obesity and type 2 diabetes, body weight fell 12.8 to 14.7% over 72 weeks versus 3.2% on placebo. Limit: Weight loss here was noticeably smaller than in people without diabetes, and that is the honest comparison to hold against the widely quoted obesity numbers. Placebo comparator. Only the two higher dose levels were tested, so the lowest is unstudied in this group. 72 weeks. Eli Lilly funded. | Garvey 2023 PMID 37385275 | Weight loss Tirzepatide |
| Tirzepatide | Human trial n = 2539 people | In adults with obesity and without diabetes, average body weight fell 15.0 to 20.9% over 72 weeks versus 3.1% on placebo, and 85 to 91% lost at least 5% of their starting weight. Limit: People with diabetes were excluded, so these numbers do not carry over to them; the companion trial in people with diabetes produced clearly smaller losses. Placebo comparator. 72 weeks says nothing about year five. Blinding is fragile when one group visibly loses a fifth of its body weight. Stopping for side effects was 4.3 to 7.1% versus 2.6% on placebo. Eli Lilly funded. | Jastreboff 2022 PMID 35658024 | Weight loss Tirzepatide |
| Tirzepatide | Human trial n = 1032 people | Among the participants who had obesity plus prediabetes, weight was still down 12.3 to 19.7% at 176 weeks versus 1.3% on placebo, and 1.3% had developed type 2 diabetes versus 13.3%, a gap that held after 17 weeks off treatment. Limit: This covers only the prediabetes subgroup, 1032 of the 2539 people in the parent trial, and diabetes onset was a key secondary endpoint rather than the trial's main question. Three years plus is the longest randomized human exposure published for this drug, which means long term thyroid, pancreas and gallbladder outcomes past about four years are simply not established. Eli Lilly funded. | Jastreboff 2025 PMID 39536238 | Weight loss Tirzepatide |
| Tirzepatide | Human trial n = 1444 people | Against a daily basal insulin titrated to target over 52 weeks in people already taking metformin, HbA1c fell 1.93 to 2.37 percentage points versus 1.34, and weight fell 7.5 to 12.9 kg while the insulin group gained 2.3 kg. Limit: Open label. The comparator was insulin, which is expected to cause weight gain, so the weight result is close to a foregone conclusion and should not be read as a fair weight loss contest. Insulin naive participants only. The paper says stopping for side effects was more common on tirzepatide but gives no numbers in the abstract. Eli Lilly funded. | Ludvik 2021 PMID 34370970 | Tirzepatide |
| Tirzepatide | Human trial | In adults with obesity and moderate to severe obstructive sleep apnea, breathing interruptions per hour of sleep fell by about 20 to 24 events more than on placebo over 52 weeks, both in people using a breathing machine and in people who were not. Limit: Two separate trials reported in a single paper, and the combined enrollment is not given in the abstract, so the participant count is left blank here rather than guessed. The endpoint was events per hour on a sleep study, which is a measurement, not an outcome people feel: it does not show fewer crashes, less daytime sleepiness over years, or less heart disease. 52 weeks. Eli Lilly funded. | Malhotra 2024 PMID 38912654 | Tirzepatide |
| Tirzepatide | Human trial n = 13299 people | In people with type 2 diabetes and established artery disease, cardiovascular death, heart attack or stroke occurred in 12.2% on tirzepatide versus 13.1% on dulaglutide over a median treatment period of about 47 months: noninferior, but not superior. Limit: This is the headline caveat for the whole drug. Tirzepatide was not shown to be better than dulaglutide for heart outcomes; the superiority test gave P equal to 0.09. The dulaglutide comparator was held at a fixed dose below the maximum sold elsewhere while tirzepatide was titrated upward, so again this is not maximum against maximum. No placebo controlled heart outcome trial of tirzepatide exists. The wider cardiorenal figure people quote, hazard ratio 0.84, comes from a post hoc analysis (PMID 41903177), not the prespecified endpoint. Eli Lilly funded. | Nicholls 2025 PMID 41406444 | Tirzepatide |
| Tirzepatide | Human trial n = 731 people | In people with obesity and heart failure with preserved ejection fraction, the combined rate of cardiovascular death or a worsening heart failure event was 9.9% versus 15.3% on placebo over a median follow-up of about two years, and symptom scores improved more. Limit: The benefit came from fewer worsening heart failure events, not from fewer deaths: cardiovascular deaths were actually higher in number on tirzepatide, 8 versus 5, on counts far too small to interpret. Symptom scores are self reported, and blinding is hard to hold once one group visibly loses weight. FDA has approved no heart failure indication on the strength of this. Eli Lilly funded. Stopping for side effects was 6.3% versus 1.4%. | Packer 2025 PMID 39555826 | Tirzepatide |
| Tirzepatide | Human trial n = 478 people | In adults with type 2 diabetes managed by diet and exercise alone, HbA1c fell by 1.87 to 2.07 percentage points over 40 weeks while the placebo group barely moved, and weight fell by 7.0 to 9.5 kg. Limit: The comparator was placebo, not a current standard treatment, so this shows the drug beats nothing rather than beating what people would otherwise be given. Only 40 weeks. Participants were early in their diabetes and had never used an injectable diabetes medicine, which is an easier group to improve. Funded by Eli Lilly, the manufacturer. The published abstract does not state the dose escalation schedule. | Rosenstock 2021 PMID 34186022 | Tirzepatide |
| Tirzepatide | Human trial n = 1428 people | Against mealtime insulin lispro over 52 weeks in people already on basal insulin, HbA1c fell 2.1 percentage points versus 1.1, weight fell 9.0 kg versus a 3.2 kg gain, and low blood sugar episodes were roughly ten times less frequent. Limit: Open label, phase 3b. The comparator is mealtime insulin, which reliably causes weight gain and low blood sugar, so two of the three headline wins are partly baked into the study design. 52 weeks. Eli Lilly funded, across 135 sites in 15 countries. | Rosenstock 2023 PMID 37786396 | Tirzepatide |
| Retatrutide | Human trial n = 537 people | Across 40 weeks in adults with type 2 diabetes not on other diabetes drugs, HbA1c fell 1.69% to 1.94% depending on dose group against 0.81% on placebo, and weight fell 11.5% to 15.3% against 2.6%. Limit: This is the only phase 3 trial of retatrutide that has been peer reviewed, and it is a diabetes trial, not one of the big obesity trials people quote. Two deaths occurred, both in one retatrutide group, both reported by the sponsor as unrelated. Lilly ran it, and the same Lilly authors appear here as on the phase 2 papers. | Bajaj 2026 PMID 42250575 | Retatrutide |
| Retatrutide | Human trial n = 338 people | Over 48 weeks, adults with obesity lost about 8.7% of body weight in the lowest dose group and about 24.2% in the highest, against 2.1% on placebo, and 83% of the highest dose group lost at least 15% of their weight. Limit: This is the trial the whole reputation rests on, and it is one trial, run and funded by Eli Lilly, with Lilly employees on the author list. It ran 48 weeks, so nothing here says what happens after that. Heart rate rose in a dose related way, peaking at 24 weeks. No independent group has ever repeated it. | Jastreboff 2023 PMID 37366315 | Weight loss Retatrutide |
| Retatrutide | Human trial n = 2339 people | TRIUMPH-1, the pivotal obesity trial, reported 80 week weight loss of about 19.0% to 28.3% by dose group against 2.2% on placebo, and 45.3% of the highest dose group losing at least 30% of their weight. Limit: There is no peer reviewed publication and no results posted on ClinicalTrials.gov. Everything known comes from a company press release dated May 21, 2026. No outside reviewer has seen the protocol, the full statistical definitions, the per group denominators behind the side effect percentages, or the serious adverse event and death listings. The release says 2,339 were randomized while the registry lists 2,335. | Lilly 2026 | Retatrutide |
| Retatrutide | Human trial n = 281 people | In adults with type 2 diabetes, HbA1c fell about 2.02% at 24 weeks in the highest dose group against essentially no change on placebo, and weight fell up to about 16.9% at 36 weeks. Limit: Same sponsor, same problem: Lilly funded, Lilly authored, never replicated. The comparison drug was a single older weekly injection at one dose, not the strongest current option. Only 79% of participants finished treatment, so the people who tolerated it least are underrepresented in the results. | Rosenstock 2023 PMID 37385280 | Retatrutide |
| Retatrutide | Human trial n = 98 people | In participants who also had fatty liver disease, liver fat fell by roughly 81% to 82% at 24 weeks in the higher dose groups against a slight rise on placebo, and up to 86% of them reached a normal liver fat level. Limit: This is a substudy of the same 338 person phase 2 obesity trial, not new participants. Liver fat on a scan is a stand in measurement: nobody biopsied these livers, and no trial has shown retatrutide changes liver scarring or any outcome a patient would feel. Lilly funded and Lilly co-authored. | Sanyal 2024 PMID 38858523 | Retatrutide |
| Retatrutide | Human trial n = 72 people | Twelve weeks of weekly injections in adults with type 2 diabetes cut HbA1c by 1.2% to 1.6% more than placebo in the higher dose groups, with weight down about 9 kg more than placebo in the top group. Limit: Tiny groups, roughly nine to twelve people per arm, so the numbers swing easily. Side effects were reported in 63% of retatrutide participants against 54% on placebo. 29 people left the study early. Funded by Eli Lilly. This was a safety and tolerability study, not a test of whether it works. | Urva 2022 PMID 36354040 | Retatrutide |
| Retatrutide | Small human study n = 45 people | The first human study reported tolerability similar to other gut hormone drugs and weight loss that lasted about six weeks after a single injection, alongside mouse work proposing that the glucagon arm adds extra calorie burning. Limit: The calorie burning claim, which is the entire rationale for adding the third receptor, is mouse data. A later independent mouse and hamster study found energy expenditure was not significantly altered. The full text is paywalled, the dose levels were never posted anywhere public, and the human portion was 45 healthy volunteers given one injection. | Coskun 2022 PMID 35985340 | Retatrutide |
| Retatrutide | Small human study n = 103 people | DXA scans in a slice of the diabetes trial showed fat mass fell substantially in the higher dose groups, with no significant change in the lowest dose group. Limit: Only 103 of the 189 people enrolled in the substudy had scans at both the start and the end, so more than 40% are missing and it is not random who dropped out. It is a substudy of an already published Lilly trial. The lead author is a Lilly employee who appears on 12 of the 16 retatrutide papers. | Coskun 2025 PMID 40609566 | Weight loss Retatrutide |
| Retatrutide | Small human study n = 619 people | Re-analysing the two phase 2 trials, a urine protein marker of kidney stress fell about 28% to 37% in the higher dose groups, with kidney filtration rate holding steady or improving slightly. Limit: Post hoc means this analysis was decided after the results were in, not planned in advance, so it generates a hypothesis and proves nothing. The authors themselves note most participants had normal urine protein to begin with and the absolute change was small. Same two Lilly trials, cut a different way. | Heerspink 2025 PMID 40630318 | Retatrutide |
| Retatrutide | Small human study | Another re-analysis of the same two phase 2 trials found blood fat markers dropped, including non-HDL cholesterol down as much as 26.9% and apoB down as much as 24.2%. Limit: Post hoc again, on the same participants as the kidney and body composition papers. Inflammation markers fell in the obesity trial but not in the diabetes trial, which is the kind of split result that post hoc analysis is prone to producing. These are blood markers, not heart attacks or strokes. | Ruotolo 2026 PMID 42608321 | Retatrutide |
| Retatrutide | Small human study | Retatrutide slows how fast the stomach empties, the same mechanism that makes gut hormone drugs curb appetite and that can change how other swallowed medicines are absorbed. Limit: PubMed carries no abstract for this paper and the full text is paywalled. The only thing that can be verified is the claim in the title. No participant count, no effect size, no time course. Nobody has published how much this matters for other drugs a person might take. | Urva 2023 PMID 37311727 | Weight loss Retatrutide |
| BPC-157 | Systematic review n = 36 studies, 1 human | Of 36 studies, 35 were in animals, where healing of tendon, ligament, muscle and bone improved. The one human study was small and retrospective. Limit: Review says plainly: no clinical safety data exist for BPC-157. | Vasireddi 2025 PMID 40756949 | Injury recovery GLOW KLOW |
| BPC-157 | Small human study n = 16 people | Patients given BPC-157 for knee pain mostly said they felt better when phoned months later. Limit: No control group, no imaging, relies on memory by phone. | Lee 2021 PMID 34324435 | Injury recovery GLOW KLOW |
| BPC-157 | Small human study n = 12 people | Women with stubborn bladder pain reported big improvements after BPC-157. Limit: Twelve people, one clinic, no comparison group. | Lee 2024 PMID 39325560 | GLOW KLOW |
| BPC-157 | Small human study n = 2 people | Two adults showed no change in heart, liver, kidney, thyroid or sugar markers after BPC-157. Limit: Two people. Far too few to call anything safe. | Lee 2025 PMID 40131143 | GLOW |
| BPC-157 | Review | Rodent studies suggest faster healing of tendon, ligament and muscle. Limit: Animal data only; not confirmed in people. | Gwyer 2019 PMID 30915550 | Injury recovery KLOW |
| BPC-157 | Review | Broad activity in animal injury models, but not approved for human use anywhere for lack of clinical data. Limit: Narrative and patent review. | Józwiak 2025 PMID 40005999 | GLOW |
| BPC-157 | Review | Describes proposed ways BPC-157 might help wounds heal, such as nitric oxide signaling and new blood vessels. Limit: Mechanisms come from rat models. | Seiwerth 2021 PMID 34267654 | Injury recovery KLOW |
| BPC-157 | Animals | Rat tendon cells in a dish grew out and moved more with BPC-157. Limit: Cells only. | Chang 2011 PMID 21030672 | Injury recovery GLOW |
| Sermorelin | Human trial n = 19 people | In a crossover study comparing 10 healthy older men with 9 younger men, two weeks of twice daily injections raised 24 hour growth hormone release and IGF-1 in the older men to levels no longer statistically different from the younger men's baseline, an effect that only reached significance at the higher of two doses tested. Limit: Two weeks is a short exposure to base a claim about reversing an age-related hormone decline on, the young and old groups were tiny, and every outcome measured was a blood hormone level, not anything the participants could feel or a doctor could measure as a real world change in strength, body composition, or function. | Corpas 1992 PMID 1379256 | Sermorelin |
| Sermorelin | Human trial n = 19 people | In 19 healthy adults aged 55 to 71 given four weeks of placebo followed by 16 weeks of the peptide, nightly injections raised IGF-1 into the normal range for younger adults within two weeks. After four months, men, but not women, showed more lean body mass, better insulin sensitivity, improved general well being, and higher libido, while skin thickness increased in both sexes. Limit: Only 19 people total, single blind rather than double blind, and the benefits split sharply by sex, with women showing almost none of the functional gains seen in men, a pattern the authors could not explain. This one small, single-center trial is a primary basis for anti-aging marketing claims made about sermorelin today. | Khorram 1997 PMID 9141536 | Sermorelin |
| Sermorelin | Human trial n = 43 people | In 43 children with hypothalamic growth hormone deficiency randomly assigned to a lower dose of the peptide, a higher dose, or growth hormone itself for six months, height velocity was lowest in the lower dose group and roughly matched between the higher dose group and the growth hormone group, though a gain in height relative to bone age only showed up in the growth hormone group. Limit: This is a randomized, multi arm comparison, which is rare in this literature, but each group held only 12 to 16 children, it ran just six months, and it was published as a conference supplement report rather than a full peer reviewed paper with complete statistics. | Neyzi 1993 PMID 8329826 | Sermorelin |
| Sermorelin | Small human study n = 7 people | In seven children with growth hormone deficiency of hypothalamic origin, continuous injections of the peptide for at least six months failed to improve the growth rate in five of the seven children; switching those same children to growth hormone itself then improved growth in all of them. Limit: Seven children from one center, with no randomization or blinding. This is one of the more discouraging results in the sermorelin literature: the peptide did not work for most of these particular patients, while growth hormone did, in the same children. | Butenandt 1989 PMID 2537727 | Sermorelin |
| Sermorelin | Small human study n = 18 people | In 18 short children who were not growth hormone deficient, a year of twice daily injections raised height velocity from about 4.8 to 7.2 cm per year, then growth slowed back toward pretreatment levels within six months of stopping, while fasting glucose, insulin, and IGF-1 all rose during treatment. Limit: This was short stature without a diagnosed hormone deficiency, not the approved use of treating growth hormone deficiency, so it does not speak to sermorelin's core indication. There was no placebo arm, only 18 patients at one center, and the growth gain reversed after treatment stopped, raising the question of whether it produces lasting height or a temporary growth spurt. | Kirk 1994 PMID 7955460 | Sermorelin |
| Sermorelin | Small human study n = 9 people | In nine children with radiation-induced growth hormone deficiency after treatment for a brain tumor or as leukemia prevention, a year of the peptide raised height velocity from about 3.3 to 6.0 cm per year, though switching those children to growth hormone itself for the following year raised velocity further, to about 7.5 cm per year. Limit: Nine patients across multiple centers is a very small base for this specific subgroup. There was no control group and no blinding, and the authors state plainly that the peptide's own effect was smaller than growth hormone's in the same children. | Ogilvy-Stuart 1997 PMID 9231053 | Sermorelin |
| Sermorelin | Small human study n = 1 people | A 62 year old man with about 20 years of largely unsupervised use of growth hormone and growth hormone releasing peptides, including a period of sermorelin combined with GHRP-6 plus ongoing nightly growth hormone, was found to have a bone spur at the front of his neck pressing on his esophagus and causing occasional trouble swallowing large bites of food. The authors raise chronic stimulation of the growth hormone axis as a possible contributor. Limit: One patient, with decades of mixed, self-directed use of at least three different growth-axis drugs at once and no medical supervision, so nothing here can be pinned on sermorelin specifically. This is a hypothesis-generating case report, not evidence of a typical outcome. | Perez 2026 PMID 42465868 | Sermorelin |
| Sermorelin | Small human study n = 110 people | In a multicenter, open label study of previously untreated prepubertal children with growth hormone deficiency, once daily injections of the peptide over one year raised mean height velocity from about 4.1 cm per year at baseline to about 8.0 cm per year at 6 months and 7.2 cm per year at 12 months, and about 74% of children were rated as responding well at 6 months. Limit: There was no placebo or growth hormone comparison group, so the growth seen here could not be checked against either doing nothing or the standard treatment. Only 86 of the 110 enrolled children had usable efficacy data. Everyone involved knew what treatment was being given, and the study was organized and funded through the manufacturer's own international study group. | Thorner 1996 PMID 8772599 | Sermorelin |
| Sermorelin | Review | This drug evaluation review summarized the sermorelin dataset available at the time: an intravenous dose was described as a fairly specific test for growth hormone deficiency, producing fewer false positives than some older provocative tests, though a normal response could not rule out a hypothalamic problem on its own. Daily injected sermorelin produced sustained height velocity gains over 12 months, and in a small number of children followed longer, over 36 months, but growth on sermorelin was smaller than growth on growth hormone itself in head to head comparisons. Limit: This is a manufacturer-adjacent drug class review from Adis International, not new data, built largely from the same small open label and comparative studies summarized elsewhere in this file. It predates any published final adult height data and any large randomized trial. | Prakash 1999 PMID 18031173 | Sermorelin |
| Tesamorelin | Human trial n = 53 people | In 53 adults with type 2 diabetes who did not have HIV, 12 weeks of tesamorelin did not change insulin sensitivity, fasting glucose or HbA1c compared with placebo, though total and non-HDL cholesterol dropped slightly in the higher dose group. Nobody left the study because their diabetes control worsened. Limit: Only 12 weeks long, in a population outside the one tesamorelin is approved for, and funded by and co-authored with the drug's maker. It shows the drug did not worsen diabetes control over this short window, but says nothing about its approved use in HIV related fat accumulation. | Clemmons 2017 PMID 28617838 | Tesamorelin |
| Tesamorelin | Human trial n = 73 people | In 73 people with HIV, abdominal obesity and controlled viral load, six months of tesamorelin shrank waist circumference more than standard care, but memory and thinking test scores improved by a similar amount in both the tesamorelin and standard care groups, with no significant difference between them. Limit: There was no placebo group, patients and researchers knew who was getting the drug, and the study itself says it was underpowered. Its own conclusion is that there is no clear benefit to cognition from short-term fat reduction with tesamorelin. | Ellis 2025 PMID 39813152 | Tesamorelin |
| Tesamorelin | Human trial n = 412 people | Over 26 weeks, adults with HIV and excess belly fat lost about 15.2% of visceral fat on CT scan while the placebo group's visceral fat grew about 5.0%. Triglycerides fell by about 50 mg per deciliter against a rise on placebo, and IGF-1 rose about 81% against a slight fall on placebo. Blood sugar measures did not differ significantly between groups. Limit: This is the pivotal trial the approval rests on. It was funded by the drug's maker, and more people on tesamorelin left the study early because of a side effect than on placebo. Twenty-six weeks says nothing about what happens with longer use or after stopping, and everyone enrolled already had HIV on antiretroviral therapy, so it says nothing about other groups. | Falutz 2007 PMID 18057338 | Tesamorelin |
| Tesamorelin | Human trial n = 404 people | In a second year-long trial, visceral fat fell about 10.9% over the first six months on tesamorelin against almost no change on placebo, reaching about 18% at twelve months in those who stayed on it the whole time. Patients switched from tesamorelin to placebo at six months quickly lost those gains, described in the paper as a rapid reversal. Limit: Same sponsor funded it. The rebound finding means whatever benefit exists appears to depend on staying on the drug, and the paper does not put a precise number of weeks on how fast it reverses. No independent group has repeated this design. | Falutz 2010 PMID 20101189 | Tesamorelin |
| Tesamorelin | Human trial n = 410 people | In patients who stayed on tesamorelin for the full 52 weeks of this extension, visceral fat reduction held at about 18% and triglycerides stayed down about 51 mg per deciliter, without a clinically meaningful change in glucose. The paper states directly that these effects do not last beyond the duration of treatment: stopping tesamorelin let visceral fat reaccumulate. Limit: This is the extension phase of the same 412 person sponsor funded trial above, not a new population, and only the people who tolerated the drug for the first 26 weeks and chose to continue are represented, so the healthiest responders are overrepresented in the 52 week numbers. | Falutz 2008 PMID 18690162 | Tesamorelin |
| Tesamorelin | Human trial n = 61 people | The first placebo-controlled trial, 61 people over 12 weeks, found the higher dose group's trunk fat fell about 9.2% against a small rise on placebo, IGF-1 rose in a dose related way, and glucose did not change. Visceral fat fell numerically more on the higher dose but that difference from placebo did not reach statistical significance. Limit: Just 12 weeks with about 20 people per arm, too small and short to confirm a visceral fat effect or to catch rare side effects. The authors themselves said longer trials with more patients were needed, which the later phase 3 trials then provided. | Falutz 2005 PMID 16052083 | Tesamorelin |
| Tesamorelin | Human trial n = 38 people | Looking only at the people from the liver fat trial above who were on newer integrase inhibitor HIV medicines, tesamorelin still cut visceral fat and liver fat significantly more than placebo over 12 months, with similar rates of side effects, including high blood sugar, between groups. Limit: A subgroup of an already small 61 person trial, so this slice has only 15 to 16 people per treatment arm. The authors describe it as the first dedicated data in this specific group, meaning there is nothing else yet to compare it against. | Russo 2024 PMID 38905488 | Tesamorelin |
| Tesamorelin | Human trial n = 410 people | In the same 410 person trial, tesamorelin lowered a clotting related marker called tPA antigen a bit more than placebo, and changes in several inflammation markers tracked with how much visceral fat a person lost. A second clotting marker, PAI-1, did not change significantly. Limit: A substudy of blood markers, not of health outcomes like heart attacks or diabetes. The authors themselves say further study is needed to know whether these small marker changes matter clinically, and it is funded by the drug's maker. | Stanley 2011 PMID 21516030 | Tesamorelin |
| Tesamorelin | Human trial n = 402 people | Pooling two phase 3 trials and splitting patients into responders, at least 8% visceral fat loss, and non-responders, responders had significantly better triglycerides, fasting glucose and HbA1c at both 26 and 52 weeks than non-responders taking the same drug. Limit: A post hoc analysis: the responder split was decided after the data were in, which can manufacture a difference that would not hold up in a trial designed to test it directly. It also means people who did not respond well to the drug saw no metabolic benefit at all, and there is no way to predict in advance who will respond. | Stanley 2012 PMID 22495074 | Tesamorelin |
| Tesamorelin | Human trial n = 48 people | In a small single-center trial, six months of tesamorelin cut visceral fat and also reduced liver fat on MRI, with over a third of the tesamorelin group reaching a normal liver fat level against 4% on placebo. Fasting glucose rose briefly at two weeks then came back in line with placebo by six months. Limit: Only 48 people completed treatment at one hospital, and the authors call it a preliminary study. It measured liver fat by imaging, not biopsy, so it cannot say whether the change reflects less liver damage. The early, temporary glucose rise is a signal worth watching even though it faded. | Stanley 2014 PMID 25038357 | Tesamorelin |
| Tesamorelin | Human trial n = 61 people | In people with HIV and fatty liver disease, a year of tesamorelin lowered liver fat by about 4.1 percentage points more than placebo, a roughly 37% relative drop, and 35% of the tesamorelin group got their liver fat below the disease threshold against 4% on placebo. Blood sugar measures did not differ between groups over 12 months. Limit: 61 people across two United States sites. Liver fat was measured by imaging, not by liver biopsy, so it cannot say whether tesamorelin changes liver scarring or any outcome a patient would feel, and the authors call for longer studies to see if the fat reduction holds up or matters clinically. | Stanley 2019 PMID 31611038 | Tesamorelin |
| Tesamorelin | Systematic review n = 909 people | Pooling four randomized trials and 909 patients, this 2026 review found tesamorelin significantly reduced visceral fat, waist size and trunk fat while increasing lean body mass, with a small improvement in total cholesterol. Side effects tied to growth hormone stimulation were more common on tesamorelin, and people were somewhat more likely to quit the drug than placebo, though that difference stopped just short of statistical significance. Limit: Only four trials qualified for pooling, and the visceral fat result varied a lot between them, a heterogeneity measure of 74%, meaning the studies did not closely agree on the size of the effect. The review itself flags long term safety, the right dosing strategy, and how long benefits last as open questions. | Ditta 2026 PMID 42538058 | Tesamorelin |
| GHK-Cu | Human trial n = 13 people | After laser skin resurfacing, a copper-peptide cream did not beat control on measured redness or wrinkles; patients did report liking it more. Limit: Thirteen people, a cream, one subjective win. | Miller 2006 PMID 16847171 | Skin and aging GLOW KLOW |
| GHK-Cu | Small human study n = 20 (blood levels only) | People with COPD had lower blood GHK; in mice, GHK-Cu reduced smoke-related muscle loss. Limit: The human part only measured blood levels; the treatment effect is in mice. | Deng 2023 PMID 36905132 | GLOW |
| GHK-Cu | Small human study n = 29 people | A scalp routine with a copper-peptide serum plus a scrub reduced flaking over 15 days. Limit: No control group, company-employed authors, peptide mixed with other actives. | Patel 2024 PMID 39449909 | Skin and aging GLOW |
| GHK-Cu | Animals | GHK-Cu packed into liposomes sped healing of scald burns in mice. Limit: Burn model, and a special delivery form rather than plain GHK-Cu. | Wang 2017 PMID 28370978 | Wound healing GLOW |
| GHK-Cu | Review | Questions whether GHK in skin products reaches where it would need to act, and calls the effectiveness data thin and inconsistent. Limit: Narrative review. | Mortazavi 2025 PMID 39963574 | Skin and aging KLOW |
| GHK-Cu | Review | Reviews evidence that GHK-Cu changes the activity of many genes tied to repair and inflammation. Limit: Written by the peptide's discoverer; gene correlations, not patient outcomes. | Pickart 2018 PMID 29986520 | Skin and aging GLOW KLOW |
| GHK-Cu | Review | Summarizes lab evidence that GHK can raise collagen and other skin-structure molecules. Limit: Same author group; no controlled human trial evaluated. | Pickart 2015 PMID 26236730 | Skin and aging Wound healing KLOW |
| Ipamorelin | Human trial n = 114 people | In adults recovering from small or large bowel resection, people getting intravenous ipamorelin reached tolerance of a solid meal in a median of about 25 hours, against about 33 hours on placebo, but the difference was not statistically significant. None of the secondary efficacy measures showed a clear benefit either. One hundred seventeen patients were enrolled, and 114 made up the safety and modified intent to treat populations. Limit: This is the only published human trial that ever tested whether ipamorelin does anything. It was designed and described by its own authors as a small proof of concept study, not a confirmatory one, and it enrolled a broad mix of surgical patients rather than one specific procedure. Its own conclusion was that there was no significant difference from placebo. A larger follow up trial was run afterward and has never been published, see the note below. | Beck 2014 PMID 25331030 | Ipamorelin |
| Ipamorelin | Small human study n = 40 people | In healthy young men given a single intravenous infusion at one of five escalating dose levels, eight men per level, ipamorelin cleared from the blood within about two hours and triggered a single burst of growth hormone release that peaked within an hour, with the size of that hormone response leveling off at the higher doses tested. Limit: Forty healthy men, one dose each, no placebo group, and no patients. The only thing measured was blood levels of the drug and of growth hormone. It shows ipamorelin does what it was designed to do to growth hormone in the blood, not that this changes anything a person would feel or benefit from. | Gobburu 1999 PMID 10496658 | Ipamorelin |
| Ipamorelin | Animals | In rats given a steroid drug known to weaken muscle and bone, adding ipamorelin alongside the steroid for three months prevented the drop in calf muscle strength and increased the rate of new bone formation compared with the steroid given alone. Limit: Rats only, and a specific steroid injury model, not an osteoporosis or muscle wasting trial in people. No human study has tested whether ipamorelin protects against steroid side effects. | Andersen 2001 PMID 11735244 | Ipamorelin |
| Ipamorelin | Animals | In rats with surgically delayed stomach emptying, a single intravenous dose of ipamorelin sped stomach emptying back toward the level of animals that had no surgery, and it reversed the loss of contraction strength seen in isolated stomach muscle tissue taken from operated animals. Limit: Animal and isolated tissue data only, funded by and co-authored with the company developing the drug for postoperative ileus. It supports a mechanism that the one human trial of the same condition then failed to confirm. | Greenwood-Van Meerveld 2012 PMID 27186127 | Ipamorelin |
| Ipamorelin | Animals | Twice daily ipamorelin injections in mice increased body fat and fat pad weight over several weeks in both normal mice and mice bred to lack growth hormone, and it raised the appetite hormone leptin and food intake. The authors concluded that growth hormone secretagogues can increase body fat through a route that does not depend on growth hormone itself. Limit: Mice, not people, and the effect measured was more body fat, not less, which is the opposite of what most people taking a growth hormone secretagogue are hoping for. This complicates the simple story that ipamorelin should improve body composition. | Lall 2001 PMID 11162489 | Ipamorelin |
| Ipamorelin | Animals | Twelve weeks of continuous ipamorelin in adult female rats increased bone mineral content measured by DXA scan and by CT scan, an effect similar in size to giving growth hormone itself. The increase tracked the overall increase in bone size and body weight rather than making the bone denser for its size. Limit: Small groups of seven or eight rats per arm, adult rats rather than a model of any bone disease, and no comparison to any treatment used in human osteoporosis. Whether this translates into any clinical bone benefit in people has never been tested. | Svensson 2000 PMID 10828840 | Ipamorelin |
| Ipamorelin | Animals | In rats that had undergone bowel surgery, repeated intravenous ipamorelin over two days increased cumulative stool output, food intake, and weight gain compared with vehicle. A single dose sped up the time to the first bowel movement but did not change the other measures. Limit: An animal surgery model, not real patients, and funded by the company developing the drug for this exact use. This is the preclinical rationale that led directly to the human ileus trial, which then found no significant benefit. | Venkova 2009 PMID 19289567 | Ipamorelin |
| Ipamorelin | Review | A 2026 critical review of peptide use in sport and bodybuilding names ipamorelin among the growth hormone secretagogues used at combinations and frequencies well outside anything ever tested in a trial. It flags cardiovascular strain, insulin resistance, dyslipidemia, and psychiatric symptoms as emerging safety concerns for this category of drugs, while noting that how many people are actually using them this way is unknown. Limit: A review of the field as a whole, not a study of ipamorelin specifically. The safety concerns raised are general to the drug class and to unsupervised, self-directed use, not findings tied to a specific ipamorelin trial or reported case. | Coutinho 2026 PMID 41880199 | Ipamorelin |
| Ipamorelin | Review | A 2026 narrative review written for sports medicine physicians groups ipamorelin with ten other unapproved peptides sold direct to patients. It notes that animal data on tissue repair and metabolism look promising for several of these compounds, but that rigorous human safety data are scarce across the group, and that there is real potential for harm. Limit: A narrative review, not new data, covering eleven different peptides at once, so ipamorelin gets only a few sentences rather than a dedicated assessment. It reflects two authors' reading of the existing literature. | Mendias 2026 PMID 41966639 | Ipamorelin |
| Ipamorelin | Animals | Pancreas tissue taken from normal rats and from rats made diabetic with a toxin released more insulin when exposed to ipamorelin in a dish, and blocking calcium channels or certain adrenaline receptors reduced that effect, pointing to a specific signaling pathway. Limit: Isolated tissue fragments in a dish, not a living animal or person, and a toxin induced rat model that is not the same as type 1 or type 2 diabetes in people. Nobody has shown this insulin effect happens in a living body, animal or human. | Adeghate 2004 PMID 15665799 | Ipamorelin |
| Ipamorelin | Animals | In rat pituitary cells, anesthetized rats, and pigs, ipamorelin released growth hormone about as strongly as an older experimental compound, GHRP-6. Unlike GHRP-6 or GHRP-2, ipamorelin did not raise cortisol or ACTH even at doses far above what was needed for growth hormone release, and it did not change levels of other pituitary hormones. This selectivity is the finding the compound is best known for. Limit: No human data at all. This is a laboratory and animal pharmacology paper from the company that invented the compound, written to describe why they thought it was a promising drug candidate, not a demonstration that it helps with any condition. | Raun 1998 PMID 9849822 | Ipamorelin |
| MOTS-c | Human trial n = 30 people | Thirty adults were randomly assigned to a single session of endurance cycling, resistance leg exercise, or no exercise. Blood MOTS-c showed a trend toward rising after endurance exercise but not resistance exercise, and was not related to fitness level, leg strength, or muscle mitochondrial DNA amount. Limit: This randomized exercise itself, not the peptide. Nobody received MOTS-c. Ten people per group is small, and the rise in MOTS-c after endurance exercise was only a trend, not a clear statistically significant increase the way it was for a related peptide, humanin, measured in the same people. | von Walden 2021 PMID 34351816 | MOTS-c |
| MOTS-c | Systematic review n = 602 people | Pooling 6 case control studies and 1 cross sectional study covering 602 people, blood MOTS-c was lower overall in people with diabetes or obesity combined. Broken out separately, though, it was lower in type 2 diabetes but higher in obesity, moving in opposite directions depending on which condition was being compared. Limit: This reviews existing observational studies, none of which gave anyone the peptide. The opposite findings for diabetes versus obesity show how inconsistent the human data actually is, and the authors note the populations pooled into this analysis differed a great deal from each other. | Zhou 2024 PMID 39160573 | MOTS-c |
| MOTS-c | Small human study n = 94 people | In 94 people on long term hemodialysis followed for a median of about 26 months, blood MOTS-c was higher than in healthy controls, and higher still in the 53 people who later died or had a cardiovascular event. Adding MOTS-c to standard risk models modestly improved how well those models sorted higher risk from lower risk patients. Limit: This is one observational cohort from a small number of centers, and it cannot show that MOTS-c causes anything, only that it tracks with worse outcomes. That direction is the opposite of what mouse studies would predict, since in mice more MOTS-c activity is tied to better metabolic health. The authors themselves say this needs testing in larger, more varied groups before it means anything clinically. | Bolignano 2024 PMID 39111290 | MOTS-c |
| MOTS-c | Small human study n = 683 people | In 683 Korean adults over age 65, genotyped for a natural DNA variant in the MOTS-c gene, men carrying the less common version had noticeably more lean muscle mass and stronger handgrip than men carrying the common version. No such difference appeared in women. Limit: This is about an inherited gene variant, not the manufactured peptide, so it says nothing about what happens if MOTS-c is given to someone. It is limited to older adults of one ethnic background, and it found no effect at all in women, which the study does not explain. | Kim 2024 PMID 39457696 | MOTS-c |
| MOTS-c | Small human study | In people with stage 5 chronic kidney disease compared with age matched people with normal kidney function, MOTS-c was lower both in skeletal muscle tissue and in blood. Lower muscle MOTS-c tracked with lower mitochondrial density and signs of oxidative stress in the muscle. Limit: This is a cross sectional comparison, it cannot say whether low MOTS-c contributes to muscle problems in kidney disease or is simply a byproduct of it. The paper does not state an overall participant count in its summary, and the finding has not been replicated in an independent cohort. | Liu 2019 PMID 31432706 | MOTS-c |
| MOTS-c | Small human study n = 85 people | Comparing 48 people with obesity to 37 people of normal weight, average blood MOTS-c did not differ between the two groups. Across everyone tested, higher MOTS-c correlated with more insulin resistance and lower MOTS-c correlated with older age. Limit: This is a single center, cross sectional snapshot that shows correlation, not cause. People with diabetes or other chronic conditions were excluded, so the sample does not represent the general population, and no exercise or drug was given to see if changing MOTS-c would change anything. | Ozkaya 2025 PMID 41004666 | MOTS-c |
| MOTS-c | Small human study | Infusing fat into the bloodstream raised circulating MOTS-c in both healthy volunteers and women with polycystic ovary syndrome, and giving insulin afterward blunted that rise, most clearly in the PCOS group. An eight week course of moderate exercise did not change resting MOTS-c levels in either group. Limit: Nobody was given MOTS-c itself, this only tracked how the body's own levels respond to fat, insulin, and exercise. The paper does not report a combined participant count in its summary, this is a single small physiology study, and it has not been independently repeated. | Ramanjaneya 2019 PMID 31066084 | MOTS-c |
| MOTS-c | Small human study | In mice of several ages, including old mice started late in life, MOTS-c improved physical performance and changed genes tied to metabolism and cell maintenance in muscle. Separately, in people, a bout of exercise raised MOTS-c levels inside skeletal muscle and in the bloodstream. Limit: The performance and aging claims are mouse only. The human portion just shows that exercise raises the body's own MOTS-c output, it does not test giving the peptide to a person, and the paper does not state how many people were in that human measurement. Two of the senior authors disclose that they are paid consultants and shareholders in a company that develops mitochondrial peptides. | Reynolds 2021 PMID 33473109 | MOTS-c |
| MOTS-c | Animals | In mice, MOTS-c activated the AMPK energy sensing pathway in skeletal muscle and blocked the weight gain and insulin resistance normally caused by a high fat diet or by aging. Limit: This is the paper that started the field, and it is mouse data only. No human trial has ever tested whether giving the peptide itself does anything in a person. Almost everything else written about MOTS-c traces back to this study and the same small group of authors' later work. | Lee 2015 PMID 25738459 | MOTS-c |
| TB-500 | Human trial n = 73 people | In people with leg ulcers, thymosin beta-4 was as safe as placebo and a minority of treated patients healed fully. Limit: One mid-stage trial; benefit over placebo was modest. | Guarnera 2010 PMID 20536470 | Wound healing KLOW |
| TB-500 | Human trial n = 9 people | Thymosin beta-4 eye drops eased discomfort and surface damage in severe dry eye versus placebo. Limit: Nine people, eye drops, many comparisons. | Sosne 2015 PMID 25826322 | GLOW |
| TB-500 | Human trial n = 96 people | In a 96-patient heart-attack trial, the main result was not statistically significant; a timing subgroup showed smaller infarcts. Mice showed less heart damage. Limit: Used the full recombinant protein, not the TB-500 fragment sold. | Zhang 2025 PMID 41229390 | GLOW |
| TB-500 | Review | Explains how thymosin beta-4 binds actin, the cell's scaffolding protein. Limit: Structure only, not a treatment study. | Bubb 2003 PMID 12852258 | KLOW |
| TB-500 | Review | Summarizes thymosin beta-4's role in cell movement and tissue repair and lists trials then under way. Limit: Author helped develop the compound. | Goldstein 2012 PMID 22074294 | Injury recovery GLOW KLOW |
| TB-500 | Review | How thymosin beta-4 was found as the cell's main actin-binding peptide. Limit: Basic science, not treatment. | Hannappel 2007 PMID 17468232 | GLOW |
| TB-500 | Review | Says phase 2 wound trials found faster repair and good tolerability. Limit: Cites the authors' own work; trial reports not separately checked here. | Kleinman 2016 PMID 27450738 | Wound healing GLOW KLOW |
| TB-500 | Review | Animal studies suggest less heart damage after injury. Limit: No human heart outcome trials cited. | Pipes 2016 PMID 27450736 | KLOW |
| Semax | Small human study n = 110 people | In patients treated within the first days after a hemispheric ischemic stroke, adding semax to standard intensive care was linked to faster recovery of neurological function on rating scales, more so for motor deficits, compared with a separate group of patients who received standard treatment alone. EEG mapping and evoked potential testing were used alongside the clinical scores to track brain function. Limit: This is one of the two studies most often cited as the foundation for semax's stroke use, and it is nearly three decades old. The comparison group was not randomized, it was a separate group of patients matched afterward for stroke severity and location, so unmeasured differences between the groups could explain part of the result. The full paper is in Russian in a journal with no English full text available online, so only the abstract can be checked, not the statistical methods behind the improvement claim. | Gusev 1997 PMID 11517472 | Semax |
| Semax | Small human study n = 187 people | In a group of patients at different stages of chronic cerebrovascular insufficiency, tracked with neurological exams, ultrasound of the neck vessels, brain imaging and eye exams, semax treatment was linked to clinical improvement, a slower disease course and fewer strokes or transient ischemic attacks over the study period, with side effects described as minor and the drug described as well tolerated even in older patients. Limit: No control or comparison group is described in the available abstract, so there is no way to tell from what is public whether patients would have looked similar without treatment. The full text sits in a Russian neurology journal with no accessible English translation, so the numbers behind terms like significant improvement and reduced risk cannot be checked. | Gusev 2005 PMID 15792140 | Semax |
| Semax | Small human study n = 110 people | In adults recovering from ischemic stroke, blood BDNF levels rose after semax treatment regardless of when rehabilitation started, and higher BDNF levels tracked with faster and better recovery on a disability scale. Patients who did not receive semax needed to start rehabilitation early to reach a similar rise in BDNF. Limit: Patients were sorted into semax and no semax groups by whether they happened to receive the drug, not by random assignment, so people who got semax may have differed from those who did not in ways the study cannot rule out. Blood BDNF level is a proxy measurement, not a symptom or a functional outcome by itself. This is one of the few semax papers with a full English abstract on PubMed, which is not true of most of the others in this file. | Gusev 2018 PMID 29798983 | Semax |
| Semax | Small human study | In glaucoma patients whose eye pressure had already been brought under control, adding semax to standard neuroprotective care was linked to better results on electrophysiological and computer based tests of the optic nerve than standard treatment alone. Limit: No patient count is given in the available abstract, and the summary reports a general advantage rather than specific numbers. The full study sits in a Russian ophthalmology journal with no accessible English translation, so how patients were assigned to groups and the figures behind the claimed advantage cannot be checked. | Kurysheva 2001 PMID 11569188 | Semax |
| Semax | Small human study | In patients with vascular, toxic allergic or inflammatory disease of the optic nerve, two ways of delivering semax to the eye region were compared against a standard treatment only control group. The semax groups showed better visual acuity, a wider visual field, and improved color vision and nerve conduction measurements than the control group. Limit: No total patient count or group sizes are given in the available abstract, and there is no statement that group assignment was random. The full text is a Russian ophthalmology journal article with no accessible English translation, so the figures behind the reported improvement cannot be independently checked. | Polunin 2000 PMID 10741256 | Semax |
| Semax | Small human study n = 27 people | In an open label trial in patients with motor neuron disease, semax did not change the course of nerve and muscle degeneration as measured by repeated needle EMG, but patients reported a better overall quality of life score, driven mainly by improved emotional state and motivation. Limit: This was an open label trial with no placebo or control group, so both patients and raters knew who was being treated, which can inflate a subjective quality of life result. Twenty seven people is a small group for a slow, variable disease. This is also the one study in this file where semax was tested against its intended physical outcome and did not change it. | Serdiuk 2007 PMID 18379501 | Semax |
| Semax | Animals | In rats, semax given by nasal application raised BDNF protein, a growth factor tied to learning and memory, specifically in the basal forebrain within a few hours, and the researchers identified a specific binding site for the peptide in that brain region. Limit: This is rat brain tissue, not a human brain, and it measures a biological marker rather than behavior or memory performance in the same experiment. The work comes from the peptide's own development group in Moscow, not an outside lab. | Dolotov 2006 PMID 16635254 | Semax |
| Semax | Animals | In rats, a single application of semax raised BDNF and its receptor trkB in the hippocampus, a brain region tied to memory, and the treated animals also showed more of a specific learned avoidance behavior used in the lab as a memory proxy. Limit: Same origin lab as the basal forebrain paper above, again in rat brain tissue. The learned avoidance task is a narrow laboratory measure and does not directly show what happens to memory in daily human life. | Dolotov 2006 PMID 16996037 | Semax |
| Semax | Animals | Using RNA sequencing in rats after a stroke like injury, researchers found semax shifted brain gene activity toward genes involved in nerve signaling and away from genes tied to inflammation, roughly the opposite pattern seen in untreated injury, across several hundred genes with a meaningfully changed activity level. Limit: This is a gene activity pattern in rat brain tissue, not a measurement of recovery, symptoms or survival. It is again the same Moscow research group that developed the drug, running the same stroke model it has published on for over a decade. | Filippenkov 2020 PMID 32580520 | Semax |
| Semax | Review | A 2026 narrative review of therapeutic peptides in aging medicine grouped semax with several unapproved research peptides, describing it as having preclinical and limited clinical evidence for neuroprotection but lacking long term safety data and systematic validation, unlike the FDA approved agents covered in the same review. Limit: This is a narrative review, not a systematic review with a published search protocol, and it says so of itself. It drew on 20 total sources across nine different peptides, so semax gets a small slice of that, and its own conclusion is that semax lacks the clinical rigor the review says other agents in its comparison group have. | Mavrych 2026 PMID 42021992 | Semax |
| Selank | Small human study n = 60 people | In 60 patients with phobic, anxiety and somatoform disorders, selank produced a clear anxiolytic effect that outlasted treatment by about a week and improved quality of life, compared with the benzodiazepine phenazepam. Limit: The English abstract gives no detail on randomization or blinding. The full paper is in a Russian journal not indexed in English on PubMed, so the comparator dosing, dropout rate and statistical methods cannot be independently checked. | Medvedev 2014 PMID 25176261 | Selank |
| Selank | Small human study n = 70 people | Adding selank to phenazepam in 40 patients with anxiety spectrum disorders reduced the usual side effects of phenazepam, such as memory and attention problems, sedation and sexual disturbances, compared with 30 patients on phenazepam alone, while keeping the anxiolytic benefit. Limit: This tests selank as an add-on to a benzodiazepine, not selank alone against placebo, so how much benefit comes from selank itself cannot be separated out. Group sizes are small and the full methods exist only in Russian. | Medvedev 2015 PMID 26356395 | Selank |
| Selank | Small human study n = 52 people | In 52 healthy volunteers given a single dose of selank, the related peptide semax, or placebo, resting state brain scans showed selank changed the connection strength between the amygdala, a region tied to anxiety, and part of the temporal cortex, in a pattern distinct from semax. Limit: Participants were healthy volunteers, not people with anxiety, so this says nothing about symptom relief. The outcome is a brain scan connectivity measurement, not a behavioral or clinical one, and it reflects a single dose rather than ongoing treatment. | Panikratova 2020 PMID 32342318 | Selank |
| Selank | Small human study | In patients with anxiety-asthenic disorders who took selank for two weeks, a marker of immune balance in the blood, the Th1 to Th2 cytokine ratio, shifted in a consistent direction, and selank changed IL-6 gene activity in blood cells taken from patients with depression but not in cells from healthy people. Limit: No participant count is given in the English abstract, there is no placebo comparison, and this paper was published in the same year and journal as the Zozulia generalized anxiety trial, so it may report on an overlapping or identical group of patients, which cannot be confirmed from the abstracts alone. The immune marker shifts were not tied to any anxiety symptom score. | Uchakina 2008 PMID 18577961 | Selank |
| Selank | Small human study n = 62 people | In 62 patients with generalized anxiety disorder and neurasthenia, selank and the older drug medazepam produced a similar reduction in anxiety on standard psychiatric rating scales, and selank also showed antiasthenic and mild stimulant like effects. A blood marker of enkephalin activity moved along with the improvement in anxiety. Limit: This is a comparator trial against another drug, not against placebo. It was published only in a Russian language journal, so its randomization, blinding and dropout numbers cannot be checked from the English abstract alone, and it has never been replicated outside Russia. | Zozulia 2008 PMID 18454096 | Selank |
| Selank | Small human study | Blood from patients with generalized anxiety disorder showed a shorter enkephalin half life and lower enkephalin-degrading enzyme activity than blood from people without anxiety, and selank added to plasma in the lab blocked that same enzyme activity, offered as the proposed mechanism behind its anxiolytic effect. Limit: The anxiety related blood finding is a lab comparison across patient groups, not a treatment trial, and no participant count is given. The enzyme blocking result was shown in mixed blood samples in the lab, not in a person who had actually taken selank, so the mechanism is a hypothesis rather than something confirmed in treated patients. | Zozulya 2001 PMID 11550013 | Selank |
| Selank | Animals | In rats made dependent on morphine, a single injection of selank reduced signs of opioid withdrawal, including convulsions and posture problems, though it was somewhat less effective than diazepam at the dose tested. Limit: Animal data only, in a withdrawal model, not a study of selank in people with opioid dependence. No human data exists testing selank for opioid withdrawal. | Konstantinopolsky 2022 PMID 36322304 | Selank |
| Selank | Review | This English language pharmacology review groups selank with the related drug phenibut as a poorly studied Russian drug with a GABA receptor mechanism that is sold to United States consumers as a dietary supplement, despite no formal safety evaluation by any regulator. Limit: It is a review, not new data, and its selank section is short. It classifies selank mainly by mechanism alongside other sedative drugs rather than assessing selank's own evidence base in depth, and most of its safety concern, including rising poison control center calls, is specifically about phenibut, not selank. | Doyno 2021 PMID 34396551 | Selank |
| Selank | Review | This review lays out the leading receptor level theory behind selank's anxiety effect: in receptor binding assays selank behaves as a positive allosteric modulator of GABA receptors, in a manner that overlaps with but is not identical to how benzodiazepines like diazepam act. Limit: The evidence behind the review's own claim comes from receptor binding assays in the lab, not from animal behavior or human trials, and the proposed mechanism has not been confirmed by an independent laboratory. | Vyunova 2018 PMID 30255741 | Selank |
| KPV | Animals | A gut transporter moved KPV into intestinal cells, and that uptake went with less inflammation. Limit: Mice only. | Dalmasso 2008 PMID 18061177 | Gut inflammation KLOW |
| KPV | Animals | KPV reduced inflammatory cell build-up in mice about as well as the full hormone. Limit: Mechanism study, not a disease outcome. | Getting 2003 PMID 12750433 | Gut inflammation KLOW |
| KPV | Animals | In two mouse models of bowel inflammation, KPV reduced colitis severity. Limit: Mice only; paper notes KPV is hard to deliver and unstable. | Kannengiesser 2008 PMID 18092346 | Gut inflammation KLOW |
| KPV | Animals | KPV packed into nanoparticles eased mouse colitis better than KPV alone. Limit: Results may owe as much to the nanoparticle as to KPV. | Xiao 2017 PMID 28143741 | Gut inflammation KLOW |
| KPV | Cells in a dish | In human skin cells in a dish, KPV switched on an anti-inflammatory signal. Limit: Cells only. | Elliott 2004 PMID 15102092 | KLOW |
How the grades work
Cells in a dish never touched a living animal. Animals means mice or rats, usually. Small human study means a handful of people with no comparison group. Human trial means people were randomly split into treated and untreated groups, which is the only kind that can show an effect is real. Review and Systematic review sum up other studies rather than running one. Full rules: How we check.
What is not in this table
Studies we could not find, studies behind a paywall with no readable abstract, and anything we have not read ourselves. We add a row only after checking the PubMed record. If we got one wrong, we fix the row on this page.
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