By research area
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This is a summary of published and preclinical research, not medical advice. Every entry describes what a study found, not what you should do. These compounds are supplied for laboratory research only.
Tirzepatide — Metabolic research (Clinical evidence)
Clinical trials report substantial average weight reduction (16–22%), generally greater than semaglutide in head-to-head comparison.
Phase 3 SURMOUNT-1 (NEJM): average weight reductions of 16.0–22.5% across dose groups over 72 weeks in adults with obesity/overweight, vs. 2.4% with placebo; 89–96% of participants achieved ≥5% body weight reduction vs. 28% on placebo. SURMOUNT-5 (head-to-head vs. semaglutide): −20.2% vs. −13.7% at 72 weeks, tirzepatide showing significantly greater reduction. SURMOUNT-MAINTAIN (The Lancet): continuing tirzepatide (5–15mg) maintained weight loss vs. switching to placebo.
Retatrutide — Metabolic research (Clinical evidence)
Phase 2 trial reports the largest average weight reduction of any compound studied here (up to 24% at 48 weeks), alongside improved cardiometabolic markers.
Phase 2 trial (NEJM): mean weight reduction up to 17.5% at 24 weeks (primary endpoint), up to 24.2% at 48 weeks (secondary endpoint), the largest reported average reduction of any compound in this catalog. Also associated with improvements in blood pressure, triglycerides, LDL/total cholesterol, HbA1c, fasting glucose/insulin. 338-participant randomized, double-blind, placebo-controlled design. Safety profile similar to other incretin-based therapies.
Semaglutide — Metabolic research (Clinical evidence)
Two-year trial data shows sustained ~15% average weight loss vs. ~3% on placebo, with GI side effects being the most common tradeoff.
STEP 1 (NEJM): −14.9% body weight vs. −2.4% placebo at 68 weeks; 86.4% achieved ≥5% weight loss vs. 31.5% on placebo. STEP 5 (2-year follow-up, Nature Medicine): −15.2% vs. −2.6% at 104 weeks, sustained over two years. GI side effects (nausea, etc.) more common than placebo (82.2% vs. 53.9%), mostly mild-to-moderate.
Cagrilintide — Metabolic research (Clinical evidence)
Monotherapy trials report ~12% average weight loss; combined with semaglutide, most participants achieved 20%+ weight loss in a large Phase 3 trial.
Monotherapy trial (3,417 participants, 68 weeks): 11.8% average weight reduction vs. 2.3% placebo; 31.6% achieved ≥15% weight loss vs. 4.7% on placebo. REDEFINE 1 (combined with semaglutide as "CagriSema"): 60% of participants achieved ≥20% weight loss, 23% achieved ≥30%; also improved blood pressure, waist circumference, lipids, glycemic control (88% of prediabetic participants returned to normoglycemia). Distinct mechanism from GLP-1s: an amylin analog, targeting satiety via a different pathway.
AOD-9604 — Metabolic research (Clinical evidence)
An early trial reported modest fat-specific loss; a larger follow-up trial found no significant effect, and development was discontinued in 2007.
A 12-week, 300-participant trial found a modest average loss of 2.6kg vs. 0.8kg placebo (fat-specific, sparing lean mass), but a larger, longer 24-week trial of 536 participants found no significant weight reduction, and development was discontinued in 2007. Never received FDA approval for any indication.
5-Amino-1MQ — Metabolic research (Community evidence)
Evidence to date is entirely preclinical, from mouse research. Any weight-loss figure quoted for this compound comes from animal models rather than people.
The evidence base is entirely preclinical: efficacy and safety data come from animal models, and the compound is sold as an unregulated research chemical with no regulatory approval. Mouse studies (diet-induced-obese mice, NNMT inhibition) reported reduced body weight and fat mass without reduced food intake, plus lower cholesterol. Vendor dosing guidance is extrapolated from that animal data.
NAD+ — Longevity research (Clinical evidence)
Trials consistently show NAD+ boosting is safe and reliably raises NAD+ levels. Evidence that this translates into a measurable anti-aging benefit is still limited and mixed.
Over a dozen human trials (up to 26 weeks, one 2-year study) consistently show NAD+ precursors are safe and well-tolerated, and reliably raise blood NAD+ levels (roughly 2x after 14 days of NR/NMN supplementation). Evidence for the anti-aging benefit this is meant to produce is weaker than the safety data: one trial found no cognitive improvement over placebo, and a broader review found "clear evidence for antiaging effects... is still scarce," with some limited efficacy shown for metabolic health and skin cancer incidence specifically.
SS-31 (Elamipretide) — Longevity research (Clinical evidence)
Real clinical trials exist and show benefit, specifically in people with diagnosed mitochondrial disease. Trials in broader populations (heart failure, general myopathy) did not meet their endpoints.
18 human clinical trials have been run. Real successes exist, specifically in people with defined mitochondrial disease: patients with primary mitochondrial myopathy showed a dose-dependent improvement on the 6-Minute Walk Test (51.2m improvement vs. 3.0m placebo at the highest dose); 48-week treatment in Barth syndrome improved walk-test performance, symptom scores, and heart physiology. Trials in heart failure and general mitochondrial myopathy populations did not meet their endpoints. Important caveat: the positive results are specific to rare, diagnosed mitochondrial disease populations, and apply to those populations; a generally healthy person is a different context.
Epithalon — Longevity research (Community evidence)
Human cell research (rather than living-patient trials) shows the compound can activate telomerase in a lab setting. Evidence in living people remains to be established through controlled trials.
Developed in Russia by Khavinson's lab and studied for over 30 years there. Real human-derived research exists: Epithalon increased telomerase activity in lymphocytes taken from human donors aged 25–88. That is cell-culture research using human-derived cells, so it measures activity in the dish rather than an outcome in a living person. Large-scale randomized human trials remain to be run, and the compound has yet to go through Western regulatory testing.
MOTS-c — Longevity research (Community evidence)
Human studies show MOTS-c naturally correlates with better metabolic markers and rises with exercise. The human data describes MOTS-c as the body produces it; testing it as an administered compound is still an open question.
Human research exists and is observational rather than a treatment trial: exercise raises circulating MOTS-c levels in humans; lower plasma MOTS-c correlates with higher fasting insulin, HbA1c, and BMI; levels are lower in Type 1 diabetes patients and in obese children. The human evidence therefore describes what MOTS-c does naturally in the body. Whether administering it reproduces those associations remains an open question.
Semax — Cognitive research (Clinical evidence)
Approved in Russia for stroke and brain-injury recovery based on real clinical trials there; smaller studies in healthy volunteers show attention and memory improvements. The findings await independent Western replication.
Semax holds Russian pharmaceutical approval for acute ischemic stroke, traumatic brain injury, optic nerve pathology, and cognitive enhancement in organic brain dysfunction. A 110-patient trial (Gusev et al., 2018) found intranasal Semax raised BDNF and improved motor/functional recovery scores over ~5 months in post-stroke patients; an earlier controlled trial (Gusev et al., 2001) found it accelerated neurological recovery after acute ischemic stroke. In healthy volunteers, doses of 250–1000mcg/kg improved attention and short-term memory with EEG changes similar to other neuroprotective drugs. Caveat: this evidence comes from Russian trials awaiting independent Western replication, and much of it involves stroke and brain-injury patients; a healthy adult is a different context.
Selank — Cognitive research (Clinical evidence)
Russian clinical studies (800+ patients across trials) report anxiety relief comparable to benzodiazepines, without the sedation or dependence risk. Large Western RCTs are still to come.
Reported across trials totaling 800+ patients, with anxiolytic effects described as comparable to benzodiazepines (e.g. vs. medazepam, vs. phenazepam) while leaving sedation, cognitive impairment and dependence out of the profile. Standardized anxiety scales (Hamilton Anxiety Rating Scale) and physiological stress markers (blood pressure, cortisol) reportedly improved vs. placebo. Caveat: large-scale, Western-style randomized controlled trials remain to be published; the evidence is Russian-language, smaller-sample research.
Cerebrolysin — Cognitive research (Clinical evidence)
A large meta-analysis (14 RCTs, ~2,900 patients) shows real stroke-recovery benefit, while a major 2012 trial found the benefit unclear in stroke generally. The evidence is genuinely mixed.
A meta-analysis of 14 randomized controlled trials (2,884 patients) found significantly improved neurological recovery after acute ischemic stroke vs. placebo, and upper-limb motor recovery improved within 3 weeks (sustained at 90 days). A large 2012 trial cast doubt on its usefulness in stroke generally, except perhaps in severe cases, and functional-independence outcomes showed only a non-significant trend favoring it. Separately, a schizophrenia-patient trial found improved cognition/memory, and an older-adult memory-loss trial found improved memory alongside unchanged verbal fluency. Whether it prevents dementia or slows general cognitive decline remains an open question.
CJC-1295 (No DAC) + Ipamorelin — Performance research (Clinical evidence)
Human trials confirm this reliably raises growth hormone and IGF-1 for days at a time. What those trials measured is the hormone response; the downstream effect on muscle, strength and recovery is still an open question, and the pairing has been studied as two separate compounds rather than as a combination.
Two randomized, placebo-controlled, double-blind human trials (28 and 49 days) found single/multiple CJC-1295 doses produced dose-dependent GH increases (2–10x) lasting 6+ days and IGF-1 increases (1.5–3x) lasting up to 28 days after repeated dosing. Important caveat: these trials measured hormone levels, so muscle growth, strength and body composition remain untested endpoints; raising GH/IGF-1 is a different claim from a proven strength result. The combined CJC-1295+Ipamorelin stack that is commonly used has been studied as its two separate compounds. The combination's rationale (complementary GH-release pathways) is mechanistic reasoning drawn from those individual trials.
Ipamorelin — Performance research (Clinical evidence)
Confirmed in human trials to raise growth hormone cleanly and briefly. The trials measured the hormone response; effects on muscle, sleep and recovery remain untested endpoints.
A randomized, double-blind, placebo-controlled human trial confirmed Ipamorelin sharply raises GH (peaking ~40 minutes post-dose, back to low levels by 6 hours) with a cleaner side-effect profile than older secretagogues like GHRP-6, leaving cortisol, prolactin and appetite largely unchanged. Trials to date have measured the hormone response itself, so body composition, sleep quality and recovery remain untested endpoints. It holds no FDA approval for any indication, and existing human data is small-scale and short-term.
GHRP-6 — Performance research (Clinical evidence)
Reliably raises growth hormone in human studies and is used as a diagnostic test for GH deficiency. Its anabolic and anti-aging applications remain unconfirmed after decades of research, and it holds no regulatory approval.
Human studies confirm GHRP-6 reliably stimulates GH release (used alongside GHRH as a validated diagnostic test for adult GH deficiency). Despite reproducible GH-stimulating effects, "the clinical use of GHRP as orally active growth-promoting agents and anabolic anti-aging drugs remains to be confirmed": early enthusiasm for it as a GH-replacement alternative was not borne out in further research. It holds no clinical approval, and the available human safety data is short-term.
Tesamorelin — Performance research (Clinical evidence)
FDA-approved on strong trial data, specifically for visceral fat in HIV-associated lipodystrophy. That is a real, well-proven effect in a population quite different from general fitness use.
The first FDA-approved GHRH analog, approved specifically for reducing visceral fat in HIV-associated lipodystrophy. Two Phase III trials (816 participants, 543 on drug during the 26-week placebo-controlled period) found 15–17% reductions in visceral abdominal fat by CT scan vs. placebo, with the effect specific to visceral fat rather than subcutaneous fat, limb fat, or overall body weight. Caveat: FDA approval covers HIV-associated lipodystrophy only. General fitness and performance use sits outside what the approval and trials establish.
IGF-1 LR3 — Performance research (Community evidence)
Cell-level research supports the mechanism, and native IGF-1 has real human data in a medical context. Evidence for this specific long-acting analog, as it is actually used, remains preclinical.
Human muscle-cell models show IGF-1 LR3 activates the Akt/mTOR pathway (increasing protein synthesis and myotube hypertrophy), and native IGF-1 studies in HIV-associated muscle wasting show meaningful lean-mass preservation. Human clinical evidence specific to IGF-1 LR3, the long-acting analog sold as a research compound, remains preclinical. Most real-world use in bodybuilding and athletic communities extrapolates from studies of native IGF-1. It holds no FDA approval for human use.
Follistatin (FST) — Performance research (Community evidence)
The single human trial used gene-therapy delivery in six muscular dystrophy patients, a different route and population from the injectable peptide. Muscle-mass evidence beyond that comes from mouse studies.
A proof-of-principle trial delivered follistatin via gene therapy (AAV1.CMV.FS344 injected directly into the quadriceps) to six Becker muscular dystrophy patients, measuring walking-distance improvement, with no abnormal safety findings across monitored organ systems. Two important caveats: the trial used gene-therapy delivery rather than the injectable peptide sold in this catalog, and it studied six patients with a specific muscular dystrophy rather than general muscle-building in healthy adults. Broader evidence (increased strength and muscle mass) comes from mouse studies.
GHK-Cu — Regenerative research (Clinical evidence)
Genuinely strong, repeated clinical trial evidence for wound healing and scar reduction in humans: one of the best-evidenced compounds in this catalog, with completed human trials behind it.
The best-evidenced compound in this category. A current Phase 2 randomized, double-blind, vehicle-controlled trial (ClinicalTrials.gov) is testing topical GHK-Cu gel on standardized skin wounds in healthy adults. Completed human studies: a 2023 Phase 2 trial in 40 post-surgical patients found 0.5% GHK-Cu gel reduced scar volume by 35% at 3 months vs. silicone (statistically significant, p=0.002); a 2021 RCT in 72 diabetic ulcer patients found 85% wound closure at 12 weeks with GHK-Cu dressings vs. 55% control; a human comparison trial found topical GHK-Cu increased collagen in 70% of volunteers, outperforming both vitamin C and retinoic acid comparators. Chronic venous ulcer trials also show accelerated healing and granulation tissue formation vs. placebo.
BPC-157 — Regenerative research (Community evidence)
Has real human trial data for an inflammatory gut condition. For the injury and tendon healing it is typically associated with, the evidence to date is preclinical: 100+ animal studies plus one small observational report.
Important distinction: BPC-157 does have real human trial data. A Phase 2 trial for ulcerative colitis (Croatia) found statistically significant dose-dependent improvement in endoscopic/clinical scores, and Croatian trials in the early 2000s found it safe and effective for inflammatory bowel disease. The injury, tendon and muscle healing use that represents the majority of how people actually use this compound rests on preclinical evidence: 100+ animal studies plus one small, low-quality observational study (7 of 12 people with chronic knee pain reported relief 6+ months after one injection). Human safety data covers the gut-condition trials; the injury-recovery use case remains preclinical.
TB-500 — Regenerative research (Community evidence)
The human trial data commonly cited for this compound comes from full-length Thymosin Beta-4, a related but larger molecule applied topically. Evidence for TB-500 itself, the 17-amino-acid fragment sold as a peptide, is preclinical.
Critical distinction: as of this research, evidence for TB-500 (the 17-amino-acid fragment sold as a peptide) is preclinical across every tissue-repair indication. The human clinical trial data that does exist (two Phase 2 trials in venous stasis ulcers and pressure ulcers, showing healing accelerated by nearly a month, safe and well-tolerated) used full-length Thymosin Beta-4, a related but larger molecule, applied topically. Preclinical (animal and cell) research on Tβ4 broadly supports accelerated wound healing mechanisms; whether TB-500 specifically, as an injected peptide, reproduces that effect is still an open question.
KPV (Alpha-MSH Fragment) — Regenerative research (Community evidence)
A well-understood anti-inflammatory mechanism, with an evidence base that is entirely preclinical: animal models and laboratory research.
A tripeptide derived from alpha-MSH with a well-studied anti-inflammatory mechanism (blocks NF-kB signaling, reducing nuclear translocation by up to 80% in lab models). Anti-inflammatory effects are documented in animal models of colitis and peritonitis. The evidence base is preclinical: animal models and laboratory research.
Thymosin Alpha-1 — Immune research (Clinical evidence)
Extensively studied (11,000+ subjects) with real, strong benefit in specific conditions like hepatitis B, while a large sepsis trial found no benefit. Evidence is condition-specific.
Studied in more than 11,000 human subjects across trials. Real, strong results exist and are specific to particular conditions: a pivotal RCT in chronic hepatitis B found 40.6% complete virological response with a 26-week course vs. 9.4% in controls; a 12-month trial in pulmonary tuberculosis patients with diabetes found significantly better sputum-clearance and lesion-resolution rates alongside increased CD3+/CD4+/NK-cell counts. Results vary by condition: a large Phase 3 sepsis trial (22 centers, China) found no significant benefit on any outcome. Mechanistically, it raises CD4+ T-cell levels and CD4/CD8 ratio, which is why it is studied in immunocompromised populations (HIV, cancer-related immunosuppression, age-related immune decline). Those trial populations are specific; a healthy adult is a different context.
LL-37 (Cathelicidin) — Immune research (Clinical evidence)
Real trial data exists, almost entirely for topical wound healing. The antimicrobial and immune mechanisms are well-studied in the lab, with human trials for those broader applications still early.
The most advanced human data is in topical wound healing: a Phase IIb RCT (148 patients) found 28.1% complete wound closure with LL-37 vs. 8.1% placebo in a large-wound subgroup; a smaller RCT in venous leg ulcers also showed improved healing. A Phase I trial tested it via intra-tumoral injection in melanoma, finding acceptable tolerability and variable biological response. Broader immune and antimicrobial mechanisms (disrupting microbial membranes, modulating inflammatory signaling) are well-documented in lab research, while "clinical translation remains in its infancy" for those broader applications.
Tymalin — Immune research (Clinical evidence)
Decades of real clinical use and striking long-term mortality data in Eastern European research. That evidence comes from clinical practice there and remains to be independently replicated under Western trial standards.
Developed in the 1970s (the same Khavinson/Morozov lab behind Epithalon) and in clinical use for 40+ years in Russia and Eastern Europe, with regulatory approval in those countries. A notable 2021 study found it improved immune status markers and clinical outcomes in elderly COVID-19 patients. Separately, described as "the longest human clinical trial ever conducted on a therapeutic peptide": a 6-year follow-up in elderly patients reportedly found a 45% reduction in cardiovascular mortality and 28% reduction in all-cause mortality. Also used as adjunct therapy for influenza, hepatitis B/C, herpes simplex, and HIV in the countries where it is used clinically. Independent replication under US/EU regulatory review remains to be done.
PNC-27 — Immune research (Community evidence)
An experimental anti-cancer research compound studied in cell cultures. Its evidence base is preclinical, and its research context is oncology rather than immune support.
Framing note: PNC-27 is a p53-derived experimental compound studied for selectively destroying cancer cell membranes in vitro. Its research context is oncology rather than the immune support this area implies. Research to date is cell-culture level (over 20 human cancer cell lines tested) with limited in vivo (animal) data; human clinical trials remain to be run. It holds no approval for human use from any regulatory authority.
GHK-Cu — Dermal research (Clinical evidence)
Strong, repeated clinical trial evidence for skin and wound healing (see Healing & recovery); smaller human trials also show real improvements in hair count and follicle density with topical use, resting on smaller trials than the skin evidence.
For skin: see the full GHK-Cu entry under Healing & recovery. The scar-reduction, wound-closure and collagen-increase trials there apply directly to the skin and aesthetic use case, extending beyond wound repair to collagen stimulation and visible skin quality. For hair specifically the evidence is real and thinner: a 2016 RCT using a GHK peptide formulation found significant hair-count increases after 6 months of topical use vs. placebo in men with pattern hair loss, and a 2015 study combining GHK-Cu with other hair-active peptides outperformed placebo on follicle density and diameter. The mechanism (VEGF upregulation, TGF-β1 suppression, Wnt/β-catenin activation in dermal papilla cells) is well-characterized in lab research. Honest summary: a well-understood mechanism, positive animal data, and a cluster of smaller positive human studies. Large-scale RCTs remain to be run.
GLOW (GHK-Cu + TB-500 + BPC-157) — Dermal research (Community evidence)
A blend built from individually-researched compounds. Evidence exists for each ingredient on its own; the combination as a whole remains to be trialed.
A combination product (GHK-Cu + TB-500 + BPC-157) built from individually-researched compounds; see each one's own entry (GHK-Cu here and under Healing & recovery; BPC-157 and TB-500 under Healing & recovery). This specific combination remains to be trialed as a whole, the same caveat as the CJC-1295+Ipamorelin stack under Physical performance. Confidence in the individual ingredients applies to those ingredients: combining compounds can change absorption, interaction effects and outcomes in ways individual-ingredient trials leave open.
KLOW (GHK-Cu + BPC-157 + TB-500 + KPV) — Dermal research (Community evidence)
A blend built from individually-researched compounds. Evidence exists for each ingredient on its own; the combination as a whole remains to be trialed.
A combination product (GHK-Cu + BPC-157 + TB-500 + KPV) built from individually-researched compounds; see each one's own entry (GHK-Cu here and under Healing & recovery; BPC-157, TB-500 and KPV under Healing & recovery). This specific combination remains to be trialed as a whole, the same caveat as the CJC-1295+Ipamorelin stack under Physical performance. Confidence in the individual ingredients applies to those ingredients: combining compounds can change absorption, interaction effects and outcomes in ways individual-ingredient trials leave open.
DSIP — Neuroendocrine research (Clinical evidence)
Real human trials exist and they disagree with each other: some show meaningful sleep improvement, one found the effect minimal compared to placebo. The evidence is genuinely mixed.
Real human trials exist, and results are inconsistent across them. One early trial: 7 severe insomnia patients given 10 DSIP injections had normalized sleep for 3–7 months in all but one case, with improved daytime mood and performance. A separate trial in 6 chronic insomniacs found longer sleep duration, higher sleep quality, fewer interruptions, and slightly more REM sleep with no daytime sedation, though the sleep-promoting effect appeared in the second hour after injection (a mild arousing effect showed in the first hour). Another controlled trial found total sleep time increased while nighttime awakenings tracked placebo, concluding the clinical significance was minimal. Overall assessment from research reviewers: "clinical research remains limited and somewhat controversial."
NEURO-CALM PM (blend) — Neuroendocrine research (Community evidence)
A blend product whose combination remains to be trialed as a whole. Evidence comes from its individual ingredients, researched separately.
A combination blend; individual components should be researched on their own merits (this catalog entry does not specify a composition that maps cleanly to the already-researched single compounds in this document). As with other blends (GLOW/KLOW, CJC-1295+Ipamorelin), this specific combination remains to be trialed; treat the blend itself as community-tier regardless of any individual ingredient's own evidence.
PT-141 (Bremelanotide) — Melanocortin research (Clinical evidence)
Genuinely FDA-approved with solid trial data (1,200+ women). The approval is specifically for a diagnosed desire disorder in premenopausal women, and there it improved desire scores while the count of satisfying sexual events, a key trial endpoint, stayed close to placebo.
FDA-approved (as Vyleesi®, June 2019) for acquired, generalized hypoactive sexual desire disorder (HSDD) in premenopausal women: the second-ever approved drug for female sexual desire disorder, and the first with a non-hormonal mechanism (acting centrally via MC4R receptors and dopamine pathways, where Viagra and Cialis work on blood flow). Trials included over 1,200 women. Important, specific caveat: it improved desire and desire-related distress scores vs. placebo, while the number of "satisfying sexual events," a key trial endpoint, stayed close to placebo. Nausea was the most common side effect (40% of the treatment group in the RECONNECT trials, resolving within ~3 hours). Used off-label in men for erectile dysfunction and low libido; the FDA approval and the trial population above are specifically premenopausal women with HSDD.