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Every study behind the numbers on this site, sorted by type of peptide. Each entry gives the authors, the journal and the year, plus a plain-English line on what that paper actually showed — so you can weigh the evidence yourself instead of taking a number on trust.
A pentadecapeptide fragment derived from a sequence in human gastric juice. The published record is almost entirely preclinical research on tendon, ligament, muscle and gastrointestinal healing. There is no completed, published human efficacy trial, and reported doses are extrapolations from weight-based research figures rather than clinically established ranges.
A synthetic fragment of thymosin beta-4, the actin-sequestering protein. Full-length Tβ4 reached human trials for dry eye and cardiac indications; the truncated research fragment sold as TB-500 has not. Dosing conventions come from the research community, loosely anchored to preclinical Tβ4 work.
The C-terminal tripeptide of α-melanocyte-stimulating hormone, studied for anti-inflammatory activity in colitis and dermatitis models without the pigmentation effects of the full hormone.
The most extensively trialled compound in this database. Approved formulations follow a fixed escalation schedule to manage gastrointestinal tolerability; the figures below reflect the STEP obesity trial titration.
A dual incretin agonist. SURMOUNT-1 established the 5/10/15 mg maintenance arms with a four-week-per-step escalation from 2.5 mg.
A triple-receptor agonist in ongoing phase 3 development. Phase 2 data reported dose-dependent weight reduction up to 12 mg weekly. Not approved anywhere; long-term safety is not established.
An amylin analogue studied alone and in fixed combination with semaglutide (CagriSema). Escalation mirrors the GLP-1 pattern.
A dual GLP-1/glucagon receptor agonist in phase 3, with notable phase 2 results in MASH as well as obesity.
A GLP-1/glucagon dual agonist developed primarily in Chinese phase 2/3 programmes.
A C-terminal fragment of human growth hormone investigated as an anti-obesity agent. Human trials were conducted, but efficacy on weight endpoints was not compelling enough to advance, which is itself informative.
A small-molecule NNMT inhibitor rather than a true peptide. Research data show reduced adiposity in diet-induced obesity models. No human trials. Commonly grouped with the peptides even though it is a different class of molecule.
An estrogen-related receptor pan-agonist described as an exercise mimetic in preclinical models. Not a peptide, no human data of any kind. Reported doses below are the weight-based research figures, given raw rather than converted, because a human-equivalent conversion is not supported.
A vascular-targeting peptidomimetic that ablates white adipose vasculature. Research studies showed weight loss alongside dose-dependent renal toxicity. Development did not proceed. This compound has a genuine documented harm signal.
An AMPK-activating nucleoside studied for ischaemia protection and as an exercise mimetic in preclinical research. Requires very large doses relative to peptides; a WADA-prohibited substance.
The most receptor-selective of the GHRP family — releases GH with minimal effect on cortisol, ACTH or prolactin, which is its main pharmacological point of interest. Human pharmacology work exists; long-term human efficacy trials do not.
A tetra-substituted GHRH(1-29) analogue without the drug affinity complex, giving a short pulse rather than sustained elevation. Frequently paired with a GHRP on the rationale of hitting two complementary receptors.
GHRH analogue conjugated to bind serum albumin, extending half-life from minutes to days. This produces sustained GH/IGF-1 elevation rather than pulses — a meaningfully different physiological profile from the no-DAC version.
The natural GHRH 1-29 fragment. Previously an approved agent for paediatric GH deficiency diagnosis and treatment before withdrawal from the US market for commercial reasons. Among the better-documented compounds in this class.
An FDA-approved GHRH analogue for HIV-associated lipodystrophy — the only compound in this class with a full approval and a defined label dose. Two large phase 3 trials support the 2 mg daily figure.
A growth hormone-releasing peptide with an approved diagnostic use in Japan for GH deficiency testing. Less receptor-selective than ipamorelin — raises prolactin and cortisol somewhat.
The original GHRP. Notably potent at stimulating appetite via ghrelin receptor activity, which for many purposes is a side effect rather than a feature.
A potent GHRP with additional cardiac CD36 receptor activity independent of GH release. Notable for rapid receptor desensitisation with continuous use.
Recombinant somatropin. An approved prescription drug with well-defined indications and a substantial adverse-effect profile including insulin resistance, oedema, arthralgia and carpal tunnel syndrome. Vials are labelled in IU; roughly 3 IU per mg.
An IGF-1 analogue engineered to resist binding-protein sequestration, giving far longer activity than native IGF-1. Carries genuine hypoglycaemia risk. Widely used as a cell-culture supplement; human research use is not supported by trial data.
A truncated IGF-1 variant with roughly tenfold higher potency at the receptor but a very short half-life, hence its reputation as a localised agent. Preclinical only.
A splice variant of IGF-1 expressed in muscle after mechanical loading, implicated in satellite cell activation. Extremely short-lived unmodified.
MGF with polyethylene glycol conjugation to extend circulating half-life from minutes to days. Entirely preclinical and community-derived dosing.
A synthetic tetrapeptide from the Khavinson bioregulator programme, associated with telomerase activation and pineal regulation claims. The supporting literature is overwhelmingly from a single Russian research group, largely in journals with limited international peer review, and has not been independently replicated at scale.
A tripeptide bioregulator directed at neuronal tissue in the Khavinson framework. Evidence base is the same single-programme literature as the other bioregulators.
A dipeptide bioregulator associated with thymic and immune claims within the same Russian research programme.
Bioregulator tetrapeptide associated with hepatic and chromatin-decondensation claims. Same evidence caveats as the rest of the class.
Bioregulator peptide directed at cartilage and connective tissue in the Khavinson framework. No independent clinical literature.
Bioregulator tripeptide associated with bronchopulmonary tissue claims.
Bioregulator tetrapeptide with reported gonadal-axis activity in the same programme literature.
Bioregulator tetrapeptide associated with hepatic and ovarian tissue claims.
Bioregulator tetrapeptide targeting prostatic tissue; related to the Prostamol/prostate peptide series.
Bioregulator tripeptide associated with vascular endothelium claims.
Bioregulator tetrapeptide directed at cortical/neural tissue; studied in peripheral nerve regeneration models within the same programme.
A senolytic peptide that disrupts the FOXO4–p53 interaction, selectively triggering apoptosis in senescent cells. The research data are striking; there is no human dosing data whatsoever, and the mechanism is intrinsically cytotoxic.
A coenzyme rather than a peptide. Direct NAD+ administration is bioavailability-limited and often poorly tolerated (stinging, flushing, nausea). Most rigorous human research uses precursors — NR or NMN — rather than NAD+ itself.
A mitochondrial-derived peptide acting via AMPK on insulin sensitivity and metabolic homeostasis. Genuinely interesting mechanism with solid research data and human observational correlations, but no human dosing trials.
A cardiolipin-targeting mitochondrial peptide — the only compound in this class with substantial registered human trial data, across Barth syndrome, primary mitochondrial myopathy and dry AMD. Results have been mixed, with several missed primary endpoints.
The principal endogenous intracellular antioxidant tripeptide. Widely administered in clinical settings; the evidence for parenteral supplementation improving outcomes in healthy subjects is thin.
A synthetic ACTH fragment analogue registered as a medicine in Russia for stroke and cognitive indications. Substantial Russian clinical literature; almost no Western replication.
A tuftsin-derived heptapeptide registered in Russia as an anxiolytic. Reported to modulate GABAergic and enkephalin systems without the sedation or dependence profile of benzodiazepines.
Not a single peptide but a standardised mixture of low-molecular-weight peptides and amino acids of porcine origin. Approved in a number of countries for stroke and dementia; Cochrane reviews of the evidence have been notably unenthusiastic.
A nonapeptide originally isolated from cerebral venous blood during induced sleep. Despite the name, controlled human sleep-architecture results have been inconsistent, and the compound has essentially no modern clinical development.
A shortened spadin analogue that blocks the TREK-1 potassium channel, proposed as a fast-acting antidepressant mechanism. Preclinical data only.
An 11-amino-acid erythropoietin derivative that engages the innate repair receptor without the erythropoietic or thrombotic effects of EPO. Studied in sarcoidosis-associated small fibre neuropathy and diabetic neuropathy with genuine registered trials.
The sole human cathelicidin-derived antimicrobial peptide. Well characterised in immunology literature for direct antimicrobial and immunomodulatory activity; also implicated in rosacea and psoriasis pathology, which cuts against naive "more is better" reasoning.
A thymic peptide approved in a number of countries as an immunomodulator, principally as adjunct therapy in chronic hepatitis B and C. One of the better-evidenced compounds here, with a defined label dose.
A 28-amino-acid neuropeptide with vasodilatory and immunomodulatory activity. The aviptadil formulation reached large registered trials in respiratory failure. Use in chronic inflammatory response syndrome is far less well evidenced. Hypotension is a real risk.
A p53-derived peptide fused to a membrane-penetrating sequence, reported to selectively lyse cancer cell membranes in vitro and in preclinical tumour models. There are no human trials. Marketing of this compound as a cancer treatment substantially outruns its evidence.
A copper-binding tripeptide present in human plasma, declining with age. The strongest evidence covers collagen synthesis, wound healing and skin remodelling. Copper-containing solutions are photosensitive and should not be mixed with certain diluents; check compatibility.
A non-selective melanocortin agonist producing pigmentation, appetite suppression and erectile effects. Carries documented safety concerns: nausea, blood pressure changes, and case reports of dysplastic naevi and melanoma associated with unregulated use. Bremelanotide (PT-141) is the selectively developed descendant.
A cosmetic peptide marketed as a SNARE-complex modulator — a "botulinum analogue." The evidence is manufacturer-sponsored cosmetic testing rather than independent research.
An FDA-approved melanocortin-4 agonist for hypoactive sexual desire disorder in premenopausal women. The 1.75 mg label dose is well defined; nausea is the dominant adverse effect and transient blood pressure elevation is documented.
An upstream regulator of GnRH release, studied extensively in reproductive endocrinology at Imperial College and elsewhere. Human doses in the literature are given by body weight or as timed infusions, not as flat mg figures — treat any flat "standard dose" with suspicion.
Native gonadotropin-releasing hormone. Pulsatile administration stimulates the axis; continuous administration paradoxically suppresses it, which is exactly why cadence matters more than dose here.
A glycoprotein hormone with LH-like activity, an approved prescription drug in fertility and hypogonadism. Vials are labelled in IU. The "HCG diet" application has been explicitly rejected by the FDA as unsupported.
A nonapeptide hormone. Long established as a clinical drug. The social-cognition research literature is large but has significant replication problems worth knowing about before reading any single result.
A fixed-ratio combination vial. Because the components are pooled at a fixed ratio, you cannot titrate one without moving the others — the practical consequence is that dosing is driven by whichever component has the narrowest window. A 70 mg vial is roughly 71% GHK-Cu by mass.
The GLOW combination with KPV added. Same fixed-ratio constraint applies, with a fourth component narrowing the titration window further.
The most common repair blend, equal parts BPC-157 and TB-500. Two sizes: the 10 mg vial holds 5 mg of each, the 20 mg vial holds 10 mg of each. The split is 50/50 either way, so every dose delivers half of it to each component regardless of which vial you have — a 1000 mcg dose is 500 mcg of each. The vial size changes how many doses you get, not the ratio. Switch the vial strength above to match what you are holding.
An equal-parts repair and anti-inflammatory pairing — 10 mg of each in a 20 mg vial, so every dose splits evenly down the middle and a 600 mcg dose is 300 mcg apiece. Both components sit in the same 200–500 mcg daily range, which makes this an unusually well-matched blend: unlike most fixed-ratio combinations, neither one caps the other. Both are preclinical, with no human efficacy trials behind either.
A GHRH analogue paired with a selective ghrelin receptor agonist — the pairing rationale is that the two receptors act synergistically on GH release. A 10 mg vial holds 5 mg of each; a 200 mcg dose therefore delivers 100 mcg of each.
An equal-thirds repair and anti-inflammatory combination — 10 mg of each component in a 30 mg vial. Because the three are pooled at a fixed 1:1:1 ratio you cannot move one without moving the others, so every dose delivers exactly one third of the total to each. A 900 mcg dose is 300 mcg apiece.
Pairs a GHRH analogue with a selective GHRP in a 17 mg vial — roughly 65% tesamorelin, 35% ipamorelin. Worth knowing before you dose it: tesamorelin’s established daily figure is 2 mg, and reaching that from this blend takes about 3.1 mg total, which also delivers around 1.1 mg of ipamorelin — roughly four times the 100–300 mcg commonly reported for it. Any fixed-ratio blend forces that trade-off; you cannot raise one without raising the other.
An equal-parts pairing of the two Russian-registered neuropeptides — 5 mg of each in a 10 mg vial, so every dose splits evenly down the middle. Both are short-acting. Worth knowing that the published figures for both compounds come from intranasal studies rather than injection, so the amounts below are the researched doses rather than an established subcutaneous schedule.
A metabolic combination in a 120 mg vial, dosed daily and anchored to MOTS-c. MOTS-c is 8.3% of the contents, so a 1 mg daily MOTS-c dose means 12 mg of blend — which also delivers 10 mg of NAD+ and 1 mg of 5-Amino-1MQ. Because the ratio is fixed, anchoring to MOTS-c puts the other two low against their own figures: NAD+ is reported at 50–100 mg per dose and 5-Amino-1MQ at 50–150 mg orally. At 1 mg MOTS-c daily a vial runs about 10 days.
Equal parts of a triple incretin agonist and an amylin analogue — 5 mg of each in a 10 mg vial, once weekly. The thing to understand before dosing it: the two components were trialled on very different scales. Retatrutide ran up to 12 mg weekly, cagrilintide only to 2.4 mg. Because a 1:1 blend moves both together, cagrilintide hits its ceiling at 4.8 mg total — and at that point retatrutide is still only at 2.4 mg, nowhere near its higher arms. Cagrilintide is what caps this blend, and pushing past it takes the amylin component beyond anything that has been tested.