Peptide encyclopedia
20 peptides indexed. Each entry carries mechanism, route of administration, half-life, legal status in your jurisdiction, and the primary sources backing every claim.
- Compounds
- 20
- Source links
- 39
- Therapeutic classes
- 9
F·Filter
01·Healing & repair
BPC-157
Also: Body Protective Compound 157, PL 14736
BPC-157 is a 15-amino-acid sequence derived from a fragment of human gastric juice protein. Across rodent models it accelerates tendon-to-bone healing, ligament repair, and gut mucosal recovery — the candidate mechanisms include enhanced angiogenesis through the VEGFR2-eNOS-NO axis, increased fibroblast migration in tendon explants, and modulation of dopaminergic and serotonergic systems. The cross-system breadth of the rodent data is striking; the human data is far thinner.
Research use only
02·GH secretagogue
CJC-1295
Also: CJC-1295 with DAC, DAC:GRF, et al.
CJC-1295 is a tetrasubstituted analog of growth-hormone-releasing hormone (GHRH 1-29) — the active fragment of native GHRH — engineered for resistance to enzymatic degradation and, in the DAC ("drug affinity complex") variant, for covalent binding to plasma albumin. The four amino-acid substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) protect against DPP-IV cleavage and proline isomerization; the DAC moiety — a maleimidopropionic acid linker on Lys³⁰ — covalently binds the cysteine-34 residue of circulating albumin, dramatically extending plasma half-life ([Teichman et al., *J Clin Endocrinol Metab* 2006, 91:799–805](https://doi.org/10.1210/jc.2005-1536)). Receptor mechanism is the same as Tesamorelin: GHRH-receptor agonism on pituitary somatotrophs, pulsatile GH release, hepatic IGF-1 production. The non-DAC form, often labeled "Modified GRF (1-29)" or "Mod GRF 1-29," shares the four substitutions but lacks the albumin tether and clears in roughly thirty minutes — a short pharmacological window suited to per-pulse dosing rather than tonic stimulation.
Research use only
03·Sleep
DSIP
Also: Delta Sleep-Inducing Peptide, WAGGDASGE
DSIP is a nine-amino-acid peptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) discovered through one of the more unusual experimental paradigms in peptide biology: Marcel Monnier's group at Basel hypnotized rabbits with electrical stimulation of the intralaminar thalamic area, dialyzed cerebral venous blood, and isolated a fraction that, when injected into recipient rabbits, induced delta-wave EEG activity characteristic of slow-wave sleep ([Schoenenberger et al., *Pflügers Arch* 1978, 376:119–129](https://doi.org/10.1007/BF00581575)). The synthetic nonapeptide reproduced the same delta and spindle EEG enhancement, with a reported ~35% increase in delta activity in neocortex and limbic cortex of treated rabbits versus controls. Despite five decades of subsequent research, no specific high-affinity receptor has been definitively identified, and the molecular mechanism by which DSIP modulates sleep architecture remains incompletely characterized. The proposed mechanism is that DSIP acts as a modulator of sleep-wake regulatory networks rather than as a direct sedative — its effects are described as state-dependent, with greater activity in subjects whose sleep is disturbed and minimal effects in healthy unaffected sleepers.
Research use only
04·Cognitive
Dihexa
Also: PNB-0408, N-hexanoyl-Tyr-Ile-(6)aminohexanoic amide
Dihexa is a chemically modified hexapeptide derivative engineered from the cognition-relevant fragment of angiotensin IV by Joseph Harding's laboratory at Washington State University ([McCoy et al., *J Pharmacol Exp Ther* 2013, 344:141–154](https://doi.org/10.1124/jpet.112.199497)). The modifications — an N-terminal hexanoyl group and a C-terminal 6-aminohexanoic acid extension — were designed to increase lipophilicity and protect against enzymatic degradation, producing a metabolically stable, orally active, blood-brain-barrier-permeant analog. Mechanistically, the cognitive activity of angiotensin IV had originally been attributed to the AT4 receptor; the Harding group's later work demonstrated that the relevant target is actually the hepatocyte growth factor (HGF) receptor c-Met. Dihexa binds HGF with high affinity and potentiates HGF activity at c-Met, driving downstream PI3K/Akt signaling and synaptogenesis. In cell-culture assays the group reported synapse-formation activity orders of magnitude greater than equivalent concentrations of brain-derived neurotrophic factor — the much-quoted "10 million times more potent than BDNF" framing originates here, and applies specifically to a synaptogenesis-in-culture endpoint, not to broad cognitive efficacy in vivo.
Research use only
05·Longevity
Epitalon
Also: Epithalon, Epithalamin, et al.
Epitalon is a synthetic tetrapeptide with the sequence Ala-Glu-Asp-Gly (AEDG), designed as a short-form analog of the polypeptide complex epithalamin extracted from bovine pineal gland. The proposed mechanism is unusual for a peptide on this site: rather than agonizing a defined receptor, Epitalon is reported to act as an epigenetic and gene-expression modulator. The most-cited primary finding (Khavinson and colleagues, *Bulletin of Experimental Biology and Medicine* 2003) showed that Epithalon administration to telomerase-negative human fetal fibroblasts in culture induced expression of the catalytic subunit of telomerase, enzymatic telomerase activity, and telomere elongation — effects the authors proposed occur through reactivation of normally silenced telomerase genes in somatic cells ([Khavinson et al., *Bull Exp Biol Med* 2003, 135:590–592](https://doi.org/10.1023/a:1025493705728)). Subsequent work from the same St. Petersburg Institute of Bioregulation and Gerontology has extended the mechanistic story to gene-expression regulation in pineal-axis tissues, melatonin-rhythm restoration, and tissue-specific epigenetic effects across animal models.
Research use only
06·Healing & repair
GHK-Cu
Also: Copper tripeptide-1, GHK-copper, et al.
GHK is the tripeptide glycyl-L-histidyl-L-lysine, a fragment of human collagen that occurs naturally in plasma and declines with age. The biologically active form on skin and in tissue is the copper(II) complex GHK-Cu, where the imidazole and amine ligands chelate Cu²⁺. The complex appears to act through several coupled pathways: it modulates the expression of a broad set of genes involved in tissue remodeling, stimulates fibroblast collagen and glycosaminoglycan synthesis, supports angiogenesis through copper-dependent mechanisms, and exhibits anti-inflammatory and antioxidant effects in dermal and other connective-tissue contexts ([Pickart and Margolina, *Int J Mol Sci* 2018, 19(7):1987](https://doi.org/10.3390/ijms19071987)). Copper itself is a required cofactor for lysyl oxidase, the enzyme that cross-links collagen and elastin — which is part of why GHK-Cu's effects on skin density and elasticity are mechanistically plausible rather than merely empirical.
Research use only
07·GH secretagogue
Ipamorelin
Also: NNC 26-0161
Ipamorelin is a synthetic pentapeptide built around two non-natural amino acids (Aib at the N-terminus, D-2-naphthylalanine and D-phenylalanine in the core) that binds the growth-hormone-secretagogue receptor — the ghrelin receptor, GHSR-1a — on pituitary somatotrophs ([Raun et al., *Eur J Endocrinol* 1998, 139:552–561](https://doi.org/10.1530/eje.0.1390552)). Receptor agonism triggers a pulsatile release of growth hormone, which drives hepatic IGF-1 production downstream. Mechanistically this differs from Tesamorelin and CJC-1295: those are GHRH analogs binding the GHRH receptor; Ipamorelin mimics ghrelin instead. The pentapeptide structure is also small enough that it crosses some tissue compartments more readily than the larger 44-amino-acid GHRH analogs.
Research use only
08·Healing & repair
KPV
Also: Lys-Pro-Val, Lysine-Proline-Valine, et al.
KPV (Lys-Pro-Val) is the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH). The mechanistic story that drives current interest is not melanocortin-receptor signaling but transporter-mediated cellular uptake: KPV enters intestinal epithelial cells and immune cells through PepT1, an oligopeptide transporter whose expression rises during intestinal inflammation. Once intracellular, the tripeptide inhibits NF-κB and MAP kinase signaling at nanomolar concentrations and suppresses pro-inflammatory cytokine secretion ([Dalmasso et al., *Gastroenterology* 2008, 134:166–178](https://doi.org/10.1053/j.gastro.2007.10.026)). Critically, the anti-inflammatory effect persists in mice with non-functional MC1R, indicating it is not melanocortin-receptor-mediated — KPV essentially acts as a small-molecule cytokine-pathway modulator that gets concentrated where it's needed because the relevant transporter is upregulated at the inflammation site.
Research use only
09·GH secretagogue
MK-677
Also: Ibutamoren, Ibutamoren mesylate, et al.
MK-677 (ibutamoren) is a non-peptide spiropiperidine designed by Merck as an orally bioavailable agonist of the growth-hormone-secretagogue receptor — the ghrelin receptor, GHSR-1a — on pituitary somatotrophs ([Nass et al., *Ann Intern Med* 2008, 149:601–611](https://doi.org/10.7326/0003-4819-149-9-200811040-00003)). Receptor agonism triggers pulsatile growth hormone release in the same downstream pathway as Ipamorelin, with the practical advantage that it is absorbed orally and clears with a half-life that supports once-daily dosing. Strictly speaking, MK-677 is not a peptide — it is a small molecule that mimics ghrelin's receptor activity. This site labels it "peptide-adjacent" because the GH-axis function it serves is the same one biohackers approach via the injectable peptides on this list, and excluding it would make the GH-secretagogue conversation less complete than it should be.
Research use only
10·Mitochondrial
MOTS-c
Also: Mitochondrial open reading frame of 12S rRNA-c
MOTS-c is a 16-amino-acid peptide encoded within the 12S ribosomal RNA gene of the mitochondrial genome — the first mitochondrial-encoded peptide to be characterized as a circulating signaling molecule rather than a structural component of the organelle. The discovery and primary characterization, by Changhan Lee and Pinchas Cohen at the University of Southern California, established a metabolic signaling pathway distinct from any known nuclear-encoded peptide hormone ([Lee et al., *Cell Metab* 2015, 21:443–454](https://doi.org/10.1016/j.cmet.2015.02.009)). MOTS-c's primary tissue target appears to be skeletal muscle, where it inhibits the folate cycle, raises AICAR levels, and activates AMP-activated protein kinase (AMPK). AMPK activation downstream produces increased glucose uptake, fatty-acid oxidation, and the broader metabolic effects associated with the cellular energy-stress response. Subsequent work from the Cohen group showed that MOTS-c can translocate to the nucleus under metabolic stress and regulate nuclear gene expression — a mitochondria-to-nucleus signaling axis that adds mechanism beyond simple peripheral hormone-like activity.
Research use only
11·Sexual function
PT-141
Also: Bremelanotide, Vyleesi, et al.
PT-141, marketed as bremelanotide and approved as Vyleesi, is a cyclic heptapeptide melanocortin receptor agonist developed from the α-melanocyte-stimulating hormone (α-MSH) family. It is a non-selective melanocortin agonist with activity at MC1, MC3, MC4, and MC5 receptors; the MC4 receptor activity, particularly in the central nervous system, is the principal mechanism for sexual-desire and arousal effects. Unlike PDE5 inhibitors (sildenafil, tadalafil), which act peripherally on the vasculature of erectile tissue, PT-141 acts centrally — in the hypothalamic and other CNS pathways that regulate sexual desire and arousal — making the mechanism more upstream and the experiential profile distinct. The cyclic structure was engineered for stability against enzymatic degradation, supporting the as-needed subcutaneous dosing profile of the FDA-approved formulation ([Kingsberg et al., *Obstet Gynecol* 2019, 134:899–908](https://doi.org/10.1097/AOG.0000000000003500)).
Prescription only
12·Metabolic / GLP-1
Retatrutide
Also: LY3437943
Retatrutide is a synthetic peptide engineered as a balanced agonist of three receptors: the glucose-dependent insulinotropic polypeptide (GIP) receptor, the glucagon-like peptide 1 (GLP-1) receptor, and the glucagon receptor ([Jastreboff et al., *N Engl J Med* 2023, 389:514–526](https://doi.org/10.1056/NEJMoa2301972)). The first two receptors share their incretin mechanism with tirzepatide and semaglutide, respectively; the addition of glucagon-receptor agonism is what distinguishes retatrutide and is hypothesized to add a pro-energy-expenditure component to the appetite-suppressive and insulin-sensitizing effects of the two incretins. Mechanistically, glucagon-receptor agonism increases hepatic glucose output, mobilizes lipids, and raises basal energy expenditure — a combination that, balanced correctly against the incretin signals, is intended to drive weight loss through both reduced energy intake and increased energy turnover. The fatty-acid modification for albumin binding produces a roughly week-long pharmacokinetic profile suited to weekly dosing.
Prescription only
13·Mitochondrial
SS-31
Also: Elamipretide, Bendavia, et al.
SS-31, marketed as elamipretide, is a four-amino-acid peptide engineered by Hazel Szeto and Peter Schiller at Cornell to selectively concentrate in the inner mitochondrial membrane and bind cardiolipin — the unique phospholipid that organizes the electron transport chain and is exclusively localized to mitochondrial inner membranes. The molecule's structure (D-Arg-2',6'-dimethylTyr-Lys-Phe-NH2) combines alternating aromatic and basic residues with a D-stereochemistry N-terminal arginine that produces 1,000- to 5,000-fold concentration in the inner mitochondrial membrane relative to extracellular space. By stabilizing cardiolipin and supporting electron-transport-chain organization, SS-31 has been reported to improve mitochondrial respiration, reduce reactive oxygen species production under stress, and protect mitochondria in models of ischemia-reperfusion injury, heart failure, and primary mitochondrial disease. The mechanism is structural and pharmacological — direct organelle targeting — rather than receptor agonism, which distinguishes it sharply from every other peptide on this site.
Prescription only
14·Cognitive
Selank
Also: TKPRPGP, Selanc
Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) built by extending the immunoglobulin-derived tetrapeptide tuftsin with a Pro-Gly-Pro tail that resists enzymatic degradation. The proposed mechanism is multimodal rather than single-receptor. Published work has documented allosteric modulation of GABA-A receptor sensitivity, reshaping of GABA-induced gene-expression patterns in human IMR-32 neuroblastoma cells (Selank alone produced no baseline mRNA changes — its effect appeared only in combination with GABA or olanzapine; [Filatova et al., *Front Pharmacol* 2017, 8:89](https://doi.org/10.3389/fphar.2017.00089)), elevated brain-derived neurotrophic factor (BDNF) in rat hippocampus, and modulation of leu-enkephalin turnover in human plasma. Unlike benzodiazepines, Selank does not appear to bind the benzodiazepine site of the GABA-A receptor directly, which is the hypothesis underlying its reported non-sedating, non-dependency-forming profile. In Russian clinical use it is administered intranasally; subcutaneous and intravenous routes appear in the experimental rodent literature.
Research use only
15·Metabolic / GLP-1
Semaglutide
Also: Ozempic, Wegovy, et al.
Semaglutide is a 31-amino-acid analog of glucagon-like peptide-1 (GLP-1) with two structural modifications: an α-aminoisobutyric acid substitution at position 8 that resists degradation by DPP-4, and a C18 fatty acid chain attached at position 26 through a γ-glutamic acid spacer that binds plasma albumin and extends the half-life to about a week ([Lau et al., *J Med Chem* 2015, 58:7370–80](https://doi.org/10.1021/acs.jmedchem.5b00726)). It acts as a full agonist at the GLP-1 receptor, which is expressed on pancreatic β-cells, on enteric neurons, and on hypothalamic and brainstem appetite-regulating circuits. Three downstream effects matter clinically: glucose-dependent insulin secretion, slowed gastric emptying, and centrally mediated appetite suppression. The central effect is the dominant driver of weight loss, not the peripheral metabolic ones.
Prescription only
16·Cognitive
Semax
Also: MEHFPGP, ACTH(4-7) Pro-Gly-Pro, et al.
Semax is a synthetic heptapeptide built by attaching a Pro-Gly-Pro tail to the C-terminus of ACTH(4-7) — the four-residue fragment Met-Glu-His-Phe — yielding the sequence MEHFPGP. The Pro-Gly-Pro extension protects against enzymatic degradation, and follow-up work has shown that the tail itself carries independent neurotrophic activity in rodent stroke models. Mechanistically Semax appears to act through several coupled pathways: in rodents it rapidly elevates brain-derived neurotrophic factor (BDNF) and TrkB receptor expression in the hippocampus, modulates dopaminergic and serotoninergic systems, and influences melanocortin-receptor signaling consistent with its ACTH origin. A representative Western-journal mechanism study reported a 25% rise in striatal 5-HIAA at two hours after Semax administration in rats, with serotonin-metabolite levels reaching 180% of baseline within 1–4 hours; dopamine concentrations were unaltered by Semax alone, but Semax pretreatment substantially enhanced the dopamine response to D-amphetamine ([Eremin et al., *Neurochem Res* 2005, 30:1493–1500](https://doi.org/10.1007/s11064-005-8826-8)). The reading is consistent with Semax acting as a neuromodulatory amplifier rather than a primary releaser.
Research use only
17·Healing & repair
TB-500
Also: Thymosin β4, Thymosin beta-4, et al.
Thymosin β4 is a 43-amino-acid acidic peptide originally isolated from bovine thymus tissue and now recognized as one of the major intracellular G-actin sequestering proteins in mammalian cells. It binds monomeric actin (G-actin) and prevents its polymerization into F-actin, regulating cytoskeletal dynamics and cell motility. The cardiac-repair literature anchored by Bock-Marquette and colleagues (Nature 2004) extends the mechanism: thymosin β4 promotes myocardial and endothelial cell migration in embryonic hearts, retains that property in postnatal cardiomyocytes, and activates an integrin-linked kinase / Akt survival pathway that improves cardiac function after coronary artery ligation in mice ([Bock-Marquette et al., *Nature* 2004, 432:466–472](https://doi.org/10.1038/nature03000)). The peptide also induces angiogenesis, supports fibroblast migration, and has anti-inflammatory and antioxidant properties in dermal and corneal repair models. The market name "TB-500" is used interchangeably in research-peptide channels with thymosin β4, although some product literature historically describes TB-500 as a synthetic fragment containing the central actin-binding motif rather than the full 43-amino-acid peptide; the academic literature studies the full molecule.
Research use only
18·GH secretagogue
Tesamorelin
Also: Egrifta, Egrifta SV, et al.
Tesamorelin is a 44-amino-acid analog of human growth-hormone-releasing hormone (GHRH) with a trans-3-hexenoyl modification on the N-terminal Tyr¹ that confers resistance to dipeptidyl-aminopeptidase-IV degradation ([Ferdinandi et al., *Basic Clin Pharmacol Toxicol* 2007, 100:49–58](https://doi.org/10.1111/j.1742-7843.2007.00008.x)). Once injected subcutaneously, it binds the GHRH receptor on pituitary somatotrophs and triggers pulsatile growth hormone release, which in turn drives IGF-1 production in the liver. Plasma half-life is roughly 26 to 38 minutes — short enough that GH and IGF-1 stay broadly within their normal pulsatile pattern rather than being chronically elevated, which is the safety story the FDA reviewed.
Prescription only
19·Immune
Thymosin α-1
Also: Thymalfasin, Zadaxin, et al.
Thymosin α-1 is a 28-amino-acid acidic peptide first isolated from the thymus and now produced synthetically as thymalfasin. It is an immunomodulator rather than an immunostimulant — the published activity profile is heterogeneous across cell types, with effects on T-cell maturation and differentiation, dendritic-cell function, natural killer cell activity, regulatory cytokine balance, and TLR-mediated innate immune signaling ([Dominari et al., *World J Virol* 2020, 9:67–78](https://doi.org/10.5501/wjv.v9.i5.67)). The clinical development arc has tracked these mechanisms: early use in chronic viral hepatitis (where T-cell exhaustion is part of the disease biology), expansion into sepsis and severe infections, adjuvant use with vaccines in immunosenescent populations, and most recently a wave of interest in long-COVID and post-viral immune dysregulation. The peptide does not act through a single receptor pathway; it is best understood as a fine-tuning agent for the adaptive immune system rather than a directional stimulant.
Prescription only
20·Metabolic / GLP-1
Tirzepatide
Also: Mounjaro, Zepbound, et al.
Tirzepatide is a 39-amino-acid synthetic peptide engineered from the native glucose-dependent insulinotropic polypeptide (GIP) backbone, with a C20 fatty diacid chain attached via a γ-glutamic-acid / OEG linker to a Lys residue for albumin binding ([Jastreboff et al., *N Engl J Med* 2022, 387:205–216](https://doi.org/10.1056/NEJMoa2206038)). It activates both the GIP and GLP-1 receptors as a full or near-full agonist; the dual incretin engagement is the molecular signature that distinguishes it from semaglutide and the rest of the GLP-1 monoagonist class. Downstream effects span the same three mechanisms as GLP-1: glucose-dependent insulin secretion, slowed gastric emptying, and central appetite suppression. The GIP component contributes additional metabolic effects — including modulation of adipose insulin sensitivity and potential alteration of nausea-pathway signaling — that may explain part of the larger weight-loss magnitude relative to GLP-1 monoagonism, though the contribution of each receptor to clinical effect is still being parsed in the literature.
Prescription only