Peptide encyclopedia
13 of 20 peptides match the filters. 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
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Reset all01·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·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
12·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
13·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