Peptide encyclopedia
4 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·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
03·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
04·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