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alphapeptide

BPC-157: research overview

Gastric-derived pentadecapeptide studied for tendon, GI, and vascular repair; reports VEGFR2-Akt-eNOS pathway engagement.

Healing. Molecular weight 1,419.55 Da; half-life 15 min. Reference material compiled from the published literature. For laboratory research only; nothing on this page is medical advice or a claim about a product.

How it is studied

BPC-157 is a synthetic pentadecapeptide (GEPPPGKPADDAGLV) derived from a partial sequence of human gastric juice 'body protection compound.' Mechanistic studies report upregulation of VEGFR2 expression and activation of the VEGFR2-Akt-eNOS angiogenic axis, modulation of growth-hormone receptor signaling in injured tissues, and counter-regulation of the dopaminergic, serotonergic, and nitric oxide systems. It is investigated as a cytoprotective and angiomodulatory agent in models of GI ulceration, tendon and ligament transection, and ischemia-reperfusion injury.

BPC-157 is a 15-residue fragment of a cytoprotective protein isolated from human gastric juice by Sikiric and colleagues. Despite a sub-30-minute plasma in rats and no published human PK, it produces durable tissue-level effects in rodent injury models — most prominently in Achilles tendon transection and ulcer studies — that have driven sustained academic and regenerative-medicine research interest.

Half-life, with its caveats

~15 min IV in rats; <30 min across IV/IM routes in rat and beagle dog (Xu et al., Front Pharmacol 2022). No published human PK. IM bioavailability 14–19% (rat), 45–51% (dog).

How to read this page

  • Mechanism describes what the published studies tested, not what a product does.
  • Reported research areas list where the compound has been studied. They are not indications.
  • Dose ranges are what the literature reports, quoted for reference. They are not dosing advice.
  • Co-factor studies carry PubMed citations; open the source before relying on a figure.
Co-factors

Compounds studied alongside it

Moderate evidence

Compounds identified in published research as sharing pathways with BPC-157, or studied alongside it in trials. Reference material only — not a recommendation, not medical advice. Citations link to PubMed.

L-arginine

Free-form L-arginine
Shared mechanism

Endothelial nitric oxide synthase pathway and vascular healing

L-arginine is the nitric-oxide synthase substrate and has been co-administered with BPC 157 across a multi-year series of rat injury models. Studies report that BPC 157 promotes endothelial nitric oxide synthase activation via the Src-Caveolin-1-eNOS pathway in isolated rat aorta and HUVEC, and rat experiments on esophagogastric anastomosis healing and perforated-cecum lesions report that L-arginine attenuates injury while the NOS inhibitor L-NAME worsens it; BPC 157 alongside either agent consolidates the NO system toward better healing. This is the most consistently reported pharmacological co-factor relationship in the BPC 157 literature. Animal-model evidence.

CitationsPMID 330514812020PMID 278954002016

Growth hormone (and growth-hormone-axis context)

Growth hormone
Shared mechanism

Growth hormone receptor upregulation and JAK2 signalling in tendon fibroblasts

BPC 157 has been reported to upregulate growth hormone receptor expression in cultured rat tendon fibroblasts at both mRNA and protein levels in a dose- and time-dependent manner. When growth hormone was added to BPC 157-pretreated fibroblasts, cell proliferation increased and JAK2 (the canonical downstream signal of the GH receptor) was activated. This places BPC 157 in the same signalling neighbourhood as the growth-hormone secretagogue / GH-axis class and is the mechanistic basis for protocols that pair BPC 157 with GH-axis peptides in tendon and connective-tissue research. Animal/cell-culture evidence.

CitationsPMID 254154722014

L-glutamine (gastrointestinal context)

Free-form L-glutamine
Shared mechanism

Intestinal mucosal repair and tight-junction integrity

L-glutamine is the conditionally essential amino acid most strongly tied to enterocyte energetics and tight-junction integrity, and has been studied alongside gut-barrier and mucosal-repair endpoints — the same territory where BPC 157 is most extensively investigated (gastric ulcer, colitis, anastomosis, fistula models). Glutamine depletion has been documented to drive villus atrophy, lower tight-junction protein expression, and raise intestinal permeability, while supplementation has been reported to restore barrier function in injury models. This is a shared-target rather than a same-study pairing: glutamine and BPC 157 are not co-administered in the published literature, but they converge on intestinal mucosal repair, which is why they appear together in GI research protocols.

CitationsPMID 277496892017PMID 342676542021
Caveat

BPC 157 literature is dominated by the Sikiric group at Zagreb and is almost entirely animal-model. The NO-system/L-arginine co-administration data is the strongest cofactor signal. Vitamin C and zinc have plausible mechanistic overlap with BPC 157's collagen and mucosal endpoints but have not been directly co-administered in the published BPC 157 studies, so they were not included as cofactors to avoid extrapolation.

All reading

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