BPC-157
Stylized molecular signature · scaled by MW
~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).
Profiled for reference only.
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How it’s 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 half-life 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.
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Tendon and ligament transection healing models
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GI mucosal injury and inflammatory bowel disease models
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Angiogenesis and microvascular repair assays
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Neuroprotection in stroke and TBI rodent paradigms
Reported in literature: 10 µg/kg/day SC or IP in rodent studies (Sikiric et al.); clinical research, not for human use
Verify each value in primary literature.
Pre-filled defaults for BPC-157.
- Concentration
- 2.50mg/mL
- Draw on U-100
- 10units
- Volume / dose
- 0.100mL
- Doses / vial
- 20
Assumes 27-gauge insulin syringe, U-100 markings. Verify before use.
Open in calculatorCo-factors and supporting compounds.
Moderate evidenceCompounds 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-arginineEndothelial 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.
Growth hormone (and growth-hormone-axis context)
Growth hormoneGrowth 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.
L-glutamine (gastrointestinal context)
Free-form L-glutamineIntestinal 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.
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.