BPC-157
A synthetic pentadecapeptide studied for angiogenesis and tissue repair.
Repair & recovery · 8 min read · updated 13 Aug 2026
Research use only. The ranges below are what published studies and community protocols report. They are reference material for laboratory research, not medical advice or a recommendation for human or veterinary use.
The compound
BPC-157
View- Type
- Pentadecapeptide
- CAS
- 137525-51-0
- Formula
- C₆₂H₉₈N₁₆O₂₂
- Mass
- ~1419.62 Da
At a glance
- Class
- Synthetic pentadecapeptide
- Sequence
- GEPPPGKPADDAGLV — 15 amino acids
- Derived from
- Body Protection Compound, a protein in human gastric juice
- Molecular weight
- ~1419.55 Da
- CAS
- 137525-51-0
- Notable property
- Stable in gastric acid — unusual for a peptide
- Vial size stocked
- 10 mg
BPC-157 is a 15-residue fragment of a larger protein isolated from human gastric juice. That origin explains its most unusual property: it is stable in gastric acid. Almost every peptide in this catalogue is destroyed within minutes of contact with stomach acid and pepsin; BPC-157 survives, which is why oral protocols exist for it and for essentially nothing else here.
The research literature on it is dominated by one group — Sikirić and colleagues in Zagreb — who have published on it for three decades across a wide range of injury models: tendon, ligament, muscle, bone, gastrointestinal mucosa, and nerve. The breadth is simultaneously the strongest and weakest feature of the evidence base. It suggests a genuinely upstream mechanism, and it also means most of the findings come from a single laboratory and have not been widely replicated elsewhere.
Human data is essentially absent. There has been no adequately powered controlled trial in humans for any indication. Everything below is rodent work plus community practice.
Mechanism in detail
The most reproducible finding is that BPC-157 promotes angiogenesis — new blood vessel formation — and that this underlies much of the tissue repair effect. Several converging pathways have been described.
- VEGFR2 upregulation: BPC-157 increases VEGF receptor 2 expression and activates the VEGFR2–Akt–eNOS pathway in endothelial cells. This is the best-characterised route to the angiogenic effect.
- Nitric oxide system: it modulates NO synthesis in both directions — counteracting L-NAME-induced vasoconstriction and moderating L-arginine-induced effects. The literature describes it as an NO-system stabiliser rather than a donor.
- FAK–paxillin signalling: promotes fibroblast adhesion and migration, the cellular basis of the tendon and ligament findings.
- Growth hormone receptor expression: increased in tendon fibroblasts, which sensitises repairing tissue to circulating GH.
- Gastrointestinal cytoprotection: BPC-157 counteracts NSAID-induced and alcohol-induced mucosal lesions in rodent models, and this was the original research context before the tendon work.
Systemic or local?
A persistent question in reported protocols is whether administration near the target tissue outperforms administration anywhere else. The rodent data cut against the local-injection theory: intraperitoneal and even oral administration produced repair at distant sites in several models, implying a systemic mechanism rather than a depot effect.
Community practice nonetheless favours administering subcutaneously near the area of interest. It costs nothing and the systemic effect is unchanged either way, so the convention persists even though the evidence does not require it.
Oral versus injected
Oral BPC-157 is a legitimate route because of the acid stability, but the two routes are not interchangeable. Oral administration produces high local concentrations along the gastrointestinal tract and comparatively low systemic exposure. For gut-focused research questions that is an advantage. For tendon, ligament or systemic questions, subcutaneous administration is the route the majority of the reported protocols use.
Storage
- Lyophilised: 2–8 °C, or −20 °C for long-term storage, protected from light.
- Reconstituted: 2–8 °C, used within about 28 days. Do not freeze.
- BPC-157 is comparatively robust for a peptide, but "robust" is relative — it still degrades at room temperature over days in solution.
Cautions
- No controlled human trials. The entire human evidence base is anecdotal.
- Angiogenesis is the core mechanism, and angiogenesis is not selectively beneficial. Any model with existing neoplastic tissue is a contraindication in the same way it is for GH.
- Reported effects on blood pressure in either direction exist in the rodent NO-system work; the human relevance is unknown.
- The concentration of evidence in one research group is a genuine limitation, not a technicality.
References & credit
- 1Sikirić P et al., Current Pharmaceutical Design (multiple reviews) — The principal body of BPC-157 research, spanning gastrointestinal, tendon and nerve models.
- 2Chang CH et al., J Appl Physiol 2011 — BPC-157 and tendon fibroblast outgrowth via the FAK–paxillin pathway.
- 3Hsieh MJ et al., J Mol Med 2017 — VEGFR2 activation and the angiogenic mechanism.
This article was written in-house. Where a dose range reflects community practice rather than a published trial, the community references we consulted are credited above and the article says which is which.