Identity synthetic pentadecapeptide, 15 amino acids (< 40 aa → peptide). Molecular formula C₆₂H₉₈N₁₆O₂₂; MW ≈ 1419.6 g/mol. A partial sequence of "Body Protection Compound" originally isolated from human gastric juice; notably stable in gastric juice. ## Development & history - Derived from a protective protein isolated from human gastric juice in the early 1990s; the research programme has been led by Predrag Sikirić and colleagues at the University of Zagreb (Croatia) for ~30 years.
- In 1993 the Croatian pharmaceutical company Pliva (then a major regional firm) partnered with the Zagreb group — alongside the US company Parke-Davis — and advanced BPC-157 for inflammatory bowel disease / ulcerative colitis under the codes PL-10, PLD-116 and PL 14736.
- A Phase 1 safety study in healthy volunteers reported it safe and well tolerated (Veljaca et al., 2003). A Phase 2 trial in ulcerative colitis was completed — but its results were never published in a peer-reviewed journal, which remains the single biggest gap in its human record.
- Pliva was later acquired (Barr, then Teva) and the programme did not continue to approval; a later Phase 1 (NCT02637284, 2015) was registered but cancelled. As a hard-to-patent natural fragment it drew little commercial investment, and it has since lived as a gray-market "research" peptide — now in the 2026 FDA compounding review. ## Mechanism (as proposed) studies attribute BPC-157's effects to several overlapping pathways — up-regulation of VEGFR2 and modulation of the nitric-oxide system via the Akt–eNOS axis (promoting angiogenesis; note that in cell culture BPC-157 shows no direct angiogenic effect and appears to act by modulating VEGF expression in vivo), growth-hormone-receptor up-regulation in tendon fibroblasts (~4-fold in one independent rat study), plus FAK/paxillin and ERK1/2 signalling and reduced inflammatory cytokines. These mechanisms are largely derived from rodent work; whether they translate to humans is unproven.