Preprint Notes / Pentadecapeptide GEPPPGKPADDAGLV
BPC-157: A Pentadecapeptide With a Three-Decade Preclinical Record and a Thin Human File
An indexed reading of the published literature on Body Protection Compound 157 — synthesis, mechanism, animal models, pharmacokinetics, regulatory status. No products. No protocols. Only the record.
Abstract
BPC-157 — also catalogued as Pentadecapeptide BPC 157, PL 14736, PL-10, and PLD-116 — is a synthetic 15-amino-acid peptide with the sequence GEPPPGKPADDAGLV, a molecular weight of 1419.55 Da, and CAS number 137525-51-0. The sequence was identified within a cytoprotective protein recovered from human gastric juice and has been studied in animal models since the early 1990s. The defining structural feature is a triple-proline tract at positions 3–5, which appears to confer resistance to gastric proteolysis and underwrites the unusual decision to administer the peptide in drinking water in many rodent protocols[11].
A 2025 systematic review in HSS Journal indexed thirty-six BPC-157 articles published between 1993 and 2024; thirty-five were preclinical, one was clinical[16]. That ratio is the single most important fact on this page. Whatever the molecule does — and it appears to do a great deal in rats — it does so in a literature that has barely crossed the species line.
01. What is BPC-157?
BPC-157 is a partial sequence taken from a larger cytoprotective protein present in gastric juice. The synthetic peptide is referred to in the literature as a stable gastric pentadecapeptide — “stable” because it survives in gastric conditions, “gastric” because of its origin, “pentadecapeptide” because it is fifteen residues long. Across published preclinical work, the peptide is described as multi-system: its effects have been catalogued in models of tendon transection, ligament injury, segmental bone defect, muscle crush, muscle detachment, gastrointestinal anastomosis, fistula formation, ischemia-reperfusion, traumatic brain injury, peripheral nerve transection, and spinal cord compression[1][3][5][8][9][12][13][14].
The research lab most associated with this body of work is Predrag Sikiric’s group at the University of Zagreb. The dominance of a single lab is a methodological concern that any honest reading of the literature must acknowledge — replication by independent groups remains thin.
02. What the research describes
Mechanism. In preclinical models the peptide is reported to modulate the nitric oxide system through endothelial nitric oxide synthase (eNOS) activation via the Akt-eNOS axis, to promote angiogenesis through the VEGFR2-PI3K-Akt-eNOS pathway, and to activate ERK1/2 MAPK and FAK-paxillin signaling relevant to fibroblast migration and collagen organization[4][20]. Macrophage polarization shifts toward an M2 anti-inflammatory phenotype.
Tendon and bone. Staresinic et al. (2003) reported that transected rat Achilles tendons treated with BPC-157 at 10 μg/kg or 10 ng/kg intraperitoneal showed increased load-to-failure, superior collagen organization, and full restoration of tendon integrity, with parallel reversal of 4-hydroxynonenal-induced growth inhibition in tendocyte cultures[1]. Sebecic et al. (1999) reported in rabbit segmental bone-defect models that 10 μg/kg BPC-157 produced bony union comparable to autologous cortical bone grafting[5].
Gastrointestinal. The molecule’s name and original rationale come from gastric cytoprotection. Reviews summarize rat anastomosis studies across esophagogastric, colocolonic, jejunoileal, and ileoileal segments showing reduced leakage and increased burst pressures[13]; fistula models — colocutaneous, duodenocolic, tracheocutaneous — report closure of external and internal defects[7][19][23].
Human evidence. Three small uncontrolled human reports from a single investigator group, all published between 2021 and 2025, are the entire published clinical file: intra-articular knee injection in 14 of 16 patients reporting pain relief; intravesicular bladder injection at 10 mg for interstitial cystitis with 80–100% symptom resolution in 12 women; and a single-arm intravenous infusion up to 20 mg in healthy volunteers reported as well tolerated with clearance within 24 hours[17]. None is a controlled trial.
03. Pharmacokinetics and regulatory standing
He et al. (2022) profiled the peptide in Sprague-Dawley rats and beagle dogs after intramuscular dosing and reported bioavailability of 14–19% in rats and 45–51% in dogs, Tmax of approximately 3 minutes in rats and 6–9 minutes in dogs, and plasma half-life under 30 minutes[11]. Metabolism generates six small peptide fragments, with proline among the terminal residues; elimination is urinary and biliary.
In September 2023 the U.S. Food and Drug Administration placed BPC-157 on its Category 2 list of bulk drug substances that may present significant safety risks, effectively excluding it from 503A pharmacy compounding. The World Anti-Doping Agency added it explicitly to the Prohibited List under section S0 (Non-Approved Substances), effective 1 January 2022, and the prohibition has remained in subsequent annual lists[16][18]. No major regulatory authority — FDA, EMA, MHRA, TGA — has approved BPC-157 for any human indication.
BPC-157 is not approved by the FDA, EMA, MHRA, or TGA for any human indication. It is on the FDA Category 2 list (September 2023) and prohibited under WADA section S0 (effective 1 January 2022).
04. What this site is, and is not
BPC157clinic.com is a research-summary publication. It does not operate a clinic, employ clinicians, prescribe medication, dispense product, recommend doses, or refer to vendors. The word clinic in the domain is used in the older sense — clinical research, the bench-and-bedside literature — not the patient-services sense.
The site has three obligations to the reader: cite the actual studies; quote doses only in the species and route they were administered; and refuse to extrapolate from a rat at 10 μg/kg to a human at any dose. The dosage page therefore frames every number as in rats, intraperitoneal or in dogs, intramuscular, never as a suggestion.