# BPC-157: The Gastric Pentadecapeptide Research Record, Plotted > BPC-157 is a 15-amino-acid cytoprotective research peptide studied across tendon, gut, and vascular repair. The literature plotted as a record — mechanism, pharmacokinetics, the human-data gap, every figure cited. The published record plotted as coordinates: a transected-tendon healing result, a formal pharmacokinetic readout, a VEGFR2-driven angiogenesis mechanism, and the precise point where the human data stop. Every figure is cited. ## What BPC-157 is, in one coordinate BPC-157 is a synthetic 15-amino-acid peptide — a pentadecapeptide — derived from a partial sequence of a protein found in human gastric juice. The full name is Body Protection Compound 157. Its sequence is `Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val`, its molecular formula `C62H98N16O22`, its molecular weight roughly `1419.53 Da`, and its CAS number `137525-51-0`. It is not a naturally circulating hormone; it is a stable fragment manufactured for study. The peptide is studied under a single framework: cytoprotection — the protection of cells and tissue from injury. Across three decades, that framework has been applied to tendon, ligament, muscle, gut, liver, kidney, and nerve models, almost entirely in rodents. The most reproduced result is mechanical: in fully transected rat Achilles tendons, BPC 157 accelerated healing across biomechanical, functional, microscopic, and macroscopic measures, and stimulated tendocyte outgrowth in vitro [1]. That is the anchor coordinate everything else is plotted against. This site reads the record the way an engineering publication reads a dataset — each study a point, each cited claim a confirmed reading, each honest gap a deliberately empty cell. The largest empty cell is the most important one: there is no large, controlled human efficacy trial of BPC-157 anywhere, and only three small human pilot studies exist [8][14]. ## BPC-157: the stable gastric pentadecapeptide The descriptor "stable gastric pentadecapeptide" is the authors' own. BPC-157 is reported to resist breakdown in human gastric juice, which is the structural reason researchers have tested oral and intragastric routes alongside injection. The peptide is frequently supplied as the acetate salt and catalogued under PubChem CID `108101`; older industrial development programs designated it `PL 14736`, `PLD-116`, and `PL-10`. The BPC-157 peptide sits in a regulatory category that this site treats as a first-class fact rather than a footnote. It is not an FDA-approved drug. In the United States, FDA placed it in 503A "Category 2" — bulk substances identified as possibly presenting significant safety risks — effective with FDA's September 29, 2023 nominated-substances update [16]. It is also prohibited in sport at all times by the World Anti-Doping Agency under the S0 non-approved-substances category [18]. The [FDA 503A compounding category](/legal-status), and what it means for access, is plotted in full on the [BPC-157 legal status](/legal-status) page, including a scheduled 2026 FDA advisory-committee discussion. What the record does not contain matters as much as what it does. Popular claims that BPC-157 builds muscle, drives weight loss, or raises testosterone are not supported by the published literature, and recent reviews flag them as unsubstantiated [9]. ## What BPC-157 is studied for in the research literature The studied outcomes cluster around three mechanisms, all read off animal and cell models, never human treatment claims. **Tissue repair.** Beyond the transected-tendon result, BPC 157 has been studied in gastric-ulcer models, where intramuscular delivery produced an ulcer-formation inhibition ratio of `45.7-65.6%` at the higher doses tested and accelerated rebuilding of the glandular epithelium [4]. A 2024 review consolidated its reported effects on intestinal anastomotic healing across rat models [10]. **Angiogenesis.** The repair effects are most consistently linked to the formation of new blood vessels. BPC157 up-regulates the VEGFR2 receptor and promotes its internalization, activating the downstream VEGFR2-Akt-eNOS (nitric-oxide) pathway; this increased vessel density in vivo and accelerated blood-flow recovery in ischemic muscle, with the effect abolished when endocytosis was blocked [3]. This is the [BPC-157 mechanism of action](/research) the rest of the record hangs from. **Cytoprotection across organs.** Rodent work has studied BPC 157 as protective of the liver after radiation injury [6], and a 2025 rat study reported reduced distant-organ damage to liver, kidney, and lung secondary to acute pancreatitis [12]. These describe what was measured in animals — they are not statements about treating any human condition. For the dose figures behind these results, see the [BPC-157 research dosage context](/dosage); for the newest 2024-2026 literature, see the [recent BPC-157 research](/recent-research) page. ## Where the human data stop The single coordinate that orients everything on this site is the boundary between animal evidence and human evidence — because for BPC-157 that boundary is unusually sharp and unusually early. The preclinical record is broad and, within the work of its core group, reproducible. The human record is three small pilot studies: a two-person intravenous safety pilot, an intra-articular knee-pain case series, and a twelve-patient intravesical interstitial-cystitis pilot [8][14]. That asymmetry is why this site refuses to translate animal results into human claims. A finding measured at `10 microg/kg` in a rat tendon is a real datum about a rat; it is not a dose, a timeline, or an outcome for a person. The 2025 musculoskeletal narrative review states the position the whole record supports: human data are extremely limited, rigorous large-scale trials are lacking, and BPC-157 should be considered investigational [14]. Reading the literature honestly means holding the breadth of the animal work and the thinness of the human work in view at the same time. ## What does BPC-157 do in the body? In animal models, BPC-157 is described as a cytoprotective, pro-angiogenic peptide that supports tissue repair across many organ systems. Its best-characterized route of action is up-regulation and internalization of the VEGFR2 receptor, driving the downstream Akt-eNOS nitric-oxide pathway [3]. Additional reported routes include the FAK-paxillin pathway and modulation of nitric-oxide and neurotransmitter systems. These are preclinical findings; the [human pilot studies](/recent-research) are too small to confirm a human effect. --- A cobalt-blueprint reading of the BPC-157 record — every finding plotted to its study, the human-data gap left as an open cell, and the FDA 503A status struck before anything else; no clinic at the bench and nothing here dispensed or sold.