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BPC-157 is a peptide, a short chain of 15 amino acids, that has mainly been researched in cells and animals, in models of injury to the stomach, liver, tendons, ligaments, muscle and bone [G1, G2, G3, G5]. Researchers have also studied it in blood-vessel growth experiments and in rodent behaviour models [G4, G5, G6]. Research in people is limited to three small reports from one clinic group and a registered trial with no posted results [G8–G11].
What is BPC-157?
A peptide is a short chain of amino acids, the building blocks of proteins. BPC-157 has 15 of them and is described as a partial sequence of "body protection compound", a protein reported in human gastric juice (stomach fluid) [G3]. Its sequence is GEPPPGKPADDAGLV and its molecular weight is 1419 [G4]. Papers also call it "stable gastric pentadecapeptide BPC 157" (pentadecapeptide means a 15-amino-acid peptide), PL-10, PL-14736 and bepecin [G4].
Much of the review literature comes from one pharmacology group at the University of Zagreb: of the 40 earlier reviews of the peptide that its 2025 review lists, the group counts 31 as its own [G4]. An independent UK review noted that "only a handful of research groups" had studied the peptide in depth over two decades [G2].
What is BPC-157 used for?
In research, BPC-157 has mainly been studied in animal models of tissue damage, and in cell experiments on the signalling behind what researchers observed [G1, G2, G3]. The research areas, in plain terms:
- Stomach and liver damage in rats, including damage caused by NSAIDs (non-steroidal anti-inflammatory drugs) [G5]. The Zagreb group calls this line of work "cytoprotection" and, in its account, extends it to models of other organs [G4].
- Cut tendons and ligaments in rats: transected Achilles and quadriceps tendons and a medial collateral ligament (knee ligament) transection model [G1].
- Muscle and bone: rat muscle that was cut or crushed [G1], muscle under body-wide insults such as high blood potassium or magnesium (hyperkalaemia, hypermagnesaemia) [G2], and a rabbit model of nonunion, a broken bone that fails to join [G1].
- Blood vessels: angiogenesis, the growth of new blood vessels, and blood flow, in chick-embryo, cell and rat experiments [G6, G7], plus the Zagreb group's rat models of blocked major vessels [G5].
- The eye: corneal models, reported by the Zagreb group [G4].
- Brain and behaviour: rodent models of anxiety-, seizure-, depression-, catalepsy- and schizophrenia-like behaviour [G5], and mouse and rat models of Parkinson's-like and Alzheimer's-like disturbances [G4], also from the Zagreb group.
Across the muscle, tendon, ligament and bone injury models, Vasireddi et al.'s review reported that preclinical studies observed better functional, structural and biomechanical (strength and mechanics) measures [G1].
Research areas at a glance
| Area | What researchers looked at | Models | How strong the evidence is |
|---|---|---|---|
| Stomach and liver | Whether induced lesions were reduced. The Zagreb group reported the lesions were counteracted in rats given the peptide [G5] | Rat stomach and liver lesion models, including NSAID-induced lesions [G5] | Animal studies (rats) [G5] |
| Tendons and ligaments | How cut tendons and ligaments repaired: better structural, functional and biomechanical tendon measures, and biomechanical and functional ligament measures, in rats [G1]. In cells, more tendon-tissue outgrowth, cell movement and survival under oxidative stress, with no direct effect on how fast cells multiplied [G3] | Transected rat Achilles and quadriceps tendons; rat medial collateral ligament transection; rat tendon tissue and tendon cells (fibroblasts) [G1, G3] | Cell and animal studies (rats) [G1] |
| Muscle and bone | Muscle structure, function and mechanics in rats, which measured better [G1]; whether non-joining bone breaks joined in rabbits, with results similar to bone marrow or bone grafting comparators [G1] | Rat muscle cut and crush models; body-wide-insult muscle models; rabbit nonunion model [G1, G2] | Animal studies (rats, rabbits) [G1] |
| Blood vessels | Vessel growth and blood flow: higher vessel density, more VEGFR2 (a blood-vessel growth receptor), faster blood-flow recovery in rats, and nitric-oxide-dependent relaxation of the aorta [G6, G7] | Chick CAM assay; human endothelial cells; rat hind-limb ischaemia (cut-off blood supply); isolated rat aorta [G6, G7] | Lab-dish, isolated-tissue and animal studies [G6, G7] |
| Brain and behaviour | Induced behavioural and brain disturbances in rodents, which the Zagreb group reported were counteracted [G4, G5] | Rodent behavioural models; Parkinson's- and Alzheimer's-like models [G4, G5] | Animal studies (mice and rats), reported in the group's reviews only [G4, G5] |
| Human studies | Measures used: pain ratings recalled by phone with no standardised tool [G8]; a symptom-response questionnaire [G9]; a blood-biomarker and vital-signs panel [G10] | 3 single-clinic reports (n = 16, 12 and 2) [G8–G10]; 1 registered phase 1 trial with no posted results [G11] | A few small reports, none randomised or controlled [G8–G10] |
How is it thought to work?
Every finding below comes from cells, tissue or animals.
Cell attachment and movement (FAK-paxillin). FAK (focal adhesion kinase) and paxillin are proteins at the points where a cell grips its surroundings and are involved in how cells spread and move. In tendon cells (fibroblasts) from rat Achilles tendon, Chang et al. observed concentration-dependent increases in FAK and paxillin phosphorylation, a chemical tag that switches proteins on, while total protein levels stayed the same [G3]. The cells also moved and spread more and formed more F-actin, the filaments of the cell's internal skeleton [G3]. Proliferation (cell multiplication), measured by an MTT assay, did not change. The authors concluded the effects were "likely mediated" by the FAK-paxillin pathway [G3]. Vasireddi et al.'s summary of several cell studies lists increased proliferation among its tendon findings, while Chang et al.'s MTT assay found no direct effect [G1, G3].
Growth-factor signalling. VEGF-A is a growth signal for blood vessels and VEGFR2 is the receptor on vessel-lining (endothelial) cells that picks it up. In human endothelial cells, Hsieh et al. found VEGFR2 mRNA and protein increased while VEGF-A did not [G6]. The receptor was drawn into the cell (internalised), which the blocking compound dynasore prevented, and the VEGFR2-Akt-eNOS signalling chain was activated over time [G6]. Vasireddi et al. summarised animal studies reporting increased VEGF expression, and one cultured rat tendon cell study reporting increased growth hormone receptor expression [G1].
Nitric oxide. Nitric oxide (NO) is a short-lived signalling gas that relaxes blood vessels; eNOS is the enzyme that makes it in the vessel lining. In isolated rat aorta, BPC-157 produced concentration-dependent relaxation that depended on the vessel lining and was blocked by L-NAME (an NO-production blocker) or haemoglobin, so the authors attributed it to nitric oxide [G7]. It did not directly relax a 3D model of vessel smooth muscle. In endothelial cells it raised phosphorylation of Src, caveolin-1 and eNOS, three linked signalling proteins; a Src inhibitor abolished this, and caveolin-1 bound less to eNOS [G7]. The Zagreb group describes a broader effect on the NO system [G4].
Inflammation signals. Preclinical studies reviewed by Vasireddi et al. reported lower COX-2 expression, lower myeloperoxidase activity, and lower IL-6 and TNF-α levels, all markers that rise with inflammation [G1].
Gwyer et al. noted that the precise mechanisms still need to be understood [G2].
What kind of studies are these?
Studies come in three broad kinds. Cell studies (in vitro) test a compound on cells or tissue in a dish. Animal studies test it in living animals such as rats; together with cell work these are called preclinical. Human (clinical) studies range from small reports with no comparison group to randomised controlled trials, where people are assigned by chance to different groups and the groups are compared.
BPC-157's evidence sits almost entirely in the first two. A 2025 systematic review, searching the research databases by set rules up to June 2024, identified 544 records published between 1993 and 2024 and, after screening, included 36 studies: 35 preclinical and 1 clinical [G1]. It graded the literature as level IV and level V evidence, the low end of a scale on which level I is the strongest [G1]. Gwyer et al. noted that the majority of the musculoskeletal work used small rodents, and wrote that efficacy "is yet to be confirmed in humans" [G2]. Vasireddi et al. reported that "No clinical safety data were found" [G1].
Three human reports have been published by one clinic group [G8–G10]:
- A retrospective chart review (2019–2020) of 16 people with knee pain of mixed causes, reached by phone. Patients rated their own pain from recall; no standardised measurement tool was used, there was no control group, and follow-up time varied [G8].
- An uncontrolled pilot in 12 women aged 39 to 76 with interstitial cystitis, assessed with the Global Response Assessment questionnaire. There was no control or placebo arm [G9].
- An IRB-approved pilot in two adults, aged 58 and 68, that recorded blood biomarkers of heart, liver, kidney, thyroid and glucose, plus vital signs, over three days [G10].
None of the three was randomised or controlled, and the largest included 16 people [G8–G10]. Separately, a phase 1 trial in healthy volunteers was registered in 2015 with an estimated enrolment of 42; its status is listed as unknown and no results have been posted [G11].
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Sources
- [G1] Vasireddi N, Hahamyan H, Salata MJ, et al. HSS J. 2025;21:485–495. doi:10.1177/15563316251355551. PMID 40756949.
- [G2] Gwyer D, Wragg NM, Wilson SL. Cell Tissue Res. 2019;377:153–159. doi:10.1007/s00441-019-03016-8. PMID 30915550.
- [G3] Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JH. J Appl Physiol. 2011;110:774–780. doi:10.1152/japplphysiol.00945.2010. PMID 21030672.
- [G4] Sikiric P, Seiwerth S, Skrtic A, et al. Pharmaceuticals (Basel). 2025;18(6):928. doi:10.3390/ph18060928. PMID 40573323.
- [G5] Sikiric P, Gojkovic S, Krezic I, et al. Pharmaceuticals (Basel). 2023;16(5):676. doi:10.3390/ph16050676. PMID 37242459.
- [G6] Hsieh MJ, Liu HT, Wang CN, et al. J Mol Med (Berl). 2017;95:323–333. doi:10.1007/s00109-016-1488-y. PMID 27847966.
- [G7] Hsieh MJ, Lee CH, Chueh HY, et al. Sci Rep. 2020;10:17078. doi:10.1038/s41598-020-74022-y. PMID 33051481.
- [G8] Lee E, Padgett B. Altern Ther Health Med. 2021;27(4):8–13. PMID 34324435.
- [G9] Lee E, Walker C, Ayadi B. Altern Ther Health Med. 2024;30(10):12–17. PMID 39325560.
- [G10] Lee E, Burgess K. Altern Ther Health Med. 2025;31(1):20–24. PMID 40131143.
- [G11] ClinicalTrials.gov NCT02637284. https://clinicaltrials.gov/study/NCT02637284
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