§ 03 FAQ
Fifteen questions, answered from the literature.
Direct answers, each anchored to a study or a regulatory document.
§ 01 Background
What is BPC-157?
BPC-157 is a synthetic peptide of fifteen amino acids — sequence GEPPPGKPADDAGLV, molecular weight 1419.55 Da. The sequence was identified within a larger cytoprotective protein found in human gastric juice [11]. Synonyms in the literature include Pentadecapeptide BPC 157, PL 14736, PL-10, and PLD-116.
Where did it come from?
The peptide was characterized and named in the early 1990s by a research group led by Predrag Sikiric at the University of Zagreb. The Croatian pharmaceutical company Pliva later registered the molecule under the development code PL 14736 and advanced an enema formulation into Phase II trials for ulcerative colitis [6]. The program was not advanced further and the full trial data were never published in a standalone peer-reviewed paper.
**Why is it called Body Protection Compound?**
The name reflects the framing of its discoverers: a peptide that protects body tissues from injury. In the literature it is described as cytoprotective across the gastrointestinal mucosa, vasculature, tendon, ligament, muscle, bone, and central nervous system in rodent injury models.
§ 02 Evidence
Does it work?
In rodents, in many models, the published literature reports that it does. In humans, the published file is three uncontrolled reports from one investigator group between 2021 and 2025 [17]. Whether that constitutes working depends on which evidence bar a reader is applying.
How many BPC-157 studies are there?
A 2025 systematic review in HSS Journal indexed thirty-six articles published between 1993 and 2024. Thirty-five were preclinical. One was clinical [16]. Many more individual experiments exist across reviews and conference papers, but the count of indexed primary articles is small relative to the size of the popular conversation.
Are there human trials?
One Phase II program ran (PL 14736, Pliva, ulcerative colitis) and was not published in full or advanced [6]. One Phase I registration (NCT02637284, PCO-02 in healthy volunteers) was cancelled in 2016. Three uncontrolled case series and one IV pilot have appeared in the literature since 2021, all from one group [17]. No randomized controlled trial has been published. No registered trial is actively recruiting in the major international registries at the time of writing.
Why is most of the research in rats?
Because that is what has been done. The Sikiric group at Zagreb produced the dominant share of the preclinical record over thirty years using rat and mouse models with occasional rabbit and dog work. Replication by independent groups at the same scale has not occurred. Whether this is a feature of the peptide's chemistry or of the research economics around an unapproved compound is not something the literature settles.
§ 03 Mechanism
How is it described as working?
The most-cited mechanism is angiogenesis through the VEGFR2-PI3K-Akt-eNOS pathway, supported by increased VEGF expression and microvascular density at injury sites in vivo [4]. A second mechanism is nitric oxide modulation across all three NOS isoforms, with the peptide acting as a modulator rather than a substrate [7][20]. In tendon fibroblasts the peptide upregulates growth hormone receptor mRNA and protein up to sevenfold and amplifies proliferation in the presence of growth hormone via JAK2 [2].
Does it act locally or systemically?
Both, depending on the study. Local injection, intra-articular injection, topical cream, and intravesicular instillation have been used in some protocols. Systemic intraperitoneal, intragastric, oral (drinking water), subcutaneous, and intramuscular routes have been used in others. Effects have been reported across all of these routes in preclinical work [11][13][14].
§ 04 Dosing in studies
What doses are used in the research?
In most rodent work, 10 μg/kg and 10 ng/kg are administered intraperitoneally, intragastrically, or per-orally in drinking water [1][3][4][7][14]. CNS work uses higher doses (e.g. 200 μg/kg in spinal cord injury models [9]). The three human reports used 10 mg intravesicular [17], single-arm IV up to 20 mg [17], and intra-articular knee injections at undisclosed exact doses [17].
What is the half-life?
Plasma half-life is under 30 minutes in both rats and dogs after intramuscular dosing, with Tmax of ~3 minutes (rat) and ~6-9 minutes (dog) [11].
Is it stable in the stomach?
Yes — this is the stable in stable gastric pentadecapeptide. The three consecutive prolines at positions 3-5 of the sequence appear to confer resistance to gastric proteolysis, which is why drinking-water administration is a documented research route [11][14].
§ 05 Regulation
What is the FDA's position?
In September 2023, the FDA 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 for human use. The agency has issued public statements identifying BPC-157 as an unapproved drug found in some wellness products [16][18].
Is it banned by WADA?
Yes. BPC-157 was added explicitly to the WADA Prohibited List under section S0 (Non-Approved Substances) effective 1 January 2022, and has remained on subsequent annual lists. The prohibition applies in and out of competition. There is no Therapeutic Use Exemption pathway because the peptide has no approved human therapeutic indication [16][18].
Is it a controlled substance?
Not under the U.S. Controlled Substances Act. State-level regulations on research chemicals vary.
§ 06 Safety
What does animal toxicology show?
Acute studies in Sprague-Dawley rats up to 20 mg/kg intramuscular and beagle dogs up to 10 mg/kg intramuscular reported no observed teratogenic, genotoxic, anaphylactic, or local toxic effects [18]. These doses are several orders of magnitude above the typical 10 μg/kg efficacy dose.
What are the theoretical concerns?
The 2025 Pharmaceuticals review (Jozwiak et al.) flags three: VEGFR2-mediated angiogenesis as a possible concern in malignant or pre-malignant settings; proline metabolites activating proline oxidase and generating reactive oxygen species; and excessive nitric oxide impairing hepatic drug metabolism [18]. These are mechanistic predictions, not findings.
Are there documented adverse events in humans?
In the three published human reports (16 + 12 + an open IV pilot), the authors reported no adverse events at the doses used [17]. Sample sizes are small. There is no published controlled long-term human safety data. There is no post-marketing surveillance — because there is no marketing.