BPC-157
BPC-157 (Body Protection Compound-157) is a 15-amino-acid synthetic peptide (sequence: Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val; MW 1419.5 Da) derived from a protein found in human gastric juice. It is the most widely-studied compound in the regenerative medicine peptide-clinic space. Preclinical data in rodents are extensive and broadly positive for musculoskeletal repair, GI healing, and neuroprotection. Human evidence as of 2026 consists of three small pilot studies (combined n < 30), one Phase I with UNKNOWN registry status and cancelled-results submission (NCT02637284), and one recruiting Phase II RCT (NCT07437547, n=120 planned). WADA lists it under S0 (Non-Approved Substances, Specified Substance) in the 2026 Prohibited List. The FDA PCAC reviewed nominations related to peptide compounds including BPC-157 in the 2024–2026 cycle for the 503A bulks list. No lifespan-extension data exist in any model organism; it has no DrugAge entry.
Identity
- PubChem CID: 9941957 (confirmed via PubChem REST API)
- ChEMBL ID: CHEMBL4297358 (confirmed via ChEMBL API; lists Development Phase 1)
- InChIKey: HEEWEZGQMLZMFE-RKGINYAYSA-N
- Molecular formula: C62H98N16O22
- Molecular weight: 1419.5 Da (average; PubChem confirmed; Jozwiak 2025 states 1419.55 Da — rounding difference; monoisotopic: 1418.70 Da)
- Sequence (15 AA): Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val
- CAS: 137525-51-0
- Class: synthetic pentadecapeptide
- WHO-INN: none assigned needs-canonical-id
- DrugBank: no entry found
- DrugAge: no entry (no lifespan-extension data in any model organism)
Derivation: BPC-157 is a partial sequence of a larger protein isolated from human gastric juice. The parent protein is not a catalogued gene product with a standard UniProt entry under the BPC-157 fragment name; no separate protein page is needed for the parent unless it is identified and sequenced further. needs-canonical-id for the endogenous parent protein.
Pharmacokinetics and delivery
- Half-life: approximately 30 minutes in human plasma per preclinical PK modelling 1; confirmed in the systematic review by Vasireddi et al. 2025 2: “metabolized in the liver with half-life <30 minutes.” Renal excretion.
- Stability: unusually stable in gastric juice — demonstrated effective after oral or intragastric administration in rat models, attributed to resistance to protease degradation 3.
- Routes studied preclinically: oral gavage, intragastric, subcutaneous (SC), intraperitoneal (IP), intravenous (IV). Animal studies use both systemic and local (intra-articular, peritendinous) injection.
- Routes in human pilots: IV infusion (Lee & Burgess 2025 4) and intravesical (Lee et al. 2024 5). The Phase II RCT (NCT07437547) uses SC injection.
- Oral bioavailability: not established by rigorous human PK study. The unusually short half-life suggests high first-pass clearance; however, the stable-in-gastric-juice property is cited as the basis for oral efficacy in rodents. The PK remains incompletely characterised. dose-response-unclear
Mechanism of action
Three overlapping mechanism clusters are described in the literature, with variable experimental support:
1. Nitric oxide (NO) system modulation (most evidence)
BPC-157 activates endothelial nitric oxide synthase (eNOS) via Akt phosphorylation, increasing NO production. NO-dependent vasodilation and endothelial cell activation are proposed to drive angiogenesis and accelerate wound healing [^mcguire2025, ^jozwiak2025]. NOS inhibition (L-NAME) attenuates BPC-157-induced wound healing in rodent models, providing pharmacological evidence that NO is a required mediator.
2. VEGFR2 / angiogenesis signalling
BPC-157 transactivates VEGFR2 (KDR/Flk-1) in endothelial cells, activating FAK and ERK1/2, driving endothelial migration and capillary sprouting [^seiwerth2018, ^jozwiak2025]. This is mechanistically distinct from direct VEGF-A binding (BPC-157 is not a VEGF analogue); the transactivation mechanism is not fully resolved at the biochemical level. no-mechanism
3. Growth hormone receptor (GHR) upregulation
BPC-157 has been reported to upregulate GHR expression in injured tissue, potentially enabling local IGF-1 autocrine/paracrine signalling to support cell proliferation and matrix synthesis 6. This mechanism is less well-characterised than the NO/VEGFR2 pathways and is primarily inferred from pharmacological experiments in rodent injury models.
Other documented activities
- Reduces pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1beta) in rodent colitis and ischaemia models.
- Stabilises platelet plug formation and resolves vessel constriction in haemorrhagic injury models 3.
- Modulates dopaminergic and serotonergic neurotransmitter pathways in rodent CNS models (mechanism unclear; reviewed in 1).
Caveat: The Sikiric laboratory (Zagreb) is responsible for the majority of BPC-157 preclinical publications. Independent replication outside this group is limited. Most mechanistic claims derive from rodent injury models; in vitro receptor-binding affinity data (Ki, Kd) for VEGFR2 or eNOS are not available in the public ChEMBL dataset. no-mechanism for the direct molecular binding event at each proposed target.
Preclinical evidence
Preclinical data are extensive (>200 papers). The following summarises results by tissue type based on the most comprehensive systematic review available 2.
Tendon and ligament healing
BPC-157 consistently improves tendon-to-bone reattachment in rodent Achilles detachment models 7 and accelerates ligament (MCL) healing in rat models 8. Biomechanical load-to-failure and histological organisation are improved vs. vehicle controls. needs-human-replication
| Study | Model | n (approx) | Design | Finding |
|---|---|---|---|---|
| Krivic 2006 7 | Male Wistar rat Achilles detachment | ~6–8/group (unconfirmed; full text not accessible) | in-vivo | Improved tendon-to-bone healing; corticosteroid aggravation opposed no-fulltext-access |
| Cerovecki 2010 8 | Male Wistar rat MCL transection (90-day endpoint) | ~6–8/group (unconfirmed; full text not accessible) | in-vivo | Improved ligament histology and biomechanical properties no-fulltext-access |
GI tract healing
The peptide’s gastric origin motivated extensive GI investigation. BPC-157 accelerates healing of gastric ulcers, colitis, fistulas, and intestinal anastomoses in rodent models [^seiwerth2021, ^seiwerth2018]. It maintains gut-barrier integrity in colitis and NSAID-induced ulcer models.
Bone healing
Fracture healing and bone density endpoints are improved in rodent fracture models.
Skeletal muscle
BPC-157 reduces myotendinous junction disruption from crush injury and toxin exposure (reviewed in Staresinic et al. 2022 9).
Neurological models
Rodent models of PD-like states, spinal cord injury, and stroke show benefit. Evidence is hypothesis-generating only. No human neurological trial has been conducted.
Aging-specific preclinical data
There are no published model-organism lifespan studies for BPC-157 and no DrugAge entry. The relevance to aging is indirect: tissue repair capacity declines with age, and the indications studied (tendinopathy, IBD) are prevalent in older adults. No study has specifically tested BPC-157 in aged animals vs. young controls to characterise age-dependent efficacy. needs-human-replication
Human evidence
Three small human pilots have been published or completed. No large placebo-controlled RCT has yet reported results.
NCT02637284 — Phase I (oral; abandoned)
- Sponsor: PharmaCotherapia d.o.o. (Zagreb, Croatia)
- Design: Randomised, placebo-controlled Phase I; healthy volunteers ages 18–35; 42 estimated enrollees; single and multiple oral doses (product name: Bepecin)
- Site: Hospital Ángeles Tijuana, Mexico
- Status: Registered December 2015; estimated primary completion February 2016; last update December 2015. Current ClinicalTrials.gov status: “UNKNOWN” (confirmed via ClinicalTrials.gov v2 API 2026-05-09). No results posted, no formal termination record.
- Outcome: No published results. The trial did not advance to Phase II. Jozwiak 2025 states: “in 2016, the researchers cancelled submission of the results” — the mechanism of cancellation is not documented in the public registry record, but the registry status is UNKNOWN rather than Terminated or Completed.
Note on enrollment: The ClinicalTrials.gov record lists 42 as the estimated (not confirmed enrolled) number; actual enrollment is unknown. needs-human-replication
Lee & Burgess 2025 — IV safety pilot (n=2)
Two healthy adults (58-year-old male, 68-year-old female) received IV infusions of 10 mg BPC-157 in 250 mL saline on day 1 and 20 mg on day 2 4. No measurable effects on cardiac, hepatic, renal, thyroid, or metabolic biomarkers; no adverse events. IRB-approved. Published in Alternative Therapies in Health and Medicine 2025 Sep;31(5):20-24 (PMID 40131143).
This is the 2025 N=2 pilot referenced in the user framing. The journal (Alternative Therapies in Health and Medicine) is not a high-impact peer-reviewed venue; the study is IRB-approved but insufficiently powered to establish safety. The finding is consistent with short-term tolerability but should not be interpreted as a safety clearance. needs-replication
Lee et al. 2024 — Interstitial cystitis pilot (n=12)
Twelve women with moderate-to-severe interstitial cystitis (unresponsive to standard treatment) received single intravesical injections of 10 mg BPC-157 5. Complete symptom resolution in 10/12 (83%); 80% improvement in 2/12. Global Response Assessment: 5/5 in all participants. No adverse events. Published in Alternative Therapies in Health and Medicine 2024 Oct;30(10):12-17 (PMID 39325560). No control arm; same journal as above; effect sizes are striking and warrant independent replication. needs-replication
Lee 2021 / Vasireddi 2025 systematic review — one retrospective clinical series
The Vasireddi 2025 systematic review 2 identified one retrospective clinical report (Lee E, Padgett B. Altern Ther Health Med. 2021;27(4):8-13 10): 12 patients received intra-articular BPC-157 alone for unspecified chronic knee pain; 11/12 (91.6%) had significant improvement on patient self-report. Vasireddi characterises this as “7 of 12 patients reported relief for >6 months” (the longer-duration subset). No control arm; retrospective design; same low-impact journal (Alternative Therapies in Health and Medicine) as the Lee IV and IC pilots. This is the only other human data point in the orthopaedic literature.
Summary of human evidence tier
| Study | Design | n | Route | Endpoint | Outcome |
|---|---|---|---|---|---|
| NCT02637284 (2015–16) | Phase I RCT | 42 (estimated) | Oral | AEs — any | Not reported; results submission cancelled 2016; registry status UNKNOWN |
| Lee & Burgess 2025 4 | Uncontrolled pilot | 2 | IV | Biomarker safety | No signal; no AEs |
| Lee et al. 2024 5 | Uncontrolled pilot | 12 | Intravesical | Symptom resolution | 10/12 complete; 2/12 80% |
| Lee 2021 10 (via Vasireddi 2025) | Retrospective | 12 (BPC-157 alone arm) | Intra-articular | Significant pain improvement (self-report) | 11/12 (91.6%); 7/12 reported relief >6 months |
needs-human-replication — No placebo-controlled RCT with a hard primary endpoint has reported results for any BPC-157 indication.
NCT07437547 — Phase II RCT (recruiting)
- Design: Randomised double-blind placebo-controlled; 120 participants ages 18–45; acute grade II hamstring muscle strain; SC injection once daily for 14 days plus standardised rehabilitation
- Endpoints: Time to return to unrestricted sport (primary); MRI injury-volume reduction at Day 14
- Site: Peking University Shenzhen Hospital, China
- Estimated completion: February 2027
- Status: Recruiting (confirmed ClinicalTrials.gov v2 API, 2026-05-09)
This is the first adequately designed controlled trial. The indication (acute sports injury, ages 18–45) is not an aging indication. clinical-trials-active: 1 reflects this single actively recruiting/ongoing trial as of 2026-05-09.
Regulatory status
WADA prohibition
BPC-157 is listed on the WADA Prohibited List under S0 — Non-Approved Substances, applicable at all times (in-competition and out-of-competition) 11. It is classified as a Specified Substance within S0 (athletes may receive reduced sanctions under defined conditions, but the substance remains fully prohibited). This category covers pharmacological substances with no current approval by any regulatory health authority for human therapeutic use.
Historical note: Vasireddi 2025 records a WADA-specific ban on BPC-157 established in 2022 (Table 1). The Jozwiak 2025 review (accepted January 2025) states BPC-157 was “temporarily banned in 2022” and “is not currently listed as banned by the WADA” — this appears to reflect the status at the time of writing prior to the effective date of the 2026 list; the WADA 2026 Prohibited List (effective January 1, 2026, confirmed 2026-05-09) does list BPC-157 under S0.
BPC-157 is also specifically prohibited by the UFC and NFL, and subject to broader peptide-hormone bans in the NBA, NHL, MLB, NAIA, PGA, and NCAA 2.
FDA 503A bulks list — PCAC review
The FDA’s Pharmacy Compounding Advisory Committee (PCAC) reviewed nominations for the 503A bulks list in the 2024–2026 cycle as part of a broad review of peptides commonly compounded at telehealth peptide clinics. BPC-157 was among compounds subject to enhanced scrutiny following FDA guidance tightening oversight of compounded peptides in 2024. At the time of this page’s seeding (2026-05-09), BPC-157 is NOT on the FDA 503A nominated bulks list for positive inclusion and its pathway to compounding regulatory approval remains blocked by the absence of FDA-approved human therapeutic use. Detailed PCAC outcome data should be verified against the FDA website directly; needs-regulatory-update. The PharmaCotherapia / PharmaQure Zagreb group is the only known entity pursuing a formal pharmaceutical development pathway.
Compounding access
Prior to increased FDA enforcement (2024), BPC-157 was one of the most commonly prescribed compounds at telehealth peptide compounding pharmacies in the US. FDA enforcement actions against compounders supplying unapproved peptides substantially restricted this access from 2024 onward.
Aging relevance
BPC-157 has no direct longevity evidence — no DrugAge lifespan data, no NIA Interventions Testing Program evaluation, no aged animal vs. young animal comparative efficacy study. Its relevance to the aging wiki is:
- Tissue repair capacity declines with age — the primary preclinical indications (tendon, ligament, muscle, GI healing) are all processes that become impaired in older adults. If BPC-157 restores normal repair capacity in aged tissues, it could address downstream consequences of stem-cell-exhaustion (satellite cell depletion in muscle) and related hallmarks. This is speculative; no aged-animal study has been published.
- Anti-inflammatory activity — GI and systemic anti-inflammatory effects in rodent models may be relevant to chronic-inflammation. This is a weak hallmark link without human evidence.
- Regulatory-medicine context — as one of the most widely-used compounded peptides before 2024 regulatory tightening, BPC-157 represents a real-world aging-medicine intervention being evaluated by the FDA and WADA. This page’s primary value is tracking that regulatory and clinical-evidence landscape.
The hallmark tag [[chronic-inflammation]] is assigned conservatively based on anti-inflammatory activity in rodent IBD and colitis models; it should not be interpreted as evidence of hallmark-level efficacy in humans. Tags for [[stem-cell-exhaustion]] and [[altered-intercellular-communication]] would be speculative and are omitted pending any aged-tissue evidence.
Safety
Preclinical: LD50 not achieved across multiple rodent species and dosing routes [^staresinic2022, ^jozwiak2025]. No organ toxicity at therapeutic doses in animal studies. No teratogenicity reported in available literature.
Human: Based on three small pilots (n=2 IV, n=12 intravesical, n=12 intra-articular retrospective) with no serious adverse events, short-term tolerability appears acceptable. These are insufficient to establish a safety profile at population scale. long-term-unknown
Theoretical concerns:
- Angiogenic activity (VEGFR2 activation) is theoretically concerning in the context of occult malignancy — stimulation of tumour angiogenesis is a potential off-target risk analogous to concerns raised about VEGF-pathway drugs.
- Peptide impurities from compounding are a practical concern not captured in the pharmaceutical-grade trials.
- GHR upregulation could theoretically influence IGF-1 signalling in ways relevant to cancer risk, though no data exist on this.
None of these theoretical risks have been quantified in human studies. long-term-unknown
Limitations and knowledge gaps
- Single-lab publication bias: the majority of BPC-157 preclinical data originate from Sikiric and Seiwerth (University of Zagreb). Independent replication outside this group is sparse. needs-replication
- Mechanism not resolved at receptor level: no binding affinity (Ki, Kd) data for VEGFR2, eNOS, or GHR are publicly available. The mechanistic claims are inferred from pharmacological inhibitor experiments and gene expression data, not from direct receptor-binding assays. no-mechanism
- No human PK data: half-life in humans (oral, SC, or IV) has not been formally characterised in a published PK study.
- No aging-specific preclinical data: no lifespan study, no aged-animal efficacy comparison.
- Phase I trial abandoned: the only formally registered Phase I trial (NCT02637284) lapsed without publishing results, leaving a gap in the dose-escalation safety literature.
- Regulatory instability: ongoing FDA and WADA review creates uncertainty about compounding access and the clinical development pathway.
- Recency search (2020–2026): PubMed search 2020–2026 for “BPC-157” returned 84 papers (searched 2026-05-09). The most recent systematic reviews (Vasireddi 2025, McGuire 2025, Jozwiak 2025) all conclude that preclinical evidence is robust but human evidence is insufficient to recommend clinical use. No new human RCT results were published in this window.
Extrapolation table (rodent → human)
| Dimension | Status |
|---|---|
| Pathway conserved in humans (NO/VEGFR2/GHR)? | yes (canonical mammalian pathways) |
| Phenotype conserved in humans (tissue repair decline)? | yes |
| Replicated in humans at efficacy level? | no |
Footnotes
Footnotes
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doi:10.3390/ph18020185 · Jóźwiak M, Bauer M, Kamysz W, Kleczkowska P · Pharmaceuticals 2025;18(2):185 · review · model: literature + patent survey · locally available: yes (DOI lookup confirmed) · n/a (review) ↩ ↩2
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doi:10.1177/15563316251355551 · Vasireddi N, Hahamyan H, Salata MJ, et al. · HSS Journal 2025 · systematic-review · n=36 studies (35 preclinical, 1 clinical) · model: rodent (35) + retrospective human series (1) ↩ ↩2 ↩3 ↩4
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doi:10.3389/fphar.2021.627533 · Seiwerth S, Milavic M, Vukojevic J, et al. (Sikiric P, corresponding) · Frontiers in Pharmacology 2021 · review · n/a (review of wound-healing models) · model: rat incisional, excisional, burn, diabetic-ulcer ↩ ↩2
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PMID 40131143 · Lee E, Burgess K · Alternative Therapies in Health and Medicine 2025 Sep;31(5):20-24 · uncontrolled pilot · n=2 (ages 58 and 68) · IV BPC-157 10 mg day 1, 20 mg day 2 · no biomarker changes; no AEs · IRB-approved · DOI not available from PubMed record ↩ ↩2 ↩3
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PMID 39325560 · Lee E, Walker C, Ayadi B · Alternative Therapies in Health and Medicine 2024 Oct;30(10):12-17 · uncontrolled pilot · n=12 women (ages 39–76; mean 58.3 yr) · single intravesical 10 mg BPC-157 · 10/12 complete symptom resolution; 2/12 80% improvement; 0 AEs · DOI not available from PubMed record ↩ ↩2 ↩3
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doi:10.2174/1381612824666180712110447 · Seiwerth S, Sikiric P, et al. · Current Pharmaceutical Design 2018 · review · n/a (review) · model: rat GI, tendon, ligament, bone healing models ↩
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doi:10.1002/jor.20096 · Krivic A, Anic T, Seiwerth S, et al. · Journal of Orthopaedic Research 2006;24(5):982-989 · in-vivo · n=~6–8/group (unconfirmed; full text not accessible — Wiley closed-access) · model: Male Wistar rat Achilles tendon post-transection (confirmed via Vasireddi 2025 Table 2) · BPC-157 improved functional and biomechanical indices, macroscopic and microscopic structures, resolved tendon-bone defect; corticosteroid aggravation opposed no-fulltext-access ↩ ↩2
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doi:10.1002/jor.21107 · Cerovecki T, Bojanic I, Brcic L, et al. · Journal of Orthopaedic Research 2010;28(9):1155-1161 · in-vivo · n=~6–8/group (unconfirmed; full text not accessible — Wiley closed-access) · model: Male Wistar rat MCL transection (90-day endpoint) (confirmed via Vasireddi 2025 Table 2) · BPC-157 reduced postinjury valgus instability and contracture, restored biomechanics, improved macroscopic and microscopic structure no-fulltext-access ↩ ↩2
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doi:10.3390/biomedicines10123221 · Staresinic M, et al. (Sikiric P, corresponding) · Biomedicines 2022;10(12):3221 · review · n/a (review of muscle healing) · model: rat crush injury, toxin-exposure models; LD50 not achieved in safety summary ↩
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PMID 34324435 · Lee E, Padgett B · Alternative Therapies in Health and Medicine 2021;27(4):8-13 · retrospective · n=16 contacted (12 received BPC-157 alone, 4 received BPC-157 + TB4) · intra-articular injection · 11/12 (91.6%) BPC-157-only patients had significant knee pain improvement; 7/12 reported relief >6 months per Vasireddi 2025 characterisation · no control arm · DOI not available from PubMed record ↩ ↩2
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World Anti-Doping Agency Prohibited List 2026 · S0 Non-Approved Substances · BPC-157 listed by name as a Specified Substance · confirmed via WADA Prohibited List webpage 2026-05-09 (effective January 1, 2026) ↩