Research Use Only: This product is supplied for laboratory research and in-vitro studies. Not for human or veterinary administration.

Hover to zoom

Identity Verified: LC-MS

(0 Reviews)

BPC-157

Gastric Pentadecapeptide: 15-amino acid sequence (GEPPPGKPADDAGLV), ≥99% purity, 4-pack format
NO System Modulation: VEGFR2-Akt-eNOS and Src-Caveolin-1-eNOS pathway research
Tissue Repair Studies: FAK-paxillin pathway activation and angiogenic signaling

Metabolic Synergy Research
In-Vitro Receptor Profiling
HPLC Verified (≥98% Purity)

$150.00In Stock

Ships same-day if ordered before 2PM EST

Encrypted Checkout

Global Express

Research Overview

BPC-157 (Body Protection Compound-157) is a synthetic pentadecapeptide derived from a protective protein found in human gastric juice. First described by Sikiric and colleagues in 1993 at the University of Zagreb, Croatia, this 15-amino acid peptide has been the subject of over 150 peer-reviewed publications spanning more than three decades. Recent systematic reviews (Vasireddi et al., 2025; McGuire et al., 2025) have analyzed 36 studies from 1993 to 2024, while a comprehensive literature and patent review (Jozwiak et al., 2025) catalogued the compound's pleiotropic beneficial effects across multiple organ systems.

BPC-157's biological effects are mediated through multiple interconnected cellular signaling pathways. The peptide activates vascular endothelial growth factor receptor-2 (VEGFR2), promoting VEGFR2 internalization through endocytosis and time-dependent activation of the VEGFR2-Akt-eNOS signaling cascade. It also modulates nitric oxide production through dual pathways: VEGF-dependent (VEGFR2-PI3K-Akt-eNOS) and VEGF-independent (Src-Cav-1-eNOS) routes. Additionally, BPC-157 activates focal adhesion kinase (FAK) and paxillin expression, enhancing cellular adhesion, migration, and survival—all essential processes in tissue repair. The peptide demonstrates exceptional stability in gastric juice for over 24 hours and maintains biological activity across a wide pH range, attributed to its four proline residues which provide structural rigidity and resistance to enzymatic degradation.

Despite growing clinical interest, only three pilot studies have examined BPC-157 in human subjects to date, and it remains an investigational compound without regulatory approval. A 2025 pilot study demonstrated that IV infusion of up to 20 mg in healthy adults produced no adverse effects on cardiac, hepatic, renal, thyroid, or metabolic biomarkers (Lee and Burgess, 2025). Another pilot study showed complete symptom resolution in 10 of 12 patients with interstitial cystitis following intravesical injection (Lee et al., 2024). Comprehensive preclinical safety evaluation across mice, rats, rabbits, dogs, and guinea pigs found negative acute toxicity at 2 g/kg, no mutagenic or genotoxic effects, and no developmental toxicity (Xu et al., 2020).

Primary Research Applications

Gastrointestinal Tract Research

Musculoskeletal Tissue Healing Studies

Angiogenesis and Vascular Research

Wound Healing and Dermatological Research

Neurological and Neuroprotective Research

Cardiovascular System Research

Ischemia-Reperfusion and Organ Protection

Cell Signaling and Molecular Biology

Mechanism of Action

Nitric Oxide (NO) System Modulation

Src-Caveolin-1-eNOS Signaling — BPC-157 stimulates phosphorylation of Src kinase, enhancing phosphorylation of Caveolin-1 (Cav-1) which reduces its inhibitory binding to endothelial nitric oxide synthase (eNOS). Liberation of eNOS from Cav-1 complexes leads to increased eNOS phosphorylation and activation, catalyzing the production of nitric oxide from L-arginine. The vasodilatory effects of BPC-157 are abolished by L-NAME (NOS inhibitor) or hemoglobin (NO scavenger), confirming NO-dependent mechanisms. BPC-157 activates both VEGF-dependent (via VEGFR2-PI3K-Akt-eNOS) and VEGF-independent (via Src-Cav-1-eNOS) pathways to NO production.

VEGFR2 and Angiogenic Signaling

VEGFR2 Activation — BPC-157 increases both mRNA and protein expression of vascular endothelial growth factor receptor-2 (VEGFR2) in vascular endothelial cells and promotes VEGFR2 internalization through endocytosis. This triggers time-dependent activation of the VEGFR2-Akt-eNOS signaling cascade, enhanced phosphorylation of Akt and eNOS leading to increased NO production, and upregulation of ERK1/2 phosphorylation with downstream activation of c-Fos, c-Jun, and Egr-1. Unlike recombinant growth factors such as bFGF, EGF, and VEGF-A which often require specific delivery systems and local application, BPC-157 demonstrates consistent efficacy across various administration routes.

FAK-Paxillin Pathway Activation

Cellular Adhesion and Migration — BPC-157 produces dose-dependent increases in focal adhesion kinase (FAK) gene and protein expression, enhanced paxillin expression and phosphorylation, significantly increased tendon fibroblast migration in transwell assay systems, promoted cell spreading and F-actin cytoskeletal remodeling, and preserved fibroblast viability under oxidative stress (H₂O₂ challenge) without artificially boosting baseline proliferation. The FAK-paxillin pathway is crucial for cellular adhesion, migration, proliferation, and survival—all essential processes in tissue repair and regeneration.

Growth Hormone Receptor Pathway

GHR Expression Enhancement — BPC-157 produces dose- and time-dependent increases in growth hormone receptor (GHR) expression in tendon fibroblasts at both mRNA and protein levels, enhanced growth hormone sensitivity through increased receptor availability, and activation of JAK2 phosphorylation (downstream mediator of GHR signaling), providing a potential mechanism for promoting tissue repair through GH/IGF-1 axis modulation.

Neurotransmitter System Modulation

Pleiotropic Neuromodulation — BPC-157 counteracts dopamine neuron destruction, vesicle depletion, receptor blockade, and receptor supersensitivity in Parkinson's disease models while improving motor abnormalities and increasing tyrosine hydroxylase expression. It demonstrates antidepressant-like effects while simultaneously counteracting serotonin syndrome, with region-specific increases in serotonin synthesis in the substantia nigra during chronic treatment. The peptide also counteracts disturbances related to glutamate, GABA, acetylcholine, and adrenaline/noradrenaline systems, operating through a cytoprotection-based modulatory mechanism that restores homeostatic balance across disrupted neurotransmitter circuits.

“The combination provides synergistic effects on metabolic parameters by targeting both hypothalamic and peripheral pancreatic pathways.”

Preclinical Research Summary

In musculoskeletal models, BPC-157 demonstrated complete restoration of walking patterns and elimination of leg contracture in rats following surgical quadriceps muscle detachment, with successful muscle-to-bone reattachment visible through microscopic examination and new bone formation with well-organized cortical structure by 3 months post-surgery. Results were consistent across dosages of 10 μg/kg and 10 ng/kg daily (Matek et al., 2025). In spinal cord injury models, single intraperitoneal injection at 200 or 2 μg/kg given 10 minutes after spinal cord compression resulted in all BPC-157-treated rats showing consistent clinical improvement and increasingly better motor function, with counteraction of vacuole formation, axon loss, edema, motoneuron loss, and demyelination, resolving spasticity and tail paralysis by day 15 (Perovic et al., 2019).

In ischemia-reperfusion injury models, 24 Wistar albino rats subjected to 45-minute lower extremity ischemia followed by 2-hour reperfusion showed that BPC-157 (20 μg/kg IP) significantly reduced distant organ damage in liver, kidney, and lung. Treatment significantly increased total antioxidant status and paraoxonase-1 activity across all three organs, and reduced sinusoidal dilation, tubular damage, and alveolar congestion in treated animals compared to controls (Demirtas et al., 2025). Comprehensive pharmacokinetic studies demonstrated plasma half-life less than 30 minutes in both rats and dogs, with peak tissue concentrations at 1 hour post-dose and highest concentrations in kidney, liver, stomach wall, thymus, and spleen—all significantly higher than plasma levels (He et al., 2022).

The first formal preclinical safety evaluation across mice, rats, rabbits, dogs, and guinea pigs found negative acute toxicity limit test at 2 g/kg (IV or oral) with no adverse effects, LD1 not achieved across wide dose ranges (6 μg/kg to 20 mg/kg), negative mutagenicity in Ames test, no chromosomal aberrations or genetic toxicity, no developmental toxicity, no anaphylactic reactions, and no gross or histologic toxicity in liver, spleen, lung, kidney, brain, thymus, prostate, or ovaries in studies up to 6 weeks (Xu et al., 2020). Two human pilot studies (2024-2025) showed that IV infusion of up to 20 mg in healthy adults produced no adverse effects on cardiac, hepatic, renal, thyroid, or metabolic biomarkers (Lee and Burgess, 2025), and intravesical injection of 10 mg in 12 patients produced no adverse events with 10 of 12 achieving complete symptom resolution (Lee et al., 2024). It is important to note that despite these promising findings, large-scale randomized controlled trials in humans have not been conducted, and the compound remains investigational without regulatory approval.