What is BPC-157?
BPC-157, also known as Body Protection Compound-157 or Pentadecapeptide BPC 157, is a synthetic peptide composed of 15 amino acids. It is derived from a partial sequence of body protection compound (BPC), a protein naturally found in human gastric juice. The peptide has the amino acid sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val, with a molecular weight of 1419.53 g/mol and the CAS registry number 137525-51-0.
Since its initial characterization, BPC-157 has been the subject of extensive preclinical research. Published studies span multiple areas including tissue repair mechanisms, gastrointestinal function, angiogenesis pathways, and neuroprotective activity. The compound is noted in the literature for its stability in human gastric juice, which distinguishes it from many other peptides that undergo rapid degradation in acidic environments.
BPC-157 is classified as a research peptide and is available exclusively for laboratory and scientific investigation. All findings described herein are derived from published preclinical studies and do not constitute medical claims.
Mechanism of Action
Published research suggests BPC-157 may interact with multiple biological pathways simultaneously, which has led researchers to investigate its potential mechanisms in detail.
Nitric Oxide (NO) System
BPC-157 has been investigated for its apparent interaction with the nitric oxide system. Studies suggest the peptide may modulate NO-mediated pathways, which are involved in vasodilation, blood flow regulation, and inflammatory responses. Research indicates that BPC-157 may help maintain NO homeostasis, potentially counteracting both the overproduction and inhibition of nitric oxide synthase (NOS) in experimental models.
Growth Factor Pathways
Laboratory studies have indicated that BPC-157 may influence the expression of several growth factors, including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), and fibroblast growth factor (FGF). The upregulation of VEGF expression has been particularly noted in wound healing models, where increased angiogenesis (formation of new blood vessels) was observed in BPC-157 treated groups compared to controls.
FAK-Paxillin Signaling
Research has demonstrated that BPC-157 may activate the focal adhesion kinase (FAK) and paxillin pathway. This signaling cascade is considered important for cell migration, adhesion, and tissue remodeling. Studies in tendon fibroblast cultures reported increased phosphorylation levels of both FAK and paxillin following BPC-157 exposure, without changes in total protein levels, suggesting the peptide may activate existing molecular pathways rather than increasing protein production.
Dopaminergic System
BPC-157 has been studied for its interactions with the dopamine system. Research in experimental models suggests the peptide may modulate dopamine receptor activity, with studies documenting apparent reversal of amphetamine-induced behavioral changes and counteraction of haloperidol supersensitivity effects.
Research & Clinical Studies
BPC-157 and Wound Healing Research
Multiple preclinical studies have investigated the potential role of BPC-157 in wound healing processes.
In a study by Seiwerth et al. (1997), three experimental murine models were utilized: one with skin tissue wounds, another with colon tissue anastomosis, and a third with synthetic sponge implantation. Following the study period, histological examination revealed that BPC-157 treated groups appeared to exhibit higher numbers of collagen fibers, reticulin development, and blood vessel formation compared to control groups.
A subsequent study by Huang et al. (2015) explored the hypothesis that BPC-157 might accelerate wound healing through multiple mechanisms. The researchers reported observations of potential improvements in granulation tissue formation, re-epithelialization, dermal remodeling, and collagen deposition. The study also suggested that BPC-157 may have enhanced the expression of vascular endothelial growth factor (VEGF) in injured skin tissues and appeared to influence human umbilical vein endothelial cell (HUVEC) proliferation and migration.
Furthermore, the study indicated that BPC-157 may regulate the phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), along with their downstream targets including c-Fos, c-Jun, and Egr-1 — proteins that play significant roles in cell growth, migration, and angiogenesis.
[1] Seiwerth S, et al. BPC 157 effect on healing. J Physiol Paris. 1997;91(3-5):173-8. PubMed ↗
[2] Huang T, et al. Body protective compound-157 enhances alkali-burn wound healing in vivo. Drug Des Devel Ther. 2015;9:2485-2499. PubMed ↗
BPC-157 and Tendon Healing Research
Chang et al. (2011) conducted experiments using cultured tendon fibroblasts derived from murine models to investigate the potential effects of BPC-157 on tendon repair processes.
The research team divided the cultures into control and BPC-157 treated groups. Following the study, several key observations were reported: the peptide appeared to promote the outgrowth of tendon fibroblasts and tissue healing; even under hydrogen peroxide (H2O2) oxidative stress conditions, BPC-157 appeared to stimulate cell survival; the peptide appeared to promote migration of tendon fibroblasts; and BPC-157 reportedly induced increased levels of phosphorylation of both PAK and paxillin proteins.
The researchers utilized Western blotting analysis and suggested that BPC-157 may activate focal adhesion kinase (FAK) and paxillin. These proteins play significant roles in cellular processes related to cell migration and adhesion. The finding that phosphorylation levels increased while total protein amounts remained unchanged led to the hypothesis that BPC-157 may primarily activate existing molecular pathways rather than inducing new protein synthesis.
The study concluded by suggesting that the peptide may impact tendon healing and cell survival through F-actin formation and activation of the FAK-paxillin pathway.
[3] Chang CH, et al. The promoting effect of pentadecapeptide BPC 157 on tendon healing. J Appl Physiol. 2011;110(3):774-80. PubMed ↗
BPC-157 and Gastrointestinal Research
BPC-157 has been extensively studied in relation to gastrointestinal healing processes. Seiwerth et al. (2018) conducted a comparative study examining BPC-157 against established angiogenic growth factors including EGF, FGF, and VEGF.
The primary hypotheses were that BPC-157 demonstrates high stability, biocompatibility, and sufficiency to exert its effects when presented independently. While the study reported improved healing parameters across multiple groups, only BPC-157 appeared to exhibit consistent results across all wound types — both chronic and acute — affecting the esophagus, stomach, duodenum, and lower gastrointestinal tract.
Separately, research into the peptide's interaction with serotonin systems has been documented. Serotonin, an enteric neurotransmitter localized in the GI tract and GI mucosa, plays a role in gastric acid secretion and gut mucosal function. Sikiric et al. (2016) reported that BPC-157 appeared to counteract the 5-HT2A receptors, potentially restricting serotonin binding and thereby modulating its action in the gastrointestinal system.
[4] Seiwerth S, et al. BPC 157 and Standard Angiogenic Growth Factors. Curr Pharm Des. 2018;24(18):1972-1989. PubMed ↗
[5] Sikiric P, et al. Brain-gut Axis and Pentadecapeptide BPC 157. Curr Neuropharmacol. 2016;14(8):857-865. PubMed ↗
BPC-157 and Muscle Healing Research
Pevec et al. (2010) investigated the potential effects of BPC-157 on muscle healing in an experimental model involving injured gastrocnemius muscle complexes. The study was designed to assess whether BPC-157 could influence recovery when muscle damage was compounded by systemic corticosteroid administration.
Murine models with gastrocnemius muscle injuries were presented with methylprednisolone (a corticosteroid known to impair healing). These models were then divided into two groups: one receiving BPC-157 and the other receiving a placebo. Both compounds were administered once every 24 hours, with examinations conducted on days 1, 2, 4, 7, and 14.
Upon examination, the corticosteroid appeared to significantly worsen muscle damage in the experimental models. However, the BPC-157 group appeared to exhibit signs of healing and restoration of the damaged gastrocnemius muscle, including apparent recovery of functional ability.
[6] Pevec D, et al. Impact of pentadecapeptide BPC 157 on muscle healing impaired by systemic corticosteroid application. Med Sci Monit. 2010;16(3):BR81-88. PubMed ↗
BPC-157 and Central Nervous System Research
Tudor et al. (2010) explored the potential of BPC-157 in the context of traumatic brain injury (TBI) using experimental murine models.
The study investigated whether BPC-157 might reduce damage caused by TBI, as assessed by early outcome measures. During the critical 24-hour post-injury period, observations indicated a reduced mortality rate in the BPC-157 group compared to controls. Additionally, the severity of traumatic lesions typically associated with TBI appeared to be less pronounced in the BPC-157 treated group.
A notable finding was considerable improvement in brain edema measurements. The researchers further hypothesized that pre-injury administration of BPC-157 might demonstrate improved ratios of conscious to unconscious states in experimental subjects.
Separately, research by Jelovac et al. (1998) examined BPC-157's interaction with the dopamine system using amphetamine-challenged models. The study reported that BPC-157 appeared to reverse amphetamine-induced excitability and caused near-complete reversal of haloperidol-induced dopamine supersensitivity.
[7] Tudor M, et al. Traumatic brain injury in mice and pentadecapeptide BPC 157 effect. Regul Pept. 2010;160(1-3):26-32. PubMed ↗
[8] Jelovac N, et al. BPC 157 blocks amphetamine stereotypy and haloperidol supersensitivity. Biol Psychiatry. 1998;43(7):511-9. PubMed ↗
Handling & Reconstitution Guidelines
Reconstitution Protocol
For laboratory use, BPC-157 lyophilized powder should be reconstituted using sterile bacteriostatic water (BAC water) or sterile saline solution. Allow the vial to reach room temperature before reconstitution. Inject the diluent slowly along the vial wall to avoid denaturing the peptide. Do not shake vigorously — gently swirl until fully dissolved.
Recommended Diluent Volume
A typical reconstitution volume is 1-2 mL of bacteriostatic water per 5mg vial, yielding a concentration suitable for precise measurement in laboratory protocols.
Post-Reconstitution Storage
Once reconstituted, the solution should be stored at 2-8C (refrigerated) and used within 30 days. For extended storage, aliquoting into single-use volumes and freezing at -20C is recommended.
Handling Precautions
Use standard laboratory personal protective equipment (PPE) including gloves and safety glasses. Work in a clean environment to minimize contamination risk. Avoid repeated freeze-thaw cycles.
Storage & Stability Information
Lyophilized Form (Unreconstituted)
Store at -20C in a sealed container protected from light and moisture. Under these conditions, the peptide maintains stability for up to 24 months. Short-term storage at 2-8C is acceptable for up to 90 days.
Reconstituted Solution
Store reconstituted BPC-157 at 2-8C (standard refrigeration). Use within 30 days of reconstitution. For longer preservation, aliquot into single-use volumes and store at -20C.
Stability Notes
BPC-157 is noted in published literature for its remarkable stability in gastric juice conditions, which distinguishes it from many research peptides. The peptide demonstrates resistance to enzymatic degradation across a wide pH range.