2,400+ researchers supplied
99+ COAs published
6-panel tested every lot
Processing within 1–3 business days
FREE SHIPFree U.S. shipping on orders over $150Free U.S. shipping on orders over $150
Free U.S. shipping on orders over $150BPC-157 is a synthetic pentadecapeptide composed of 15 amino acids, with the sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val.
It is a portion of a protein that occurs naturally in human gastric juice, commonly referred to as Body Protection Compound (BPC). Native BPC helps maintain gastrointestinal integrity under normal physiological conditions.
BPC-157 is stable and soluble in water. As a synthetic peptide, BPC-157 is not produced endogenously in this exact form but is designed to replicate a biologically active fragment of the parent protein found in gastric secretions [1].
The peptide has been the subject of extensive preclinical research, particularly in the context of cellular proliferation, angiogenesis, and tissue repair mechanisms. BPC-157 has been studied in animal and in vitro models as a tool for investigating pathways associated with:
All research involving BPC-157 remains within the domain of experimental studies, and it is not approved for human therapeutic use.
BPC-157 has been extensively studied in preclinical models for its modulatory effects on inflammation, particularly in relation to tissue injury and repair processes [1].
In various rodent studies, administration of BPC-157 reduced markers of inflammation in models of gastrointestinal, musculoskeletal, and neural injury. By modulating inflammation, rat studies suggest that various BPC variants modulate pain, while BPC-157 predominantly reduces acute pain in incisional and formalin-induced pain [2]. In a rat model of allodynia, it also reduced pain by protecting nerve integrity from capsaicin [3].
BPC may also modulate the nitric oxide (NO) system. It counteracts both excessive and deficient NO activity, supporting endothelial integrity and attenuating leukocyte infiltration in inflamed tissues.
This dual regulation may contribute to its observed ability to balance pro-inflammatory and anti-inflammatory signaling cascades [4].
In experimental colitis models, for example, BPC-157 administration was associated with:
BPC-157 also promotes angiogenesis (blood vessel growth) and stabilizes vascular function at sites of injury. This angiogenic support not only facilitates tissue repair but may also limit secondary inflammation resulting from ischemia and oxidative stress [5].
Research in tendon and ligament injury models similarly highlights reductions in edema and inflammatory cell presence following BPC-157 exposure.
These findings are derived from animal studies, and while promising, they await confirmation in human clinical research to fully understand its therapeutic relevance.
BPC-157 can facilitate regeneration across various tissue types, including:
A key feature identified in these models is BPC-157’s capacity to modulate cellular and immune environments in ways that promote structural integrity and restoration of injured sites.
In rat models of tendon fibroblasts, BPC-157 significantly upregulated growth hormone receptor expression, and enhanced the responsiveness of these cells to endogenous growth hormone [6].
This interaction promotes cell proliferation and tissue regeneration, increasing expression of proliferation markers:
These results suggest a supportive role in tendon repair processes at the molecular level, enhancing the body's natural regenerative mechanisms.
BPC-157 may influence stem cell activity indirectly by optimizing the local microenvironment of injured tissues.
While direct stimulation of stem cell differentiation by BPC-157 has not been definitively proven, its actions on surrounding tissues, blood vessels, and extracellular matrix components are believed to indirectly enhance stem cell-mediated repair processes.
BPC-157 has been extensively studied in preclinical models for its protective and regenerative effects on the gastrointestinal (GI) tract [7].
Research in rat models of ileoileal anastomosis healing, for instance, shows that BPC-157:
BPC-157 reduced adhesion formation and necrosis, while accelerating the resolution of edema and inflammatory infiltrates in treated animals compared to controls.
Additional experimental models of intestinal injury, including those involving perforations, fistulas, or induced colitis, report that BPC-157 administration supported gut integrity by:
The peptide’s influence on nitric oxide pathways and its modulation of endothelial function are proposed mechanisms underlying these benefits.
While clinical trials in humans remain limited, the consistent findings across animal models offer a compelling basis for future investigation into its application in gut health contexts.
Bees are crucial pollinators whose populations are in significant declines. Research suggests that BPC-157 may help to improve bee health and survival. In bees, BPC-157 improves colony strength and enhances certain aspects of immune responses [8]. Supplementation of bee diets with the peptide reduced the infection load of the Nosema ceranae, a one-celled fungal parasite. BPC-157 also attenuates gut damage from N. ceranae infections [8]. Overall, BPC-157 may be beneficial in beekeeping.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). BPC-157 is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
Research-grade compound with certificate of analysis. Full analytical testing on every lot.
Snapshot BPC-157 and Thymosin Beta-4 are research peptides investigated for complementary roles in tissue protection, vascular signaling, and cytoskeletal remodeling. The overlapping yet distinct mechanisms that may support coordinated repair biology, though combination evidence remains early and primarily exploratory. What Is BPC-157? BPC-157 (Body Protection Compound-157) is a synthetic 15-amino acid peptide based on a naturally occurring fragment of human gastric protein. The peptide is stable in the gastric environment and has systemic effects. It has been studied for its role in tissue protection, angiogenesis, and cellular repair signaling. Unlike many peptides that act through a single receptor, BPC-157 appears to influence multiple biological pathways involved in vascular integrity, inflammation modulation, and cell migration [1, 2, 3]. Preclinical research shows that BPC-157 interacts with signaling systems relevant to tissue homeostasis during stress and injury, such as [4, 5]: Nitric oxide (NO) VEGF-related angiogenic signaling Cytoprotective mechanisms What Is Thymosin Beta-4? Thymosin Beta-4 (TB-4) is a 43-amino acid peptide naturally expressed in many tissues, with high concentrations in platelets, immune cells, and sites of tissue injury [6]. It plays a central role in actin regulation, binding to monomeric actin (G-actin) and influencing cytoskeletal remodeling, cell migration, and wound repair processes [7]. In research models, Thymosin Beta-4 supports [8, 9]: Angiogenesis Stem cell recruitment Anti-inflammatory signaling These effects contribute to coordinated tissue regeneration across epithelial, musculoskeletal, and cardiovascular systems. Unlike growth factors that directly stimulate proliferation, TB-4 is a regulatory peptide, helping cells respond appropriately to injury or stress by organizing structural and signaling pathways. BPC-157–Thymosin-Beta-4 Synergy and Complementary Mechanisms of Action Although BPC-157 and Thymosin Beta-4 (TB-4) are distinct peptides with different primary functions, their mechanisms of action are highly complementary. Mechanistically, BPC-157 is associated with cytoprotection and vascular signaling, while Thymosin Beta-4 is more involved in cytoskeletal remodeling and cell migration. Together, these activities span multiple phases of tissue response to injury or stress. Vascular integrity and angiogenesis BPC-157 supports endothelial stability and angiogenic signaling, partly through interactions with nitric oxide pathways and VEGF-related mechanisms [10]. TB-4, in parallel, promotes angiogenesis by facilitating endothelial cell migration and organization via actin dynamics [11]. In combination, these effects may support both vascular signaling and structural assembly during tissue repair. Inflammation modulation and tissue protection BPC-157 can be cytoprotective, helping tissues maintain function under inflammatory or ischemic stress [12]. TB-4 contributes to immune regulation by influencing macrophage behavior and reducing excessive inflammatory signaling in injury models [13]. These overlapping but non-redundant roles can potentially coordinate the inflammatory microenvironment. Cell migration and repair coordination TB-4’s role in actin sequestration and cytoskeletal flexibility is critical for cell migration, a key step in wound closure and regeneration. BPC-157, meanwhile, appears to support the biochemical conditions that allow migrating cells to survive, attach, and integrate into repairing tissue. This creates a conceptual framework in which TB-4 mobilizes cells, while BPC-157 supports the environment they move into. Evidence for Combined Investigation Currently, direct studies examining BPC-157 and Thymosin Beta-4 together are limited, particularly in human clinical contexts. Most available evidence comes from separate in vitro and in vivo studies that describe overlapping outcomes. A retrospective observational study evaluated whether intra-articular administration of BPC-157, alone or in combination with Thymosin Beta-4 (TB-4), improved knee pain in 17 patients with different kinds of knee pain [14]. Twelve patients with differing types of knee injuries received 4 mg of BPC-157, while 4 patients the combination of BPC-157 + TB-4 in various doses, including 2 mg BPC-157 + 3 mg TB-4, 2 mg BPC-157 + 3 mg TB-4, 3 mg BPC-157 + 4.5 mg TB-4, and 4 mg BPC-157 + 6 mg TB-4). 11 of 12 patients who received BPC-157 treatment alone reported significant improvement in knee pain. Whereas, 3 out of 4 patients who received the combination of BPC-157 and TB-4 reported significant improvement. The one patient in the combination group who did not experience pain improvement received 2 mg of BPC-157 + 3 mg of TB-4, even though another patient receiving the same dose experienced relief. 50%+ of patients in this study experienced pain relief for 6 months to 1 year. Overall, this was a small retrospective study involving a heterogeneous group of patients with promising results. It’s widely known that pain alone is not an indicator of damage or tissue repair, which might have been better assessed with pre- and post-treatment imaging [15]. Therefore, larger, controlled studies incorporating objective imaging and functional outcomes are needed to clarify efficacy, durability, and comparative benefits. Doses and Ratios In rats, intramuscular administration of BPC-157 results in a half life of about 30 minutes in the blood [5]. In human tissues, it is estimated that levels may drop from peak amounts by 50% within 24 hours post-administration. As a result, daily administration may be essential to maintain its effects. TB-4 has a longer half life as it binds to plasma proteins and actin in tissues, resulting in effects that may last days or weeks. The daily administration of TB-4 may allow the peptide to build up. Anecdotally, the 1:1 combo of BPC-157 and TB-4 is within the typical dosage ranges of both peptides. Daily doses of 300–500 mcg of each peptide are well-tolerated, with fatigue being a potential side effect. This combination delivers synergistic immune and tissue-healing benefits. References 1 Seiwerth, S., Brcic, L., Vuletic, L. B., Kolenc, D., Aralica, G., Misic, M., et al. (2014) BPC 157 and blood vessels. Curr. Pharm. Des., Curr Pharm Des 20, 1121–1125 2 Vasireddi, N., Hahamyan, H., Salata, M. J., Karns, M., Calcei, J. G., Voos, J. E., et al. (2025) Emerging use of BPC-157 in orthopaedic sports medicine: A systematic review. HSS J., SAGE Publications 21, 15563316251355551 3 Chang, C.-H., Tsai, W.-C., Lin, M.-S., Hsu, Y.-H. and Pang, J.-H. S. (2011) The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J. Appl. Physiol., American Physiological Society 110, 774–780 4 Hsieh, M.-J., Lee, C.-H., Chueh, H.-Y., Chang, G.-J., Huang, H.-Y., Lin, Y., et al. (2020) Modulatory effects of BPC 157 on vasomotor tone and the activation of Src-Caveolin-1-endothelial nitric oxide synthase pathway. Sci. Rep., Springer Science and Business Media LLC 10, 17078 5 McGuire, F. P., Martinez, R., Lenz, A., Skinner, L. and Cushman, D. M. (2025) Regeneration or risk? A narrative review of BPC-157 for musculoskeletal healing. Curr. Rev. Musculoskelet. Med., Springer Science and Business Media LLC 18, 611–619 6 Goldstein, A. L., Hannappel, E., Sosne, G. and Kleinman, H. K. (2012) Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opin. Biol. Ther. 12, 37–51 7 Xue, B., Leyrat, C., Grimes, J. M. and Robinson, R. C. (2014) Structural basis of thymosin-β4/profilin exchange leading to actin filament polymerization. Proc. Natl. Acad. Sci. U. S. A. 111, E4596–605 8 Philp, D., Huff, T., Gho, Y. S., Hannappel, E. and Kleinman, H. K. (2003) The actin binding site on thymosin beta4 promotes angiogenesis. FASEB J., Wiley 17, 2103–2105 9 Ye, L., Zhang, P., Duval, S., Su, L., Xiong, Q. and Zhang, J. (2013) Thymosin β4 increases the potency of transplanted mesenchymal stem cells for myocardial repair. Circulation, Ovid Technologies (Wolters Kluwer Health) 128, S32–41 10 Hsieh, M.-J., Liu, H.-T., Wang, C.-N., Huang, H.-Y., Lin, Y., Ko, Y.-S., et al. (2017) Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. J. Mol. Med., J Mol Med (Berl) 95, 323–333 11 Selmi, A., Malinowski, M., Brutkowski, W., Bednarek, R. and Cierniewski, C. S. (2012) Thymosin β4 promotes the migration of endothelial cells without intracellular Ca2+ elevation. Exp. Cell Res., Elsevier BV 318, 1659–1666 12 Sikiric, P., Skrtic, A., Gojkovic, S., Krezic, I., Zizek, H., Lovric, E., et al. (2022) Cytoprotective gastric pentadecapeptide BPC 157 resolves major vessel occlusion disturbances, ischemia-reperfusion injury following Pringle maneuver, and Budd-Chiari syndrome. World J. Gastroenterol., Baishideng Publishing Group Inc. 28, 23–46 13 Zhu, Z., Liao, Y., Mou, Q., Liu, H., Shen, Y., Zhu, L., et al. (2025) Thymosin β4 regulates tissue inflammatory response in mouse nonalcoholic fatty liver disease by promoting macrophage M2-type polarization. J. Inflamm. Res. 18, 5791–5809 14 Lee, E. and Padgett, B. (2021) Intra-articular injection of BPC 157 for multiple types of knee pain. Altern. Ther. Health Med., Altern Ther Health Med 27, 8–13 15 Raja, S. N., Carr, D. B., Cohen, M., Finnerup, N. B., Flor, H., Gibson, S., et al. (2020) The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises: concepts, challenges, and compromises. Pain, Ovid Technologies (Wolters Kluwer Health) 161, 1976–1982
Snapshot Cagrilintide is a synthetic long-acting amylin analogue studied for its role in appetite regulation and metabolic coordination. By enhancing amylin-mediated satiety signaling and slowing gastric emptying, it supports smaller meal size and smoother post-meal nutrient handling. Its complementary pathway has drawn interest alongside GLP-1 agonists for layered appetite and energy-balance signaling. What is Cagrilintide peptide? Cagrilintide is a 37-amino acid, long-acting synthetic analogue of amylin, a peptide hormone that is co-secreted with insulin by pancreatic β-cells and plays a key role in appetite regulation, gastric emptying, and post-meal metabolic signaling [1]. Endogenous amylin acts as a satiety signal, helping coordinate how the body interprets meal size and nutrient intake. Cagrilintide mimics these physiologic actions while exhibiting enhanced molecular stability and prolonged activity compared with endogenous amylin [2]. Cagrilintide benefits Weight loss Cagrilintide’s association with weight regulation is rooted in its ability to amplify amylin-mediated satiety signaling, rather than by directly altering metabolic rate or energy expenditure. A multicenter, randomized, double-blind phase 2 trial evaluated the dose response, safety, and tolerability of cagrilintide [3]. A total of 706 overweight or obese participants were randomized to once-weekly cagrilintide (0.3–4.5 mg), once-daily liraglutide 3.0 mg, or placebo for 26 weeks, followed by a 6-week off-treatment period. Results showed that cagrilintide: Produced dose-dependent reductions in body weight that were significantly greater than placebo at all tested doses (p < 0.05). Resulted in mean weight loss ranging from 6.0% to 10.8% compared to 3.0% with placebo (p < 0.05). At the highest dose (4.5 mg), resulted in greater weight loss than liraglutide (10.8% vs. 9.0%). Cagrilintide was generally well tolerated, with the most common adverse events including nausea, constipation, and diarrhea, as well as injection-site reactions. Cagrilintide leads to clinically meaningful, dose-dependent weight reduction with an acceptable safety profile. Blood sugar Cagrilintide’s relevance to blood-sugar regulation is indirect and comes from its influence on meal timing, gastric emptying, and postprandial signaling. A randomized phase 2 trial evaluated the efficacy and safety of combined semaglutide and cagrilintide (CagriSema) compared with either agent alone in adults with type 2 diabetes and overweight or obesity [4]. Ninety-two participants were treated for 32 weeks with once-weekly injections of CagriSema, semaglutide, or cagrilintide, escalated to a target dose of 2.4 mg. All participants were on metformin, with or without an SGLT2 inhibitor. Results showed that CagriSema: Reduced body weight significantly more than with either monotherapy: CagriSema: 15.6%, Semaglutide: 5.1%, and Cagrilintide: 8.1%. Produced a greater reduction in HbA1c than cagrilintide alone, but not a statistically significant improvement compared with semaglutide alone. Mean HbA1c reduction: CagriSema: −2.2%, Semaglutide: −1.8%, and Cagrilintide: −0.9%. Reduced fasting plasma glucose similarly, with CagriSema outperforming cagrilintide but not semaglutide. No severe hypoglycaemia or fatal adverse events were observed, indicating that combined amylin and GLP-1 receptor agonism offers additive benefits for weight loss and glycemic control. Appetite regulation Amylin receptors are highly expressed in brain regions involved in integrating sensory input, nutrient status, and fullness cues, particularly within the brainstem and hypothalamus [5]. By engaging these receptors in a sustained manner, cagrilintide reinforces the signals that indicate meal completion and energy sufficiency, affecting both meal size and eating frequency. This can reduce reward-driven or habitual eating behaviors, especially those that occur independently of physiological hunger. Cagrilintide side effects, synergies, and contraindications Side effects Because amylin influences gastric emptying and central appetite centers, some individuals on cagrilintide may experience nausea, early fullness, or reduced appetite, especially during initial exposure. Observed effects are dose- and context-dependent, aligning with its role as a regulatory peptide rather than a forceful metabolic driver. Synergies with other metabolic peptides While GLP-1–based peptides primarily influence insulin and glucose secretion, amylin analogues like cagrilintide contribute distinct satiety and gastric-emptying signals. Together, these pathways engage multiple, non-redundant nodes to influence appetite perception. This layered signaling approach allows for enhanced appetite regulation without relying on a single pathway. Contraindications and considerations Like other peptides that influence gastrointestinal motility and appetite signaling, cagrilintide may not be appropriate in contexts where delayed gastric emptying or altered digestive rhythm could be problematic, like in patients with pre-existing gastroparesis or gastrectomies. Cagrilintide should also be evaluated in the context of overall metabolic signaling balance, particularly when combined with other appetite-modulating compounds. References 1 Edwards, B. J. and Morley, J. E. (1992) Amylin. Life Sci., Life Sci 51, 1899–1912 2 Cao, J., Belousoff, M. J., Johnson, R. M., Keov, P., Mariam, Z., Deganutti, G., et al. (2025) Structural and dynamic features of cagrilintide binding to calcitonin and amylin receptors. Nat. Commun., Springer Science and Business Media LLC 16, 3389 3 Lau, D. C. W., Erichsen, L., Francisco, A. M., Satylganova, A., le Roux, C. W., McGowan, B., et al. (2021) Once-weekly cagrilintide for weight management in people with overweight and obesity: a multicentre, randomised, double-blind, placebo-controlled and active-controlled, dose-finding phase 2 trial. Lancet, Elsevier BV 398, 2160–2172 4 Frias, J. P., Deenadayalan, S., Erichsen, L., Knop, F. K., Lingvay, I., Macura, S., et al. (2023) Efficacy and safety of co-administered once-weekly cagrilintide 2·4 mg with once-weekly semaglutide 2·4 mg in type 2 diabetes: a multicentre, randomised, double-blind, active-controlled, phase 2 trial. Lancet, Elsevier BV 402, 720–730 5 Fu, W., Patel, A., Kimura, R., Soudy, R. and Jhamandas, J. H. (2017) Amylin receptor: A potential therapeutic target for Alzheimer’s disease. Trends Mol. Med. 23, 709–720