BPC-157 Also Known As

BPC-157 | Body Protection Compound | Pentadecapeptide | PL10 | PL14736 | Bepecin

What is BPC-157?

BPC-157(body protection compound)is a small molecule peptide that is found naturally in gastric juices/stomach acid.

This peptide protects, heals and restores tissues by the building of new blood vessels and upregulating growth factors such as Vascular Endothelial Growth Factor (VEGF), Epithelial Growth Factor (EGF), Nerve growth factor (NGF)  and by interacting with the nitric oxide system (NOS), and promotion of new blood vessel formation (Angiogenesis).

These factors lead to an enhanced anabolic healing effect in both the upper and lower GI tract; having an antiulcer effect; and produce a therapeutic effect on all inflammatory bowel diseases, all surprisingly free of side effects. It also enhances growth hormone receptors which can further enhance healing processes systemically, not just in the GIT.

BPC also stimulates granulation tissue via stimulation of growth factors (NGF, EGF) which enhances collagen organisation and enhances wound healing.

Can BPC-157 Work Orally?

BPC as arginine salt (the form used by LVLUP health), almost completely resistant to gastric juices and high temperatures, meaning that unlike other peptides and other forms of BPC157, it can pass through without being denatured or broken down by stomach acid and digestive enzymes; then it can then be absorbed via the gastrointestinal tract to have local healing effects or it can be absorbed into circulation to have systemic healing effects via the growth factors listed above and the mechanisms listed below.

BPC 157 Mechanisms of Action

– Gastro-protective

– Anti-Ulcer

– Nitric Oxide Modulation (NO)

– Anti- Inflammatory

– Cytoprotective

– Upregulates Growth Hormone (GH) Receptors

– Reduces Neuro-inflammation

– Immune Modulating.

– Stimulates Angiogenesis (Blood Vessel Formation)

– Nootropic and Anxiolytic effects (Dopamine and Serotonin receptor modulation)

BPC 157 Studies / References:

Butler, R. J., Marchesi, S., Royer, T., & Davis, I. S. (2007). Effective Therapy of Transected Quadriceps Muscle in Rat:Gastric Pentadecapeptide BPC 157. Journal of Orthopaedic Research September25(June), 1121–1127. https://doi.org/10.1002/jor

Brcic, L., Brcic, I., Staresinic, M., Novinscak, T., Sikiric, P., & Seiwerth, S. (2009). Modulatory effect of gastric pentadecapeptide BPC 157 on angiogenesis in muscle and tendon healing. Journal of Physiology and Pharmacology : An Official Journal of the Polish Physiological Society60 Suppl 7, 191–196.

Cerovecki, T., Bojanic, I., Brcic, L., Radic, B., Vukoja, I., Seiwerth, S., & Sikiric, P. (2010). Pentadecapeptide BPC 157 (PL 14736) improves ligament healing in the rat. Journal of Orthopaedic Research28(9), 1155–1161. https://doi.org/10.1002/jor.21107

Chang, C. H., Tsai, W. C., Hsu, Y. H., & Pang, J. H. S. (2014). Pentadecapeptide bpc 157 enhances the growth hormone receptor expression in tendon fibroblasts. Molecules, 19(11), 19066–19077. https://doi.org/10.3390/molecules191119066

Chang, C. H., Tsai, W. C., Lin, M. S., Hsu, Y. H., & Su Pang, J. H. (2011). The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. Journal of Applied Physiology110(3), 774–780. https://doi.org/10.1152/japplphysiol.00945.2010


Gjurasin, M., Miklic, P., Zupancic, B., Perovic, D., Zarkovic, K., Brcic, L., Sikiric, P. (2010). Peptide therapy with pentadecapeptide BPC 157 in traumatic nerve injury. Regulatory Peptides160(1–3), 33–41. https://doi.org/10.1016/j.regpep.2009.11.005


Gwyer, D., Wragg, N. M., & Wilson, S. L. (2019). Gastric pentadecapeptide body protection compound BPC 157 and its role in accelerating musculoskeletal soft tissue healing. Cell and Tissue Research377(2), 153–159. https://doi.org/10.1007/s00441-019-03016-8


Perovic, D., Kolenc, D., Bilic, V., Somun, N., Drmic, D., Elabjer, E., … Sikiric, P. (2019). Stable gastric pentadecapeptide BPC 157 can improve the healing course of spinal cord injury and lead to functional recovery in rats. Journal of Orthopaedic Surgery and Research14(1), 1–12. https://doi.org/10.1186/s13018-019-1242-6


Pevec, D., Novinscak, T., Brcic, L., Sipos, K., Jukic, I., Staresinic, M., … Sikiric, P. (2010). Impact of pentadecapeptide BPC 157 on muscle healing impaired by systemic corticosteroid application. Medical Science Monitor16(3), 81–88. https://pubmed.ncbi.nlm.nih.gov/20190676/


Seiwerth, S., Sikiric, P., Grabarevic, Z., Zoricic, I., Hanzevacki, M., Ljubanovic, D., … Kolega, Z. (1997). BPC 157’s effect on Healing. Journal of Physiology Paris91(3–5), 173–178. https://doi.org/10.1016/S0928-4257(97)89480-6


Sever, A. Z., Sever, M., Vidovic, T., Lojo, N., Kolenc, D., Vuletic, L. B., … Sikiric, P. (2019). Stable gastric pentadecapeptide BPC 157 in the therapy of the rats with bile duct ligation. European Journal of Pharmacology847(January), 130–142. https://doi.org/10.1016/j.ejphar.2019.01.030


Sikiric, P. (1999). The pharmacological properties of the novel peptide BPC 157 (PL-10). Inflammopharmacology7(1), 1–14. https://doi.org/10.1007/s10787-999-0022-z


Sikiric, P., Petek, M., Rucman, R., Seiwerth, S., Grabarevic, Z., Rotkvic, I., … Karakas, I. (1993). A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. Journal of Physiology – Paris87(5), 313–327. https://doi.org/10.1016/0928-4257(93)90038-U


Sikiric, P., Seiwerth, S., Rucman, R., Kolenc, D., Vuletic, L. B., Drmic, D., Grgic, T., Strbe, S., Zukanovic, G., Crvenkovic, D., Madzarac, G., Rukavina, I., Sucic, M., Baric, M., Starcevic, N., Krstonijevic, Z., Bencic, M. L., Filipcic, I., Rokotov, D. S., & Vlainic, J. (2016). Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications. Current neuropharmacology14(8), 857–865. https://doi.org/10.2174/1570159×13666160502153022


Staresinic, M., Sebecic, B., Patrlj, L., Jadrijevic, S., Suknaic, S., Perovic, D., … Sikiric, P. (2003). Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth. Journal of Orthopaedic Research21(6), 976–983. https://doi.org/10.1016/S0736-0266(03)00110-4

Larazotide acetate


Also Known As

AT1001 | Octapeptide

What is Larazotide?

Larazotide acetate is an oral peptide derived from zonula occludens that acts as a tight junction regulator and zonulin antagonist. It binds to receptors of apical intestinal cells and antagonises zonulin, preventing the opening of the epithelial intestinal tight junctions caused by gluten/gliadin, glyphosate, pro-inflammatory cytokines, zonulin bacterial antigens such as lipopolysaccharide (LPS) and bacterial dysbiosis.

Zonulin is a main target of Larazotide acetate; the zonulin protein opens tight junctions and causes intestinal hyper-permeability (leakiness) and increases the passage of stressors into circulation and the lamina propria; eliciting an immune response and inflammation.
Subsequent tissue damage, immune dysfunction, blood-brain barrier breakdown, neuroinflammation, increased liver detoxification burden and allergic/histamine responses result when the first line barrier breaks down.

Larazotide acetate has been shown in the 2012 study by Gopalakrishnan et al to “inhibit gliadin-induced macrophage accumulation in the intestine and preserve normal TJ structure, as well as inhibited the increase in TJ permeability elicited by basolaterally applied cytokines”.

Larazotide acetate is being touted as a promising “non-dietary treatment for coeliac disease”. It has passed, and is also currently being researched in multiple clinical trials, with a growing body of evidence showing promise in the scientific literature for those with coeliac disease and other bowel diseases.

Larazotide Mechanisms of Action:

Larazotide is an inhibitor of paracellular permeability and a zonlin antagonist.

In celiac disease, one pathway that allows fragments of gliadin protein to get past the intestinal epithelium and subsequently trigger an immune response begins with binding of indigestible gliadin fragments to the chemokine CXC motif receptor 3 (CXCR3) on the luminal side of the intestinal epithelium (see this page).
This leads to the induction of myeloid differentiation factor 88 (MYD88) and the release of zonulin into the lumen.

Zonulin then binds to epidermal growth factor receptor (EGFR) and protease-activated receptor 2 (PAR2) in the intestinal epithelium.
This complex then initiates a signalling pathway that eventually results in tight junction disassembly and increased intestinal permeability.

Larazotide acetate intervenes in the middle of this pathway by blocking zonulin receptors, thereby preventing tight junction disassembly and associated increase in intestinal permeability.


Larazotide Studies:

Gopalakrishnan, S., Tripathi, A., Tamiz, A. P., Alkan, S. S., & Pandey, N. B. (2012). Larazotide acetate promotes tight junction assembly in epithelial cells. Peptides, 35(1), 95–101. https://doi.org/10.1016/j.peptides.2012.02.016

Gopalakrishnan, S., Durai, M., Kitchens, K., Tamiz, A. P., Somerville, R., Ginski, M., Paterson, B. M., Murray, J. A., Verdu, E. F., Alkan, S. S., & Pandey, N. B. (2012). Larazotide acetate regulates epithelial tight junctions in vitro and in vivo. Peptides, 35(1), 86–94. https://doi.org/10.1016/j.peptides.2012.02.015

Kelly, C. P., Green, P. H., Murray, J. A., Dimarino, A., Colatrella, A., Leffler, D. A., Alexander, T., Arsenescu, R., Leon, F., Jiang, J. G., Arterburn, L. A., Paterson, B. M., Fedorak, R. N., & Larazotide Acetate Celiac Disease Study Group (2013). Larazotide acetate in patients with coeliac disease undergoing a gluten challenge: a randomised placebo-controlled study. Alimentary pharmacology & therapeutics, 37(2), 252–262. https://doi.org/10.1111/apt.12147

Khaleghi, S., Ju, J. M., Lamba, A., & Murray, J. A. (2016). The potential utility of tight junction regulation in celiac disease: focus on larazotide acetate. Therapeutic advances in gastroenterology, 9(1), 37–49. https://doi.org/10.1177/1756283X15616576

Leffler, D. A., Kelly, C. P., Abdallah, H. Z., Colatrella, A. M., Harris, L. A., Leon, F., Arterburn, L. A., Paterson, B. M., Lan, Z. H., & Murray, J. A. (2012). A randomized, double-blind study of larazotide acetate to prevent the activation of celiac disease during gluten challenge. The American journal of gastroenterology, 107(10), 1554–1562. https://doi.org/10.1038/ajg.2012.211

Serena, G., Kelly, C. P., & Fasano, A. (2019). Nondietary Therapies for Celiac Disease. Gastroenterology clinics of North America, 48(1), 145–163. https://doi.org/10.1016/j.gtc.2018.09.011

Valitutti, F., & Fasano, A. (2019). Breaking Down Barriers: How Understanding Celiac Disease Pathogenesis Informed the Development of Novel Treatments. Digestive diseases and sciences, 64(7), 1748–1758. https://doi.org/10.1007/s10620-019-05646-y

Yoosuf, S., & Makharia, G. K. (2019). Evolving Therapy for Celiac Disease. Frontiers in Pediatrics, 7, 193. https://doi.org/10.3389/fped.2019.00193


Larazotide Clinical Trials

NCT00492960 Study to Assess the Efficacy of Larazotide Acetate for the Treatment of Celiac Disease Phase 2 – Completed
NCT00620451 Randomized, Double-Blind, Placebo-Controlled Study of Larazotide Acetate in Subjects With Active Celiac Disease. Phase 2 – Completed
NCT00889473 Study of the Efficacy of Larazotide Acetate to Treat Celiac Disease Phase 2 – Completed.
NCT01396213 A Double-blind Placebo-controlled Study to Evaluate Larazotide Acetate for the Treatment of Celiac Disease. Phase 2 – Completed.
NCT00362856 Safety and Tolerability Study of Larazotide Acetate in Celiac Disease Subjects – Underway.

KPV Tripeptide

Also Known As

Lysine Proline Valine | Tripeptide | a-MSH Fragment

What is KPV?

KPV is an oral peptide derived from alpha MSH (Melanocyte Stimulating Hormone) that acts potently on immune-mediated inflammatory conditions such as dermatitis, bowel diseases, allergic asthma, and arthritis by inactivating pro-inflammatory pathways.

It is found naturally in the body as a breakdown product of aMSH.


– Improves Gut Health

– Mast Cell Stabilisation / Reduces histamine

– Assists post toxic-mould exposure

– Anti Inflammatory

– Anti Microbial

– Wound Healing

– Skin Healing

– Protect against Nerve Damage

– Strengthen Immune System


Detailed mechanisms:

In a mice model of colitis (colon inflammation), oral administration of KPV (added to drinking water) inhibited the activation of NF-κB and MAP kinase inflammatory signalling pathways and reduced pro-inflammatory cytokine secretion.
– Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178. doi:10.1053/j.gastro.2007.10.026

KPV exerts its anti-inflammatory activities through inhibition of NF-kappaB translocation and activation of MC(1) receptor/cAMP.
– Mandrika I, Muceniece R, Wikberg JE. Effects of melanocortin peptides on lipopolysaccharide/interferon-gamma-induced NF-kappaB DNA binding and nitric oxide production in macrophage-like RAW 264.7 cells: evidence for dual mechanisms of action. BiochemPharmacol. 2001;61(5):613-21.
– Haddad JJ, Lauterbach R, Saadé NE, Safieh-garabedian B, Land SC. Alpha-melanocyte-related tripeptide, Lys-d-Pro-Val, ameliorates endotoxin-induced nuclear factor kappaB translocation and activation: evidence for involvement of an interleukin-1beta193-195 receptor antagonism in the alveolar epithelium. Biochem J. 2001;355(Pt 1):29-38.

In an animal model of colitis, KPV significantly reduced intestinal inflammation.
– Rajora N, Boccoli G, Catania A, et al. α-MSH modulates experimental inflammatory bowel disease. Peptides. 1997;18:381–385.

– Oktar BK, Ercan F, Ye en BC, et al. The effect of α-melanocyte stimulating hormone on colonic inflammation in the rat. Peptides. 2000;21:1271–1277.

KPV fights inflammation by inhibiting tumuor necrosis factor-α stimulated NF-κB activity and suppressing antigen-induced lymphocyte proliferation.
– Kelly JM, Moir AJ, Carlson K, et al. Immobilized α-melanocyte stimulating hormone 10–13 (GKPV) inhibits tumor necrosis factor-α stimulated NF-κB activity. Peptide. 2006;27:431–437.
-Cooper A, Robinson SJ, Pickard C, et al. α-melanocyte-stimulating hormone suppresses antigen-induced lymphocyte proliferation in humans independently of melanocortin 1 receptor gene status. J Immunol. 2005;175:4806–4813.

KPV suppresses inflammation through modulation of physiological responses in host defence.
-Hiltz ME, Lipton JM. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB J. 1989;3(11):2282-4.

KPV exhibits its anti-inflammatory effect through inhibition of IL-1beta functions.
-Getting SJ, Schioth HB, Perretti M. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides. J PharmacolExpTher. 2003;306(2):631-7.

KPV fights inflammation by stimulating cAMP generation in a concentration- dependent way.
-Schiöth HB, Muceniece R, Mutule I, Wikberg JE. New melanocortin 1 receptor binding motif based on the C-terminal sequence of alpha-melanocyte-stimulating hormone. Basic ClinPharmacolToxicol. 2006;99(4):287-93.

KPV combats inflammation by significantly inhibiting NF-kappaB activity.
– Kelly JM, Moir AJ, Carlson K, Yang Y, Macneil S, Haycock JW. Immobilized alpha-melanocyte stimulating hormone 10-13 (GKPV) inhibits tumor necrosis factor-alpha stimulated NF-kappaB activity. Peptides. 2006;27(2):431-7.

Several studies have shown a significant reduction of pro‐inflammatory substances such as IL1 β, IL6, TNFα, IL8, Groα, and interferon γ (IFNγ) following KPV treatment.
-Luger T A, Scholzen T, Grabbe S. The role of α‐melanocyte stimulating hormone in cutaneous biology. J Invest DermatolSympProc 1997287–93.
– Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases. Endocr Rev. 2008;29(5):581-602.

In murine models of colitis, KPV treatment showed significant anti-inflammatory effects which suggests that it can be an important therapeutic option in treating inflammatory bowel disease.
– Klaus Kannengiesser, MD, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease, Inflammatory Bowel Diseases, Volume 14, Issue 3, 1 March 2008, Pages 324–331, https://doi.org/10.1002/ibd.20334.

In a mice model of ulcerative colitis, oral administration of KPV loaded into hyaluronic acid (HA)-functionalized polymeric nanoparticles (NPs) was effective in alleviating intestinal inflammation.
– Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Mol Ther. 2017 Jul 5;25(7):1628-1640. doi: 10.1016/j.ymthe.2016.11.020. Epub 2017 Jan 28. PMID: 28143741; PMCID: PMC5498804.