Earn 0 reward points

We’re sorry we’re out of stock, but we can let you know as soon as this product becomes available again.

Enter your details below and we’ll email you once this item is back in stock.

Your NameYour Email Address



Supplied for Research Purposes Only

This information and product is provided for research purposes only. We do not provide any advice on the usage of these products as UK Law prevents this. Customers should check the legality of this product in their own country prior to purchase.

Benefits and uses:

accelerated bone and joint healing

the treatment of stomach ulcers

accelerated wound healing

accelerated cellular renewal

accelerated bone and joint healing

lower intestine injury such as inflammation and fistulas

repair organ ailment

lessen muscle loss

encourage angiogenesis to aid in the development of muscle and growth

affecting neurotransmitter activity and aiding in the treatment of mental health concerns

blood pressure reduction

lessen the negative consequences of elevated potassium levels

The therapeutic effects of body protein compound 157 (BPC-157) on the stomach and intestinal tract have led to evidence of a wide spectrum of effects on the body. [26,27,30] It has been demonstrated to be an anti-ulcer, relieve inflammatory bowel syndrome, increase angiogenesis, stimulate tendon and tissue mending, and even have an impact on brain health. [1,14,15,9,28, 29] The mucous membrane loses integrity as we age, so BPC-157 may be a useful treatment for ageing populations. [16,31,32]

Angiogenesis and BPC-157

Angiogenesis has a profound impact on ageing and, if reversed, could extend life and improve general health. By upregulating angiogenesis, researchers have discovered that BPC-157 is a potent tool for good ageing. [33,34] The development of new capillaries within an organism is the angiogenesis process. [1] After age 55, the likelihood of developing an ischemia increases every 10 years. [2,35,36] This is significant since the recovery from ischemia depends on the angiogenesis of blood vessels. A balance between cardiovascular tissue and blood vessels has been proven to raise the risk of heart failure, as has the downregulation of angiogenesis, which has also been demonstrated to induce heart difficulties. [6, 37,38,39] Age-related health problems and life expectancy may be postponed if angiogenesis can be stimulated.

How Angiogenesis Works

Many angiogenic pathway components that are crucial to the ageing process lose function as people get older. [40,41] HIF-1, PCG-1, and endothelial nitric oxide synthase (eNOS) levels have been observed to significantly decline with age, according to research [3, 42, 43, 44]. These are all vital components of the angiogenic pathway (figure 1), and HIF-1 and PCG-1 support VEGF, one of the essential growth factors that controls capillary formation. [45,46] HIF-1 and PCG-1 levels fall as we become older. [4,47] Nitric oxide, which is produced by eNOS and directly triggers the angiogenic process, is crucial to this process. As we age, however, eNOS may become decoupled from its cofactor tetrahydrobiopterin, which leads in a reduction of NO in the endothelial cells that line capillaries. [5,48,49] Peptides like BPC-157 can stop angiogenesis in its tracks. Angiogenesis is a well-understood mechanism. [50]

BPC-157 has a variety of impacts on the body, but its part in angiogenesis is one of the most crucial for lifespan. L. Bric et colleagues. examined how angiogenesis affected the muscles and tendons of injured mice. In mice treated with BPC-157, he discovered a significantly higher angiogenic response. [51] The mice's muscle and tendon regeneration was quicker as a result of this technique than it was for the control group. [4] This occurs as a result of the BPC-157 upregulating some of the crucial elements of the previously covered Angiogenic pathway. It has been demonstrated that in the rats fed BPC-157, it upregulates VEGF, CD34, and FVIII. [4,52,] We have examined how VEGF affects angiogenesis because it increases the activity of the eNOS enzyme and, consequently, the body's NO levels, which are necessary for capillary renewal. [4,52] The actions of the NOS-inhibitors and the NO-precursor have been demonstrated to be deactivated by BPC-157, which has also shown to have a direct impact on the levels of NO in the organism. [7,54] These directly influence angiogenesis. [55,56] The development of endothelial cells exhibits the expression of CD34 and FVIII. [8,53,57] The angiogenesis process is active if CD34 and FVIII expression are higher. [58]

Tissues for Healing and BPC 157

The repair of torn muscles or tendons can be significantly impacted by the activation of angiogenesis. [59,60] When using BPC-157, researchers discovered a substantial difference in how quickly muscles and tendons may heal. [4,61] Because the muscle cells' enzyme activity was able to return to normal levels more quickly, the muscles were able to return to normal both macroscopically (there was no post-injury leg contracture) and microscopically. [4] Due to the peptide's ability to upregulate angiogenesis, it may be highly helpful in assisting the elderly recover from muscle and tendon injuries as well as stroke. [62,63]

Brain and BPC-157

We have seen that BPC-157 has a wide spectrum of affects on the body, making its influence on the brain particularly intriguing. [26,64] We'll concentrate on how it affects the GI tract and the brain's wellness. BPC-157 affects the brain in a therapeutic way via the gut via the Gut-Brain Axis (GBA). It functions as a two-way communication hub for the intestinal and central nervous systems. [9,65] This ties the stomach and its health to the emotional and neurological areas of the brain. [66] This helps to maintain the general homeostasis of the GI tract and serves as a way to keep the gastric juices in the stomach in balance. [67] Additionally, studies have linked this to more complex cognitive processes including emotion and motivation. [9,65,66] The vagus nerve, which connects the enteric nervous system and the central nervous system, mediates all of this. [68] The precise targeting of the gut by BPC-157, which in turn affects the brain, results from this crosstalk between the brain and the stomach. [10] BPC-157 is an effective cytoprotective and anti-ulcer agent for the stomach. [69] The effects on the brain are achieved by preserving the integrity of the GI mucus. [11,70]

According to studies, BPC-157 helps the GI tract achieve homeostasis while also regulating the serotonergic and dopaminergic systems. [71] This is achieved by promoting the regeneration of nerve cells in injured neurons caused by excessive neurotransmitter stimulation. [11] BPC-157 enhances nerve regeneration and wellness in a variety of ways. In the brain, BPC-157 activates the Egr-1, NAB2, and JAK-2 genes. [9,72,73,74] In rat fibroblasts that have been stimulated by nerve growth factor to create PC12 cells, the Erg-1 gene product has been discovered. [12] Erg-1 was shown to be upregulated in the cell nucleus of this PC12 cell line, a model for cell differentiation in Rat fibroblasts, indicating its likely connection to nerve regeneration. [12.75,76] NAB2 has also shown to be crucial for the brain during both gene transcription and the myelination of neurons. Because it regulates the length of the poly-A tail at the 3' end of mRNA, which is crucial for the preservation of mRNA and the creation of proteins in the brain, it is crucial for transcription. [13,77,78] This pathway is crucial because it guards against demyelination, which is brought on by conditions like multiple sclerosis (MS). [17] Although the exact mechanism is still unclear, the JAK-2 pathways are important in cytokine modulation and immune function. Although mice with the JAK-2 gene knocked out perished at the eighth week of their lives, compared to a mouse's usual lifespan of two years, it has shown to be crucial. [18]

As they have been demonstrated to maintain equilibrium between the central/neural dopaminergic and serotonergic systems, these pathways are crucial for the brain and its higher level of processing. [19,20,79] In particular brain areas, it has been demonstrated to particularly promote the release of serotonin. [80] As dopaminergic and serotonergic systems in older populations deteriorate, this can aid in their repair. Dopamine levels have been declining from young adulthood by 10% every ten years. [21,81,82] A decline in cognitive and motor function is linked to this. [83,84] As dopamine levels fall, so do the number of dopamine receptors. [85] This is significant since BPC-157 has demonstrated the ability to balance the amount of dopamine receptors in the brain. [9] As humans age, serotonin levels likewise decline, [86] which causes synaptic plasticity and neurogenesis to decline. [87] As we age, this is crucial for maintaining the brain's effectiveness because synaptic plasticity loss prevents synaptic pruning. [21,88] Beyond ageing and dopaminergic and serotonergic homeostasis, the therapeutic benefits are also present. It can be used to treat stomach sores brought on by NSAIDs, alcohol, or insulin, according to research. [9] Parkinson's sufferers have also found that it helps them because it interacts with the MPTP, which harms dopaminergic parts of the basal ganglia permanently. [24] Amphetamine-related harm to the central dopaminergic system, including neuronal death, decreased dopaminergic activity, and dopaminergic vesicle depletion, has also been demonstrated to be reversed by BPC-157. [9,25] BPC-157 has also been used in older MS populations. The NAB2 pathway appears to interact with neurons to lessen demyelination in the brain, which accounts for the improvement in symptoms in rats that had been given cuprizone to produce MS. [9] BPC-157 has a variety of physiological effects and can be extremely helpful in a clinical context for people who have brain, GI, or blood vascular issues who could benefit from this treatment.


[1] Folkman, J. (1984). Angiogenesis. Developments in Cardiovascular Medicine Biology of Endothelial Cells, 412-428. doi:10.1007/978-1-4613-2825-4_42

[2] Yousufuddin, M., & Young, N. (2019). Aging and ischemic stroke. Aging, 11(9), 2542–2544. https://doi.org/10.18632/aging.101931

[3] Lähteenvuo, J., & Rosenzweig, A. (2012). Effects of Aging on Angiogenesis. Circulation Research, 110(9), 1252-1264. doi:10.1161/circresaha.111.246116

[4]Novinscak T, Brcic L, Staresinic M, et al. Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat. Surg Today. 2008;38(8):716-725. doi:10.1007/s00595-007-3706-2

[5] Vásquez-Vivar, J., Kalyanaraman, B., Martásek, P., Hogg, N., Masters, B. S., Karoui, H., . . . Pritchard, K. A. (1998). Superoxide generation by endothelial nitric oxide synthase: The influence of cofactors. Proceedings of the National Academy of Sciences, 95(16), 9220-9225. doi:10.1073/pnas.95.16.9220

[6] Isner, J. M., & Losordo, D. W. (1999). Therapeutic angiogenesis for heart failure. Nature Medicine, 5(5), 491-492. doi:10.1038/8374

[7] Grabarevic, Z., Tisljar, M., Artukovic, B., Bratulic, M., Dzaja, P., Seiwerth, S., . . . Kos, J. (1997). The influence of BPC 157 on nitric oxide agonist and antagonist induced lesions in broiler chicks. Journal of Physiology-Paris, 91(3-5), 139-149. doi:10.1016/s0928-4257(97)89478-8

[8] Siemerink, M. J., Klaassen, I., Vogels, I. M., Griffioen, A. W., Van Noorden, C. J., & Schlingemann, R. O. (2012). CD34 marks angiogenic tip cells in human vascular endothelial cell cultures. Angiogenesis, 15(1), 151–163. https://doi.org/10.1007/s10456-011-9251-z

[9] Carabotti, M., Scirocco, A., Maselli, M. A., & Severi, C. (2015). The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Annals of gastroenterology, 28(2), 203–209.

[10] Rhee, S. H., Pothoulakis, C., & Mayer, E. A. (2009). Principles and clinical implications of the brain-gut-enteric microbiota axis. Nature reviews. Gastroenterology & hepatology, 6(5), 306–314. https://doi.org/10.1038/nrgastro.2009.35

[11] 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 neuropharmacology, 14(8), 857–865. https://doi.org/10.2174/1570159x13666160502153022

[12] X M Cao, R A Koski, A Gashler, M McKiernan, C F Morris, R Gaffney, R V Hay, V P Sukhatme Molecular and Cellular Biology May 1990, 10 (5) 1931-1939; DOI: 10.1128/MCB.10.5.1931

[13] González-Aguilera, C., Tous, C., Babiano, R., de la Cruz, J., Luna, R., & Aguilera, A. (2011). Nab2 functions in the metabolism of RNA driven by polymerases II and III. Molecular biology of the cell, 22(15), 2729–2740. https://doi.org/10.1091/mbc.E11-01-0055

[14] Sikiric, P., Seiwerth, S., Rucman, R., Turkovic, B., Rokotov, D. S., Brcic, L., . . . Sebecic, B. (2012). Focus on Ulcerative Colitis: Stable Gastric Pentadecapeptide BPC 157. Current Medicinal Chemistry, 19(1), 126-132. doi:10.2174/092986712803414015

[15] Seiwerth, S., Rucman, R., Turkovic, B., Sever, M., Klicek, R., Radic, B., Drmic, D., Stupnisek, M., Misic, M., Vuletic, L. B., Pavlov, K. H., Barisic, I., Kokot, A., Japjec, M., Blagaic, A. B., Tvrdeic, A., Rokotov, D. S., Vrcic, H., Staresinic, M., … Sikiric, P. (2018). BPC 157 and Standard Angiogenic Growth Factors. Gastrointestinal Tract Healing, Lessons from Tendon, Ligament, Muscle and Bone Healing. Current Pharmaceutical Design, 24(18), 1972–1989. https://doi.org/10.2174/1381612824666180712110447

[16] Tarnawski, A. S., Ahluwalia, A., & Jones, M. K. (2014). Increased susceptibility of aging gastric mucosa to injury: the mechanisms and clinical implications. World journal of gastroenterology, 20(16), 4467–4482. https://doi.org/10.3748/wjg.v20.i16.4467

[17] Love S. (2006). Demyelinating diseases. Journal of clinical pathology, 59(11), 1151–1159. https://doi.org/10.1136/jcp.2005.031195

[18] Neubauer H, Cumano A, Müller M, Wu H, Huffstadt U, Pfeffer K (May 1998). "Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis". Cell. 93 (3): 397–409. doi:10.1016/S0092-8674(00)81168-X. PMID 9590174.

[19] Sikiric, P., Jelovac, N., Jelovac-Gjeldum, A., Dodig, G., Staresinic, M., Anic, T., Zoricic, I., Rak, D., Perovic, D., Aralica, G., Buljat, G., Prkacin, I., Lovric-Bencic, M., Separovic, J., Seiwerth, S., Rucman, R., Petek, M., Turkovic, B., Ziger, T., Boban-Blagaic, A., … Babic, S. (2002). Pentadecapeptide BPC 157 attenuates chronic amphetamine-induced behavior disturbances. Acta pharmacologica Sinica, 23(5), 412–422.

[20] Boban Blagaic, A., Blagaic, V., Mirt, M., Jelovac, N., Dodig, G., Rucman, R., Petek, M., Turkovic, B., Anic, T., Dubovecak, M., Staresinic, M., Seiwerth, S., & Sikiric, P. (2005). Gastric pentadecapeptide BPC 157 effective against serotonin syndrome in rats. European journal of pharmacology, 512(2-3), 173–179. https://doi.org/10.1016/j.ejphar.2005.02.033

[21] Peters R. (2006). Ageing and the brain. Postgraduate medical journal, 82(964), 84–88. https://doi.org/10.1136/pgmj.2005.036665

[22] O’Mahony et al., 2015 S.M. O’Mahony, G. Clarke, Y.E. Borre, T.G. Dinan, J.F. Cryan

Serotonin, tryptophan metabolism and the brain-gut-microbiome axis

Behav. Brain Res. (2015), 10.1016/j.bbr.2014.07.027

[23] National Center for Biotechnology Information (2020). PubChem Compound Summary for CID 108101. Retrieved August 4, 2020 from https://pubchem.ncbi.nlm.nih.gov/compound/108101.

[24] Sian J, Youdim MBH, Riederer P, et al. MPTP-Induced Parkinsonian Syndrome. In: Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven; 1999. Available from: https://www.ncbi.nlm.nih.gov/books/NBK27974/

[25] Sikiric P., Marovic A., Matoz W., Anic T., Buljat G., Mikus D., Stancic-Rokotov D., Separovic J., Seiwerth S., Grabarevic Z., Rucman R., Petek M., Ziger T., Sebecic B., Zoricic I., Turkovic B., Aralica G., Perovic D., Duplancic B., Lovric-Bencic M., Rotkvic I., Mise S., Jagic V., Hahn V. A behavioral study of the effect of pentadecapeptide BPC 157 in Parkinson’s disease models in mice and gastric lesions induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydrophyridine. J. Physiol. Paris. 1999;93(6):505–512. [http://dx.doi.org/10.1016/S0928-4257(99) 00119-9]. [PMID: 10672997].

[26] Sikiric, P., Seiwerth, S., Rucman, R., Turkovic, B., Stancic Rokotov, D., Brcic, L., Sever, M., Klicek, R., Radic, B., Drmic, D., Ilic, S., Kolenc, D., Vrcic, H., & Sebecic, B. (2011). Stable gastric Pentadecapeptide BPC 157: Novel therapy in gastrointestinal tract. Current 

Pharmaceutical Design, 17(16), 1612-1632. https://doi.org/10.2174/138161211796196954

[27] Pentadecapeptide BPC 157 interaction with other systems in gastric protection. (1995). Gastroenterology, 108(4), A220. https://doi.org/10.1016/0016-5085(95)23539-6

[28] Huang, T., Zhang, K., Sun, L., Xue, X., Zhang, C., Shu, Z., Mu, N., Gu, J., Zhang, W., Wang, Y., Zhang, Y., & Zhang, W. (2015). Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro. Drug design, development and therapy, 9, 2485–2499. https://doi.org/10.2147/DDDT.S82030

[29] Filosevic, A., Waldowski, R. A., Vidovic, T., Sikiric, P., & Drmic, D. (2017). Stable gastric pentadecapeptide BPC 157 antagonizes hydrogen peroxide induced oxidative stress in Drosophila melanogaster. The FASEB Journal, 31(1_supplement), 667-14.[30] Chang, C. H., Tsai, W. C., Lin, M. S., Hsu, Y. H., & Pang, J. H. S. (2011). The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. Journal of applied physiology.

[31] Park, J. M., Lee, H. J., Sikiric, P., & Hahm, K. B. (2020). BPC157 Rescued NSAID-cytotoxicity Via Stabilizing Intestinal Permeability and Enhancing Cytoprotection. Current Pharmaceutical Design.

[32] Sikirić, P., Petek, M., Ručman, R., Seiwerth, S., Grabarević, Z., Rotkvić, I., ... & Lang, N. (1993). A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. Journal of Physiology-Paris, 87(5), 313-327.

[33] Seiwerth, S., Brcic, L., Batelja Vuletic, L., Kolenc, D., Aralica, G., Misic, M., ... & Sikiric, P. (2014). BPC 157 and blood vessels. Current pharmaceutical design, 20(7), 1121-1125.

[34] Seiwerth, S., Sikiric, P., Grabarevic, Z., Zoricic, I., Hanzevacki, M., Ljubanovic, D., ... & Turkovic, B. (1997). BPC 157's effect on healing. Journal of Physiology-Paris, 91(3-5), 173-178.

[35] Xu, K., Sun, X., Puchowicz, M. A., & LaManna, J. C. (2008). Increased sensitivity to transient global ischemia in aging rat brain. In Oxygen Transport to Tissue XXVIII (pp. 199-206). Springer, Boston, MA.

[36] Davis, M., Mendelow, A. D., Perry, R. H., Chambers, I. R., & James, O. F. W. (1995). Experimental stroke and neuroprotection in the aging rat brain. Stroke, 26(6), 1072-1078.

[37] Ware, J. A., & Simons, M. (1997). Angiogenesis in ischemic heart disease. Nature medicine, 3(2), 158-164.

[38] Tomita, S., Mickle, D. A., Weisel, R. D., Jia, Z. Q., Tumiati, L. C., Allidina, Y., ... & Li, R. K. (2002). Improved heart function with myogenesis and angiogenesis after autologous porcine bone marrow stromal cell transplantation. The Journal of thoracic and cardiovascular surgery, 123(6), 1132-1140.

[39] Bosch-Marce, M., Okuyama, H., Wesley, J. B., Sarkar, K., Kimura, H., Liu, Y. V., ... & Zhou, Y. F. (2007). Effects of aging and hypoxia-inducible factor-1 activity on angiogenic cell mobilization and recovery of perfusion after limb ischemia. Circulation research, 101(12), 1310-1318.

[40] Koike, T., Vernon, R. B., Gooden, M. D., Sadoun, E., & Reed, M. J. (2003). Inhibited angiogenesis in aging: a role for TIMP-2. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 58(9), B798-B805.

[41] Sadoun, E., & Reed, M. J. (2003). Impaired angiogenesis in aging is associated with alterations in vessel density, matrix composition, inflammatory response, and growth factor expression. Journal of Histochemistry & Cytochemistry, 51(9), 1119-1130.

[42] Mechanisms of adaptive angiogenesis to tissue hypoxia.

Fong GH

Angiogenesis. 2008; 11(2):121-40.

[43] Pugh C, Ratcliffe P. Regulation of angiogenesis by hypoxia: Role of the hif system. Nat Med. 2003;9:677–684. 

[44] Lee S, Wolf P, Escudero R, Deutsch R, Jamieson S, Thistlethwaite P. Early expression of angiogenesis factors in acute myocardial ischemia and infarction. N Engl J Med. 2000;342:626–633.

[45] Hu, K., Babapoor-Farrokhran, S., Rodrigues, M., Deshpande, M., Puchner, B., Kashiwabuchi, F., Hassan, S. J., Asnaghi, L., Handa, J. T., Merbs, S., Eberhart, C. G., Semenza, G. L., Montaner, S., & Sodhi, A. (2016). Hypoxia-inducible factor 1 upregulation of both VEGF and ANGPTL4 is required to promote the angiogenic phenotype in uveal melanoma. Oncotarget, 7(7), 7816–7828. https://doi.org/10.18632/oncotarget.6868[46] Zhang, K., Lu, J., Mori, T., Smith-Powell, L., Synold, T. W., Chen, S., & Wen, W. (2011). Baicalin increases VEGF expression and angiogenesis by activating the ERR{alpha}/PGC-1{alpha} pathway. Cardiovascular research, 89(2), 426–435. https://doi.org/10.1093/cvr/cvq296

[47] Yeo E. J. (2019). Hypoxia and aging. Experimental & molecular medicine, 51(6), 1–15. https://doi.org/10.1038/s12276-019-0233-3

[48] Lubomirov, L. T., Papadopoulos, S., Pütz, S., Welter, J., Klöckener, T., Weckmüller, K., Ardestani, M. A., Filipova, D., Metzler, D., Metzner, H., Staszewski, J., Zittrich, S., Gagov, H., Schroeter, M. M., & Pfitzer, G. (2017). Aging-related alterations in eNOS and nNOS responsiveness and smooth muscle reactivity of murine basilar arteries are modulated by apocynin and phosphorylation of myosin phosphatase targeting subunit-1. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 37(3), 1014–1029. https://doi.org/10.1177/0271678X16649402

[49] Chen, K., Pittman, R. N., & Popel, A. S. (2008). Nitric oxide in the vasculature: where does it come from and where does it go? A quantitative perspective. Antioxidants & redox signaling, 10(7), 1185–1198. https://doi.org/10.1089/ars.2007.1959

[50] Hsieh, M. J., Liu, H. T., Wang, C. N., Huang, H. Y., Lin, Y., Ko, Y. S., Wang, J. S., Chang, V. H., & Pang, J. S. (2017). Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. Journal of molecular medicine (Berlin, Germany), 95(3), 323–333.

[51] Seiwerth, S., Sikiric, P., Grabarevic, Z., Zoricic, I., Hanzevacki, M., Ljubanovic, D., Coric, V., Konjevoda, P., Petek, M., Rucman, R., Turkovic, B., Perovic, D., Mikus, D., Jandrijevic, S., Medvidovic, M., Tadic, T., Romac, B., Kos, J., Peric, J., & Kolega, Z. (1997). BPC 157’s effect on healing. Journal of Physiology-Paris, 91(3–5), 173–178. https://doi.org/10.1016/s0928-4257(97)89480-6

[52] Hsieh, M.-J., Liu, H.-T., Wang, C.-N., Huang, H.-Y., Lin, Y., Ko, Y.-S., Wang, J.-S., Chang, V. H.-S., & Pang, J.-H. S. (2016). Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. Journal of Molecular Medicine, 95(3), 323–333. https://doi.org/10.1007/s00109-016-1488-y

[53]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 research, 28(9), 1155-1161.

[54] Balenovic, D., Bencic, M. L., Udovicic, M., Simonji, K., Hanzevacki, J. S., Barisic, I., ... & Coric, M. (2009). Inhibition of methyldigoxin-induced arrhythmias by pentadecapeptide BPC 157: a relation with NO-system. Regulatory peptides, 156(1-3), 83-89.

[55] Pipili‐Synetos, E., Sakkoula, E., & Maragoudakis, M. E. (1993). Nitric oxide is involved in the regulation of angiogenesis. British journal of pharmacology, 108(4), 855-857.

[56] Cooke, J. P. (2003). NO and angiogenesis. Atherosclerosis Supplements, 4(4), 53-60.

[57] Alaiti, M. A., Ishikawa, M., Masuda, H., Simon, D. I., Jain, M. K., Asahara, T., & Costa, M. A. (2012). Up‐regulation of miR‐210 by vascular endothelial growth factor in ex vivo expanded CD 34+ cells enhances cell‐mediated angiogenesis. Journal of cellular and molecular medicine, 16(10), 2413-2421.

[58] Clara, C. A., Marie, S. K., de Almeida, J. R. W., Wakamatsu, A., Oba‐Shinjo, S. M., Uno, M., ... & Rosemberg, S. (2014). Angiogenesis and expression of PDGF‐C, VEGF, CD 105 and HIF‐1α in human glioblastoma. Neuropathology, 34(4), 343-352.

[59] Eming, S. A., Brachvogel, B., Odorisio, T., & Koch, M. (2007). Regulation of angiogenesis: wound healing as a model. Progress in histochemistry and cytochemistry, 42(3), 115-170.

[60] Pettet, G. J., Byrne, H. M., McElwain, D. L. S., & Norbury, J. (1996). A model of wound-healing angiogenesis in soft tissue. Mathematical biosciences, 136(1), 35-63.

[61] 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 research, 1-7.

[62] Peake, J., Gatta, P. D., & Cameron-Smith, D. (2010). Aging and its effects on inflammation in skeletal muscle at rest and following exercise-induced muscle injury. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 298(6), R1485-R1495.

[63] Hsieh, M.-J., Liu, H.-T., Wang, C.-N., Huang, H.-Y., Lin, Y., Ko, Y.-S., Wang, J.-S., Chang, V. H.-S., & Pang, J.-H. S. (2016). Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. Journal of Molecular Medicine, 95(3), 323–333. https://doi.org/10.1007/s00109-016-1488-y

[64] Staresinic, M., Petrovic, I., Novinscak, T., Jukic, I., Pevec, D., Suknaic, S., ... & Zoric, Z. (2006). Effective therapy of transected quadriceps muscle in rat: gastric pentadecapeptide BPC 157. Journal of orthopaedic research, 24(5), 1109-1117.

[65] Foster, J. A., & Neufeld, K. A. M. (2013). Gut–brain axis: how the microbiome influences anxiety and depression. Trends in neurosciences, 36(5), 305-312.

[66] Cryan, J. F., & O’mahony, S. M. (2011). The microbiome‐gut‐brain axis: from bowel to behavior. Neurogastroenterology & Motility, 23(3), 187-192.

[67] Mayer, E. A., Tillisch, K., & Gupta, A. (2015). Gut/brain axis and the microbiota. The Journal of clinical investigation, 125(3), 926-938.

[68] Bonaz, B., Bazin, T., & Pellissier, S. (2018). The vagus nerve at the interface of the microbiota-gut-brain axis. Frontiers in neuroscience, 12, 49.

[69] Xue, X. C., Wu, Y. J., Gao, M. T., Li, W. G., Zhao, N., Wang, Z. L., ... & Zhang, Y. Q. (2004). Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats. World journal of gastroenterology, 10(7), 1032.

[70] Ilić, S., Brčić, I., Mešter, M., Filipović, M., Sever, M., Kliček, R., ... & Berkopić, L. (2009). Over-dose insulin and stable gastric pentadecapeptide BPC 157. attenuated gastric ulcers, seizures, brain lesions, hepatomegaly, fatty liver, breakdown of liver glycogen, profound hypoglycemia and calcification in rats. Journal of physiology and pharmacology, 60(S7), 107.

[71] Jelovac, N., Sikiric, P., Rucman, R., Petek, M., Marovic, A., Perovic, D., ... & Miklic, P. (1999). Pentadecapeptide BPC 157 attenuates disturbances induced by neuroleptics: the effect on catalepsy and gastric ulcers in mice and rats. European journal of pharmacology, 379(1), 19-31.

[72] Tkalcević, V. I., Cuzić, S., Brajsa, K., Mildner, B., Bokulić, A., Situm, K., Perović, D., Glojnarić, I., & Parnham, M. J. (2007). Enhancement by PL 14736 of granulation and collagen organization in healing wounds and the potential role of egr-1 expression. European journal of pharmacology, 570(1-3), 212–221. https://doi.org/10.1016/j.ejphar.2007.05.072

[73] Chang, C. H., Tsai, W. C., Lin, M. S., Hsu, Y. H., & 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 physiology (Bethesda, Md. : 1985), 110(3), 774–780. https://doi.org/10.1152/japplphysiol.00945.2010

[74] .-H. Chang, W.-C. Tsai, Y.-H. Hsu, and J.-H. Pang, “Pen-tadecapeptide BPC 157 enhances the growth hormone re-ceptor expression in tendon fibroblasts,”Molecules, vol. 19,no. 11, pp. 19066–19077, 2014.

[75] Topilko, P., Levi, G., Merlo, G., Mantero, S., Desmarquet, C., Mancardi, G., & Charnay, P. (1997). Differential regulation of the zinc finger genes Krox‐20 and Krox‐24 (Egr‐1) suggests antagonistic roles in Schwann cells. Journal of neuroscience research, 50(5), 702-712.

[76] Jones, E. A., Jang, S. W., Mager, G. M., Chang, L. W., Srinivasan, R., Gokey, N. G., Ward, R. M., Nagarajan, R., & Svaren, J. (2007). Interactions of Sox10 and Egr2 in myelin gene regulation. Neuron glia biology, 3(4), 377–387. https://doi.org/10.1017/S1740925X08000173

[77] St-Sauveur, V. G., Soucek, S., Corbett, A. H., & Bachand, F. (2013). Poly (A) tail-mediated gene regulation by opposing roles of Nab2 and Pab2 nuclear poly (A)-binding proteins in pre-mRNA decay. Molecular and cellular biology, 33(23), 4718-4731.

[78] Lucerna, M., Mechtcheriakova, D., Kadl, A., Schabbauer, G., Schäfer, R., Gruber, F., ... & Binder, B. R. (2003). NAB2, a corepressor of EGR-1, inhibits vascular endothelial growth factor-mediated gene induction and angiogenic responses of endothelial cells. Journal of Biological Chemistry, 278(13), 11433-11440.

[79] Sikiric, P., Hahm, K.-B., Blagaic, A. B., Tvrdeic, A., Pavlov, K. H., Petrovic, A., Kokot, A., Gojkovic, S., Krezic, I., Drmic, D., Rucman, R., & Seiwerth, S. (2020). Stable Gastric Pentadecapeptide BPC 157, Robert’s Stomach Cytoprotection/Adaptive Cytoprotection/Organoprotection, and Selye’s Stress Coping Response: Progress, Achievements, and the Future. Gut and Liver, 14(2), 153–167. https://doi.org/10.5009/gnl18490

[80] Tohyama, Y., Sikirić, P., & Diksic, M. (2004). Effects of pentadecapeptide BPC157 on regional serotonin synthesis in the rat brain: alpha-methyl-L-tryptophan autoradiographic measurements. Life sciences, 76(3), 345–357. https://doi.org/10.1016/j.lfs.2004.08.010

[81] Austin, J. H., Connole, E., Kett, D., & Collins, J. (1978). Studies in aging of the brain. V. Reduced norepinephrine, dopamine, and cyclic AMP in rat brain with advancing age. Age, 1(4), 121-124.

[82] Creasey, H., & Rapoport, S. I. (1985). The aging human brain. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society, 17(1), 2-10.

[83] Rinne, J. O. (1987). Muscarinic and dopaminergic receptors in the aging human brain. Brain Research, 404(1-2), 162-168.

[84] Rinne, J. O. (1987). Muscarinic and dopaminergic receptors in the aging human brain. Brain Research, 404(1-2), 162-168.

[85] de Keyser, J., De Backer, J. P., Vauquelin, G., & Ebinger, G. (1990). The effect of aging on the D1 dopamine receptors in human frontal cortex. Brain research, 528(2), 308-310.

[86] Wester, P., Hardy, J. A., Marcusson, J., Nyberg, P., & Winblad, B. (1984). Serotonin concentrations in normal aging human brains: relation to serotonin receptors. Neurobiology of aging, 5(3), 199-203.

[87] Kojic, L., Gu, Q., Douglas, R. M., & Cynader, M. S. (1997). Serotonin facilitates synaptic plasticity in kitten visual cortex: an in vitro study. Developmental Brain Research, 101(1-2), 299-304.

[88] Fernandez, S. P., Muzerelle, A., Scotto-Lomassese, S., Barik, J., Gruart, A., Delgado-García, J. M., & Gaspar, P. (2017). Constitutive and acquired serotonin deficiency alters memory and hippocampal synaptic plasticity. Neuropsychopharmacology, 42(2), 512-523.

Be the first to review this product.

Leave a review