Pentadecapeptide BPC157

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Last update: 2017-10-16 23:46
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Raw Peptides Powder Pentadecapeptide BPC157

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Alias: Booly Protection Compound 15, Pentadecapeptide, BPC 157
CAS: 137525-51-0
Sequence: Gly-Glu-Pro-Pro-Pro-Gly- Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val
MF: C62H98N16O22
MW: 1419.53552
Purity: 99%
Appearance: White Lyophilized Powder
Method of Analysis: HPLC
Storage: Lyophilized peptides although stable at room temperature for 3 months, should be stored desiccated below -18° C. Upon reconstitution of the peptide it should be stored at 4° C between 2-21 days and for future use below -18° C.

Dececription;

The anti-nociceptive effects of a newly synthesized pentadecapeptide coded BPC 157 (an essential fragment of new organoprotective gastric juice peptide BPC) was evaluated in comparison with aspirin reference standards, in various experimental models of indirect/direct nociception and neurotoxicity: writhing (acetic acid/magnesium sulphate), tail pinching, hot-plate, and capsaicin application. BPC 157 administered either in the ng or μg per kg range, intraperitoneally, significantly reduced the reactions in the writhing (inflammatory and non-inflammatory, prostaglandin-dependent and independent) and tail pinching tests.

BPC 157 markedly increased the in vitro migration of tendon fibroblasts in a dose-dependent manner as revealed by transwell filter migration assay. BPC 157 also dose dependently accelerated the spreading of tendon fibroblasts on culture dishes. The F-actin formation as detected by FITC-phalloidin staining was induced in BPC 157-treated fibroblasts. The protein expression and activation of FAK and paxillin were determined by Western blot analysis, and the phosphorylation levels of both FAK and paxillin were dose dependently increased by BPC 157 while the total amounts of protein was unaltered. In conclusion, BPC 157 promotes the ex vivo outgrowth of tendon fibroblasts from tendon explants, cell survival under stress, and the in vitro migration of tendon fibroblasts, which is likely mediated by the activation of the FAK-paxillin pathway.
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