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The published research base, predominantly preclinical with growing clinical extension, identifies several mechanisms of action
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To achieve this, we optimized the well-known peptide tripeptide-1 (GHK) by separately grafting the integrin v3-binding motif RGD and the chondroitin sulfate (CS)-binding motif sOtx2 onto it, forming two chimeric targeting peptides, RGD-GHK and sOtx2-GHK
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BPC 157 activated the Src-Cav-1-eNOS signal pathway and reduced eNOS/Cav-1 binding in vascular endothelial cells It is known that phosphorylation of Src can promote Cav-1 activation and subsequent endocytosis of tyrosine kinase receptors and eNOS activation 20,24
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