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BPC-157: NO system modulation, VEGF/FGF-2 upregulation, FAK-paxillin pathway, gastric juice stability GHK-Cu: Cu2+-dependent gene regulation (~4,000 genes), TGF-beta signaling, collagen/decorin synthesis, SOD/catalase induction BPC-157: No metal cofactor required – activity is sequence-dependent GHK-Cu: Copper stoichiometry (1:1) is essential – apo-GHK shows reduced bioactivity BPC-157 Research Areas: Gut & Tendon Studies The majority of BPC-157 research originates from a single laboratory group (Sikiric et al., University of Zagreb), which has published extensively on its effects in rodent models

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Tendon and ligament repair Rodent models of transected Achilles tendon, medial collateral ligament injury and tendon-to-bone healing have been used to study BPC-157. The proposed mechanism involves increased fibroblast migration and outgrowth from tendon explants, mediated by FAK-paxillin signalling and upregulation of growth-hormone receptor expression in tendon fibroblasts