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Multiple preclinical studies have identified that BPC-157 increases vascular endothelial growth factor (VEGF) protein and gene expression, a critical pathway in tissue repair and regeneration
Where BPC-157 and TB-500 act primarily through actin/cytoskeletal and growth-factor pathways, GHK-Cu's mechanism is dominated by transcriptional reprogramming via copper-dependent gene regulation, making it a complementary research tool when investigators wish to dissect transcription-driven from structural-protein-driven repair phenotypes
The integrity of the endothelium and oxidative damage could be restored and reversed respectively, which was linked to the increased expression and internalisation of VEGFR2
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