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BPC-157 works through at least five confirmed molecular mechanisms: eNOS upregulation increasing nitric oxide (L-NAME blockade confirms NO-dependence), VEGFR2 upregulation driving angiogenesis (+44% CD31+ microvessel density, abolished by anti-VEGFR2 antibody), FAK-paxillin pathway activation driving cell migration (+3852% scratch closure, abolished by FAK inhibitor), growth hormone receptor sensitisation relevant to tendon-to-bone healing, and NF-B suppression reducing TNF- and IL-6

It is the most abundant molecule (endogenous antioxidant) with the lowest molecular weight