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Tendon injuries initially suffer from: Poor blood supply Limited vascularity Slow nutrient delivery In rodent models, BPC-157 appears to: Upregulate VEGFR2 signalling Increase capillary density Improve microvascular perfusion Mechanistically: BPC-157 VEGFR2 activation PI3K/Akt pathway eNOS phosphorylation Increased nitric oxide Improved angiogenesis More vascularity = better nutrient and oxygen delivery to fibroblasts

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Failure to detect the presence of toxic AA produced as metabolites from candidate drugs early in drug development can result in costly late attrition

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