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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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Studies in animals show that AHK-Cu not only improves blood flow to existing hair follicles, but that it can promote the growth of new hair follicles by encouraging the growth of blood vessels

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It also modulates nitric oxide pathways to reduce inflammation and accelerate tendon-to-bone healing