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C max , peak concentration of drug in plasma

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

MOTS-c improves metabolic flexibility, insulin sensitivity, and cellular energy regulation by acting on mitochondrial signaling

It shows there's a relentless drive to iterate and improve upon existing molecules

As we get older, the production of both slows down

This may temporarily support metabolic efficiency and energy production during structured weight loss