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1) Pro-angiogenic signaling (VEGFR2 Akt eNOS) In cell and animal models, BPC-157 increases VEGFR2 expression/internalization and activates downstream Akt-eNOS signaling, supporting endothelial tube formation and blood-flow recovery after ischemia

Chen H, Yang P, Xue P, Li S, Dan X, Li Y, et al

Nrf2, a key transcription factor in oxidative stress response, is typically degraded by KEAP1 under normal conditions (71)

This has been purported to potentially increase the average lifespan of various experimental models by 1131% and may reduce mortality in murine models by a suggested 52%