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Mechanistically, much of BPC-157s activity is attributed to angiogenesis and modulation of the nitric oxide (NO) system, as reviewed by Sikiric et al

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This phenotype was explored in both mouse models and in vitro with an anti-IL-23 antibody to block IL-23 signaling where mice experienced prolonged survival and decreased tumor burden, and CD8 + cells in mice and in vitro showed enhanced cytotoxicity in the IL-23-depleted state [154] (Fig