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From a molecular point of view, the necroptosis pathway is initiated by auto- and trans-phosphorylation of RIPK1 and RIPK3 at Ser-227, resulting in stimulation of their kinase activity and assembly of a heterodimer protein complex termed necrosome via their RIPK homotypic interaction motif domains (Fulda, 2013

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BPC-157, by contrast, operates largely through modulation of the nitric oxide (NO) system and upregulation of growth factor expression, including VEGF and EGF, supporting angiogenesis and granulation tissue formation

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