By interrupting their interaction, were effectively collapsing the structural foundation that allows fibrosis to progress. Unlike traditional therapies that attempt to inhibit FAKs enzymatic activity often with poor specificity and side effects FN-2012 works by disrupting protein-protein binding
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Endothelial damage reduces nitric oxide bioavailability and elevates endothelin-1 levels, producing chronic vasoconstriction and segmental ischemiaan internal counterpart of Raynauds phenomenon within the mesenteric circulation [29,30]
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