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Another potential pathway that enhances FXR activity involves the release of the growth factor fibroblast growth factor (FGF) 19 from the intestine upon bile acid binding to FXR, 66 which has shown beneficial effects on MASH in animal models, although results are conflicting

126 The upregulation of IDH1 may represent a common metabolic adaptation for diminishing oxidative stress and supporting macromolecular synthesis, consequently promoting tumor growth and therapy resistance

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Both are studied for lipolytic activity, but AOD-9604 has additional published data on cartilage and bone research applications