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FGF19dCTD is a research-grade biologic variant of fibroblast growth factor 19 (FGF19) engineered by deleting the C-terminal domain (CTD). This structural modification specifically abolishes the protein's ability to interact with the co-receptor βKlotho, which is required for FGF19 to activate FGFR1c, FGFR2c, and FGFR3c. Consequently, FGF19dCTD acts as a selective activator of fibroblast growth factor receptor 4 (FGFR4), which can be activated in a βKlotho-independent manner. In preclinical models, FGF19dCTD has been shown to regulate bile acid metabolism by suppressing CYP7A1 expression in the liver and modulating lipid metabolism, while lacking the glucose-lowering and insulin-sensitizing effects associated with wild-type FGF19. It serves as a critical tool for dissecting the receptor-specific pathways of FGF19 signaling and understanding the differential physiological effects of selective FGFR4 activation versus broader FGF receptor activation.
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