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Discovery of First-in-Class FXR and HSD17B13 Dual Modulator for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease.
J Med Chem
January 2025
School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, P. R. China.
Metabolic dysfunction-associated steatohepatitis (MASH) is a complex disease driven by diverse metabolic and inflammatory pathways. Farnesoid X receptor (FXR) is a promising target for MASH due to its role in bile acid and lipid metabolism, while HSD17B13 regulates liver lipid droplet homeostasis. However, the existing HSD17B13 inhibitors have several druglike property challenges due to the common phenolic structure, a key pharmacophore for the HSD17B13 inhibitor.
View Article and Find Full Text PDFDiscovery of Fluorescent Probe ABDS-2 for Farnesoid X Receptor Modulator Characterization and Cell-Based Imaging.
Anal Chem
January 2025
School of Basic Medical Sciences, Guangzhou Νational Laboratory, Guangzhou Medical University, Guangzhou 511436, China.
The farnesoid X receptor (FXR) regulates key physiological processes, such as bile acid homeostasis and lipid metabolism, making it an important target for drug discovery. However, the overactivation of FXR often leads to adverse effects. This study presents the development of a novel fluorescent probe utilizing the computer-aided drug design (CADD) approach to optimize linkers between more potent warhead and FITC fluorescent groups.
View Article and Find Full Text PDFThe histamine pathway is a target to treat hepatic experimental erythropoietic protoporphyria.
Cell Mol Gastroenterol Hepatol
January 2025
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ, USA. Electronic address:
Background & Aims: Erythropoietic protoporphyria (EPP) is caused by mutations in ferrochelatase which inserts iron into protoporphyrin-IX (PP-IX) to generate heme. EPP is characterized by PP-IX accumulation, skin photosensitivity, cholestasis, and end-stage liver disease. Despite available drugs that address photosensitivity, treatment of EPP-related liver disease remains an unmet need.
View Article and Find Full Text PDFDuodenal-jejunal bypass ameliorates MASLD in rats by regulating gut microbiota and bile acid metabolism through FXR pathways.
Hepatol Commun
February 2025
Department of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Background: Although bariatric and metabolic surgical methods, including duodenal-jejunal bypass (DJB), were shown to improve metabolic dysfunction-associated steatotic liver disease (MASLD) in clinical trials and experimental rodent models, their underlying mechanisms remain unclear. The present study therefore evaluated the therapeutic effects and mechanisms of action of DJB in rats with MASLD.
Methods: Rats with MASLD were randomly assigned to undergo DJB or sham surgery.
FXR Activation Accelerates Early Phase of Osteoblast Differentiation Through COX-2-PGE-EP4 Axis in BMP-2-Induced Mouse Mesenchymal Stem Cells.
Molecules
December 2024
Graduate School of Pharmaceutical Sciences, Hiroshima International University, 5-1-1, Hirokoshingai, Kure 737-0112, Japan.
Farnesoid X receptor (FXR), a nuclear receptor, is expressed in calvaria and bone marrow stromal cells and plays a role in bone homeostasis. However, the mechanism of FXR-activated osteoblast differentiation remains unclear. In this study, we investigated the regulatory mechanism underlying FXR-activated osteoblast differentiation using bone morphogenetic protein-2 (BMP-2)-induced mouse ST-2 mesenchymal stem cells.
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