A Phase 2, Randomized, Double-Blind, Double-Dummy, Placebo-Controlled Study Evaluating the Safety and Efficacy of Semaglutide, and the Fixed-Dose Combination of Cilofexor and Firsocostat, Alone and in Combination, in Subjects With Compensated Cirrhosis (F4) Due to Nonalcoholic Steatohepatitis (NASH)

The goals of this clinical study are to learn more about the study drugs, semaglutide (SEMA) with the fixed-dose combination (FDC) of cilofexor/firsocostat (CILO/FIR), and understand whether they cause fibrosis improvement and Nonalcoholic Steatohepatitis (NASH) resolution in participants with cirrhosis due to NASH.

Start Date09 Aug 2021

Sponsor / Collaborator

Gilead Sciences, Inc.

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100 Clinical Results associated with FXR x ACC2 x ACC1

100 Translational Medicine associated with FXR x ACC2 x ACC1

0 Patents (Medical) associated with FXR x ACC2 x ACC1

Literatures (Medical) associated with FXR x ACC2 x ACC1

01 Jun 2013·HepatologyQ1 · MEDICINE

Adiponectin, bile acids, and burnt-out nonalcoholic steatohepatitis: New light on an old paradox

Q1 · MEDICINE

Communications

Author: Trauner, Michael ; Claudel, Thierry

This article discusses the adiponectin, bile acids, and burnt-out nonalcoholic steatohepatitis.Role of adiponectin in advanced NASH patients have great potential to reveal new mol. mechanisms responsible for progression from NASH to cirrhosis were discussed.Correlation between hepatic adiponectin staining and AMPK and acetyl-CoA carboxylase 1 and 2 (ACC1/ACC2) phosphorylation were discussed.The gut microbiota is also able to alter bile acid metabolism and signaling by way of deconjugation and dehydroxylation, resulting in formation of secondary more hydrophobic BA with altered ligand binding properties for TGR5 and farnesoid X receptor were discussed.

01 Jan 2011·Biological and Pharmaceutical BulletinQ4 · MEDICINE

Fibroblast Growth Factor 19 Treatment Ameliorates Disruption of Hepatic Lipid Metabolism in Farnesoid X Receptor (Fxr)-Null Mice

Q4 · MEDICINE

Article

Author: Sakaida, Yumi ; Matsuzawa, Hitomi ; Yamazoe, Yasushi ; Yoshinari, Kouichi ; Miyata, Masaaki

Human fibroblast growth factor 19 (FGF19) is an enterohepatic hormone that is involved in the regulation of hepatic metabolism of bile acids, lipids, and glucose. Farnesoid X receptor (Fxr)-null mice exhibit steatosis-like symptoms, showing higher hepatic lipid levels than with the wild-type mice. We investigated the influence of FGF19 treatment on hepatic lipogenesis in Fxr-null mice. Recombinant FGF19 treatment (400 µg/kg/d) for 3 d prevented the accumulation of lipid droplets and decreased serum alanine aminotransferase activity and hepatic lipid levels, including those of triglycerides and free fatty acids. The treatment significantly decreased the hepatic mRNA levels of acetyl-CoA carboxylase 1 (Acc1), Cd36, and sterol regulatory element-binding protein-1c (Srebp-1c) as well as those of acetyl-CoA carboxylase 2 (Acc2), stearoyl CoA desaturase 1 (Scd1), and Cyp7a1. FGF19 treatment (4 µg/kg/d) for 3 d also decreased the hepatic free fatty acid levels and mRNA levels of Acc1, Cd36, and Srebp-1c. These results indicate that FGF19-mediated signaling ameliorates disrupted hepatic lipogenesis in Fxr-null mice.

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