fk-866 and Colitis--Ulcerative

fk-866 has been researched along with Colitis--Ulcerative* in 1 studies

Other Studies

1 other study(ies) available for fk-866 and Colitis--Ulcerative

Article	Year
NAD metabolism fuels human and mouse intestinal inflammation. Gut, 2018, Volume: 67, Issue:10 Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD. We investigated the impact of NAMPT inhibition by the small-molecule inhibitor FK866 in the dextran sulfate sodium (DSS) model of colitis and the azoxymethane/DSS model of colitis-associated cancer. The impact of NAD depletion on differentiation of mouse and human primary monocytes/macrophages was studied in vitro. Finally, we tested the efficacy of FK866 compared with dexamethasone and infliximab in lamina propria mononuclear cells (LPMNC) isolated from patients with IBD.. Our data emphasise the importance of NAD immunometabolism for mucosal immunity and highlight FK866-mediated NAMPT blockade as a promising therapeutic approach in acute intestinal inflammation. Topics: Acrylamides; Animals; Cell Differentiation; Colitis, Ulcerative; Colonic Neoplasms; Dexamethasone; Energy Metabolism; Gastrointestinal Agents; Humans; Infliximab; Intestinal Mucosa; Macrophages; Mice; Monocytes; NAD; Nicotinamide Phosphoribosyltransferase; Piperidines	2018

Article

Year

NAD metabolism fuels human and mouse intestinal inflammation.

Gut, 2018, Volume: 67, Issue:10

Nicotinamide phosphoribosyltransferase (NAMPT, also referred to as pre-B cell colony-enhancing factor or visfatin) is critically required for the maintenance of cellular nicotinamide adenine dinucleotide (NAD) supply catalysing the rate-limiting step of the NAD. We investigated the impact of NAMPT inhibition by the small-molecule inhibitor FK866 in the dextran sulfate sodium (DSS) model of colitis and the azoxymethane/DSS model of colitis-associated cancer. The impact of NAD depletion on differentiation of mouse and human primary monocytes/macrophages was studied in vitro. Finally, we tested the efficacy of FK866 compared with dexamethasone and infliximab in lamina propria mononuclear cells (LPMNC) isolated from patients with IBD.. Our data emphasise the importance of NAD immunometabolism for mucosal immunity and highlight FK866-mediated NAMPT blockade as a promising therapeutic approach in acute intestinal inflammation.

Topics: Acrylamides; Animals; Cell Differentiation; Colitis, Ulcerative; Colonic Neoplasms; Dexamethasone; Energy Metabolism; Gastrointestinal Agents; Humans; Infliximab; Intestinal Mucosa; Macrophages; Mice; Monocytes; NAD; Nicotinamide Phosphoribosyltransferase; Piperidines

2018