| Literature DB >> 28112924 |
Elizabeth A Jurica1, Ximao Wu1, Kristin N Williams1, Andres S Hernandez1, David S Nirschl1, Richard A Rampulla1, Arvind Mathur1, Min Zhou1, Gary Cao1, Chunshan Xie1, Biji Jacob1, Hong Cai1, Tao Wang1, Brian J Murphy1, Heng Liu1, Carrie Xu1, Lori K Kunselman1, Michael B Hicks1, Qin Sun1, Dora M Schnur1, Doree F Sitkoff1, Elizabeth A Dierks1, Atsu Apedo1, Douglas B Moore1, Kimberly A Foster1, Mary Ellen Cvijic1, Reshma Panemangalore1, Neil A Flynn1, Brad D Maxwell1, Yang Hong1, Yuan Tian1, Jason J Wilkes1, Bradley A Zinker1, Jean M Whaley1, Joel C Barrish1, Jeffrey A Robl1, William R Ewing1, Bruce A Ellsworth1.
Abstract
A novel series of pyrrolidine-containing GPR40 agonists is described as a potential treatment for type 2 diabetes. The initial pyrrolidine hit was modified by moving the position of the carboxylic acid, a key pharmacophore for GPR40. Addition of a 4-cis-CF3 to the pyrrolidine improves the human GPR40 binding Ki and agonist efficacy. After further optimization, the discovery of a minor enantiomeric impurity with agonist activity led to the finding that enantiomers (R,R)-68 and (S,S)-68 have differential effects on the radioligand used for the binding assay, with (R,R)-68 potentiating the radioligand and (S,S)-68 displacing the radioligand. Compound (R,R)-68 activates both Gq-coupled intracellular Ca2+ flux and Gs-coupled cAMP accumulation. This signaling bias results in a dual mechanism of action for compound (R,R)-68, demonstrating glucose-dependent insulin and GLP-1 secretion in vitro. In vivo, compound (R,R)-68 significantly lowers plasma glucose levels in mice during an oral glucose challenge, encouraging further development of the series.Entities:
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Year: 2017 PMID: 28112924 DOI: 10.1021/acs.jmedchem.6b01559
Source DB: PubMed Journal: J Med Chem ISSN: 0022-2623 Impact factor: 7.446