| Literature DB >> 27190605 |
Alexander M Taylor1, Alexandre Côté1, Michael C Hewitt1, Richard Pastor2, Yves Leblanc1, Christopher G Nasveschuk1, F Anthony Romero2, Terry D Crawford2, Nico Cantone1, Hariharan Jayaram1, Jeremy Setser1, Jeremy Murray2, Maureen H Beresini2, Gladys de Leon Boenig2, Zhongguo Chen3, Andrew R Conery1, Richard T Cummings1, Leslie A Dakin1, E Megan Flynn2, Oscar W Huang2, Susan Kaufman2, Patricia J Keller1, James R Kiefer2, Tommy Lai3, Yingjie Li3, Jiangpeng Liao3, Wenfeng Liu3, Henry Lu3, Eneida Pardo1, Vickie Tsui2, Jian Wang3, Yongyun Wang3, Zhaowu Xu3, Fen Yan3, Dong Yu3, Laura Zawadzke1, Xiaoqin Zhu3, Xiaoyu Zhu3, Robert J Sims1, Andrea G Cochran2, Steve Bellon1, James E Audia1, Steven Magnuson2, Brian K Albrecht1.
Abstract
CBP and EP300 are highly homologous, bromodomain-containing transcription coactivators involved in numerous cellular pathways relevant to oncology. As part of our effort to explore the potential therapeutic implications of selectively targeting bromodomains, we set out to identify a CBP/EP300 bromodomain inhibitor that was potent both in vitro and in cellular target engagement assays and was selective over the other members of the bromodomain family. Reported here is a series of cell-potent and selective probes of the CBP/EP300 bromodomains, derived from the fragment screening hit 4-methyl-1,3,4,5-tetrahydro-2H-benzo[b][1,4]diazepin-2-one.Entities:
Keywords: Bromodomain; CBP; CREBBP; EP300; benzodiazepinone
Year: 2016 PMID： 27190605 PMCID： PMC4867486 DOI： 10.1021/acsmedchemlett.6b00075
Source DB: PubMed Journal: ACS Med Chem Lett ISSN： 1948-5875 Impact factor: 4.345