| Literature DB >> 26155854 |
Emmanuel H Demont, Chun-wa Chung, Rebecca C Furze, Paola Grandi1, Anne-Marie Michon1, Chris Wellaway, Nathalie Barrett, Angela M Bridges, Peter D Craggs, Hawa Diallo, David P Dixon, Clement Douault, Amanda J Emmons, Emma J Jones, Bhumika V Karamshi, Kelly Locke, Darren J Mitchell, Bernadette H Mouzon, Rab K Prinjha, Andy D Roberts2, Robert J Sheppard, Robert J Watson, Paul Bamborough.
Abstract
Overexpression of ATAD2 (ATPase family, AAA domain containing 2) has been linked to disease severity and progression in a wide range of cancers, and is implicated in the regulation of several drivers of cancer growth. Little is known of the dependence of these effects upon the ATAD2 bromodomain, which has been categorized as among the least tractable of its class. The absence of any potent, selective inhibitors limits clear understanding of the therapeutic potential of the bromodomain. Here, we describe the discovery of a hit from a fragment-based targeted array. Optimization of this produced the first known micromolar inhibitors of the ATAD2 bromodomain.Entities:
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Year: 2015 PMID： 26155854 DOI： 10.1021/acs.jmedchem.5b00772
Source DB: PubMed Journal: J Med Chem ISSN： 0022-2623 Impact factor: 7.446