{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Loddick SA"],"funding":["Medical Research Council"],"pagination":["1715-27"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3769207"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(9)"],"pubmed_abstract":["Continued androgen receptor (AR) expression and signaling is a key driver in castration-resistant prostate cancer (CRPC) after classical androgen ablation therapies have failed, and therefore remains a target for the treatment of progressive disease. Here, we describe the biological characterization of AZD3514, an orally bioavailable drug that inhibits androgen-dependent and -independent AR signaling. AZD3514 modulates AR signaling through two distinct mechanisms, an inhibition of ligand-driven nuclear translocation of AR and a downregulation of receptor levels, both of which were observed in vitro and in vivo. AZD3514 inhibited testosterone-driven seminal vesicle development in juvenile male rats and the growth of androgen-dependent Dunning R3327H prostate tumors in adult rats. Furthermor"],"journal":["Molecular cancer therapeutics"],"pubmed_title":["AZD3514: a small molecule that modulates androgen receptor signaling and function in vitro and in vivo."],"pmcid":["PMC3769207"],"funding_grant_id":["G0800889","G0800889/1","G0900871"],"pubmed_authors":["Robinson DM","Gaughan L","Womack C","Wilson J","Broadbent N","Loddick SA","Critchlow SE","Brooks AN","Thomason AG","Barry ST","Brave SR","Bradbury RH","Jacobs VN","Rabow A","Robson CN","Mouchet E","Walker GE","Ross SJ","Shaheen FS","Stratton NC","Trueman D","Cumberbatch M","Wedge SR","Jones RD","Dunkley TP"],"additional_accession":[]},"is_claimable":false,"name":"AZD3514: a small molecule that modulates androgen receptor signaling and function in vitro and in vivo.","description":"Continued androgen receptor (AR) expression and signaling is a key driver in castration-resistant prostate cancer (CRPC) after classical androgen ablation therapies have failed, and therefore remains a target for the treatment of progressive disease. Here, we describe the biological characterization of AZD3514, an orally bioavailable drug that inhibits androgen-dependent and -independent AR signaling. AZD3514 modulates AR signaling through two distinct mechanisms, an inhibition of ligand-driven nuclear translocation of AR and a downregulation of receptor levels, both of which were observed in vitro and in vivo. AZD3514 inhibited testosterone-driven seminal vesicle development in juvenile male rats and the growth of androgen-dependent Dunning R3327H prostate tumors in adult rats. Furthermor","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Sep","modification":"2025-04-19T11:23:48.138Z","creation":"2019-03-27T01:15:47Z"},"accession":"S-EPMC3769207","cross_references":{"pubmed":["23861347"],"doi":["10.1158/1535-7163.MCT-12-1174","10.1158/1535-7163.mct-12-1174"]}}