Journal
CANCER RESEARCH
Volume 71, Issue 4, Pages 1208-1213Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN_10-3398
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Funding
- Canadian Institutes of Health Research [MOP79308, PPP90150, MOP89902]
- U.S. Army [W81XWH-05-0058, W81XWH-07-1-0260]
- U.S. National Cancer Institutes [2R01 CA105304]
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Androgen ablation therapy remains the gold standard for the treatment of advanced prostate cancer, but unfortunately, it is not curative, and eventually the disease will return as lethal castration-resistant prostate cancer (CRPC). Mounting evidence supports the concept that development of CRPC is causally related to continued transactivation of androgen receptor (AR). All current therapies that target the AR are dependent on the presence of its C-terminal ligand-binding domain (LBD). However, it is the N-terminal domain (NTD) of the AR that is the Achilles' heel of AR activity, with AF-1 being essential for AR activity regardless of androgen. Recent efforts to develop drugs to the AR NTD have yielded EPI-001, a small molecule, sintokamide peptides, and decoys to the AR NTD with EPI-001, the best characterized and most promising for clinical development based upon specificity, low toxicity, and cytoreductive antitumor activity. Cancer Res; 71(4); 1208-13. (C)2011 AACR.
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