Inhibitor of Androgen Receptor (AR) dependent gene expression.
MJC13 inhibits the positive regulation of androgen receptor (AR) signaling by the cochaperone protein FKBP52. The molecule inhibits hormone-induced dissociation of the FKBP52, nuclear translocation of AR and AR dependent gene expression. MJC13 inhibits proliferation of the androgen-dependent prostate cancer cell lines LNCaP and LAPC4.
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American journal of modern chromatography, 1(1), 1-11 (2015-01-17)
MJC13 is a novel molecule that has potential use for the treatment of hormone refractory prostate cancer (HRPC). The purpose of this work was to develop a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for quantification of MJC13. Itraconazole was used
Androgen ablation therapy is the most common treatment for advanced prostate cancer (PCa), but most patients will develop castration-resistant prostate cancer (CRPC), which has no cure. CRPC is androgen-depletion resistant but androgen receptor (AR) dependent. AR is a nuclear receptor
The growth of prostate cancer is dependent on the androgen receptor (AR), which serves as a ligand-specific transcription factor. Although two immunophilins, FKBP51 and FKBP52, are known to regulate AR activity, the precise mechanism remains unclear. We found that depletion
The androgen receptor (AR) surface-directed antagonist MJC13 inhibits AR function and proliferation of prostate cancer (PC) cells. These effects are related to arrest of an AR/chaperone complex in the cytoplasm. Here, we compared MJC13 and classic AR antagonists such as
Proceedings of the National Academy of Sciences of the United States of America, 108(29), 11878-11883 (2011-07-07)
Drugs that target novel surfaces on the androgen receptor (AR) and/or novel AR regulatory mechanisms are promising alternatives for the treatment of castrate-resistant prostate cancer. The 52 kDa FK506 binding protein (FKBP52) is an important positive regulator of AR in
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