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
FKBP52 and β-catenin have emerged in recent years as attractive targets for prostate cancer treatment. β-catenin interacts directly with the androgen receptor (AR) and has been characterized as a co-activator of AR-mediated transcription. FKBP52 is a positive regulator of AR
Pharmaceutical development and technology, 21(1), 121-126 (2014-11-08)
MJC13, a novel FKBP52 targeting agent, has potential use for the treatment of castration-resistant prostate cancer. The purpose of this work was to develop a solution formulation of MJC13, and obtain its efficacy profile in a human prostate cancer xenograft
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
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