| HRA000921
(Open Access)
|
Clinical resistance such as androgen receptor (AR) mutation, AR overexpression and AR splice variants restrict the second-generation antiandrogens benefit in castration-resistant prostate cancer (CRPC) patients. Several strategies have been involved in the development of novel antiandrogens to circumvent the occurring resistance. In this work, based on rational drug design, we discovered and identified a bifunctional small molecule Z15 as a potent AR antagonist and the AR selective degrader. Here, in this bioproject, we performed a RNA-seq to analysis the influence of Z15 on prostate cancer cells. |
