Abstract
Background: Inhibition of the androgen receptor (AR) is the mainstay treatment for advanced prostate cancer. While initially effective, the disease ultimately progresses to metastatic castration-resistant prostate cancer (mCRPC), which is lethal. All current AR-targeted therapies directly or indirectly target the ligand binding domain (LBD). We have developed the EPI and sintokamide (SINT) compounds which target the AR N-terminal domain (NTD), allowing for sustained inhibition in the context of constitutively active AR-splice variants and mutations which often drive resistance to current AR-targeted therapies.
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