Abstract
Background: Androgen receptor (AR) signaling is a main driver of prostate cancer progression and remains a crucial target for therapeutic intervention even in late stages of the disease. While current antiandrogen therapies that directly or indirectly target the AR ligand binding domain (LBD) are initially effective, resistance ultimately develops and new methods of inhibiting the AR pathway are needed. Recent advances in targeted protein degradation using the PROteolysis TArgeting Chimera (PROTAC) technology demonstrate that AR-LBD targeted PROTACs can selectively degrade AR but not splice variant forms of AR that are found in advanced castration-resistant prostate cancer (CRPC) patients.
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