ARCC-4 selectively degrades AR via the proteasome but not PR-A or PR-B suppression[1] and it shows efficacy against clinically relevant AR mutations[1]. ARCC-4 maintains activity despite elevated androgen levels[1]. ARCC-4 enhances protein-protein interactions between AR and VHL, thereby promoting the association of the trimeric complex[1] and it induces apoptosis and inhibiting proliferation of AR-amplified prostate cancer cells[1]. ARCC-4 (0.1-10,000 nM; 20 hours) potently degrades AR with a D50 of 5?nM and Dmax of over 95%[1]. ARCC-4 (100?nM; 12 hours) shows near complete AR degradation (>98%) in prostate cancer cells[1].