The N-terminal AR antagonists such as EPI-002 (1), sintokamide A (2), and IMTPPE (3) (Figure 1) that were obtained from screening natural compound libraries have been demonstrated to have in vitro capability in inhibiting AR transactivation and AR-positive prostate cancer cell proliferation and in vivo anti-tumor efficacy in CRPC xenograft models [13]. The gene discussed is AR; the disease is neoplasm.