AR antagonist 17

AR antagonist 17 (Compound C13) shows excellent AR antagonistic activity and antiproliferative effects against AR-positive PCa cell lines (LNCaP (IC_{50 = 1.02 μM), C4−2B (IC50 = 3.86 μM), 22RV1 (IC50 = 8.45 μM), and VCaP (IC50 = 5.72 μM)), accompanied by low toxicity on normal cell lines 3T3 and Ges-1 (IC50 > 20 μM)^[1].
AR antagonist 17 (0.2-2 μM, 2 weeks) completely inhibits clonal proliferation in LNCaP cells^[1].
AR antagonist 17 (0.02-2 μM, 48 h) dose-dependently suppresses the dihydrotestosterone (DHT)-induced transcriptional levels of prostate-specific antigen (PSA), and remarkably suppresses mRNA levels of two AR-regulated downstream genes, FKBP5 and TMPRSS2 in LNCaP cells^[1].
AR antagonist 17 (0.1-10 μM, 24 h) dose-dependently inhibits endogenous PSA protein expression but has no significant effect on AR protein expression in LNCaP cells^[1].
AR antagonist 17 (0.1-10 μM, 4 h) inhibits DHT-induced AR dimerization in a dose-dependent manner, and completely blocks this process at 10 μM in 293T cells^[1].
AR antagonist 17 (10 μM, 8 h) can cause AR to remain mainly in the cytoplasm and effectively prevent AR nuclear translocation in LNCaP cells^[1].
AR antagonist 17 demonstrates excellent antagonistic activity against these clinically prevalent AR resistance mutations, ARF877L/T878A (IC50 = 0.35 μM), ARW742C (IC50 = 0.50 μM), ARF877L (IC50 = 0.070 μM)^[1].
AR antagonist 17 (2 μM, 48 h) significantly suppresses eight clinically relevant PCa recurrence markers: KLK3 (encoding PSA), TMPRSS2, KLK2, NKX3.1, SLC45A3, PMEPA1, TARP, and TM4SF1, alongside cancer-related processes, apoptosis regulators STK39, HERC3, and GRIN3A in LNCaP cells^[1].
AR antagonist 17 (2 μM, 48 h) significantly inhibits the expression of the pan-cancer-related biomarkers for DNA biosynthesis and repair, including EXO1, CYP11A1, PGC, RRM2, and FAM111B in LNCaP cells^[1].}

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.