AR antagonist 17 

AR antagonist 17 is a selective, orally active, low brain-penetrant Androgen Receptor (AR) antagonist (IC₅₀ = 0.010 μM), effectively blocking AR dimerization and nuclear translocation, and demonstrating potent efficacy in several castration-resistant prostate cancer (CRPC) cells. AR antagonist 17 showed superior efficacy against variant drug-resistant AR mutants. AR antagonist 17 can inhibit tumor growth in an LNCaP xenograft model without apparent toxicity. AR antagonist 17 can be used for the study of castration-resistant prostate cancer (CRPC)^[1].

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.

AR antagonist 17 (5 mg/kg, oral gavage, 2-8 h) has low blood-brain barrier permeability in SD Rats, may have better safety and reduce central nervous system-related side effects^[1].
AR antagonist 17 (40 mg/kg, oral gavage, twice daily for 32 days) demonstrates significant tumor growth suppression throughout the treatment duration and does not induce significant body weight loss or other signs of toxicity during the experiment in CB17 SCID mice^[1].

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

499.53

C₂₁H₂₀F₃N₃O₄S₂

3064715-04-1

CC1=C(C=C(O1)C2=CC=CC(C(F)(F)F)=C2)C(NC3=NC(CN4CCS(=O)(CC4)=O)=CS3)=O

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• [1]. Liao J, et al. Discovery of N-(thiazol-2-yl) Furanamide Derivatives as Potent Orally Efficacious AR Antagonists with Low BBB Permeability. J Med Chem. 2025 Sep 25;68(18):19688-19713.  [Content Brief]