Androgen receptor allosteric antagonist 1

D36 (30 μM; 48 h) disrupts the AR/gelsolin interaction in a mammalian two-hybrid screening assay in HepG2 cells and inhibits R1881-induced AR transcriptional activation in an MMTV-luciferase reporter assay in LNCaP cells^[1].
D36 (5-30 μM; 48 h) allosterically inhibits AR activity in an MMTV-luciferase reporter dose-response assay in LNCaP cells, decreasing Vmax and slightly increasing EC₅₀ (<3-fold), with a calculated Ki of 9.0 μM^[1].
D36 (1-40 μM; 24 h) dose-dependently inhibits R1881 (500 pM)-induced PSA mRNA expression in a qPCR assay in LAPC4 cells and suppresses the expression of multiple endogenous AR target genes in LNCaP cells^[1].
D36 (1 nM-100 μM; 7 days) inhibits both basal and androgen-stimulated proliferation in cell proliferation assays in LAPC4, LNCaP (SR/SRAR), and VCaP cells; it retains full antagonist activity in AR-overexpressing hormone-refractory models (SRAR LNCaP, VCaP), with DNA content not reduced below baseline levels, indicating no cytotoxicity^[1].
D36 (20-30 μM; 24 h) causes only a modest reduction in AR protein levels (normalized to GAPDH) in Western blot assays in LAPC4 and LNCaP cells^[1].
D36 (30 μM; 4 h) does not induce AR nuclear translocation in a nuclear-cytoplasmic fractionation assay in SRAR LNCaP cells (unlike R1881, OHF, and Csx), and inhibits the recruitment of AR and cofactors (Pol II, p300, SRC1, TRAP220) to the PSA enhancer in a ChIP assay^[1].
D36 (20-150 μM; SPR injection) directly binds to full-length AR saturated with R1881 in a surface plasmon resonance assay, with K_d=90 μM, kon=135 M^-1s^-11, and koff=0.012 s^-1[1].
D36 (near IC₅₀ concentration) effectively competes with R1881 for AR binding in a 3H-R1881 whole-cell competition binding assay in VCaP cells^[1].

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