ARD-1676

ARD-1676 (4 days) inhibits the growth of VCaP human prostate cancer cells, with an IC₅₀ of 11.5 nM after 4 days of co-incubation with 0.1 nM R1881^[1].
ARD-1676 (4 days) inhibits the growth of human prostate cancer LNCaP cells, with an IC₅₀ of 2.8 nM after 4 days of co-incubation with 0.1 nM R1881^[1].
ARD-1676 (10-100 nM; 1-24 h) induces rapid degradation of AR in human prostate cancer cell lines VCaP and LNCaP. At concentrations of 10 nM and 100 nM, the degradation rate exceeds 50% within 1 h, and reaches the maximum degradation level at 3-6 h^[1].
ARD-1676 (0.03-30 nM; 24 h) potently inhibits AR-regulated KLK3 and TMPRSS2 gene expression in VCaP and LNCaP human prostate cancer cells^[1].
ARD-1676 (1 nM-10 μM; 24 h) potently and efficiently degrades most clinically relevant AR mutants (including wild-type, point, and deletion mutants) in HEK293 cells, but exhibits low activity against AR^L702H and AR^S889G mutants^[1].
ARD-1676 (0.1-1000 nM; 15 min-48 h) potently and rapidly induces proteasomal degradation of polyglutamine AR^112Q in Tet-on PC12 cells. Its effect takes effect as early as 15 min and persists for up to 48 h, and it also effectively degrades both cytoplasmic and nuclear pools of this misfolded protein^[2].
ARD-1676 (100 nM; 24 h) potently reduces AR protein levels in control and SBMA patient-derived iMNs without altering AR mRNA expression or inducing cytotoxicity^[2].

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