MI891

MI891 (0-10 μM) abrogates PXR activation by Rifampicin (HY-B0272) and displays antagonistic activity with an IC₅₀ of 378 nM^[1].
MI891 (0-20 μM, 48 h) suppresses both rifampicin-induced and basal (constitutive) CYP3A4 mRNA expression in HepaRG cells^[1].
MI891 (1-10 μM) disrupts the wt-PXR-LBD/SRC1-VP16 interaction, does not activate the obstructed mutated PXR LBD in wild-type (wt-PXR LBD) or triple mutant (S208W/S247W/C284W) in HepG2 cells^[1].
MI891 (48 h) shows no binding activity (EC₅₀ > 10 μM) in wild-type CAR; requires high concentrations to activate CAR (EC₅₀ = 137 μM) and has no significant activation of either CARwt or CAR3 variant in human CARwt and CAR3 in HepG2 cells^[1].
MI891 (10 μM, 48 h) exhibits selective antagonism and inverse agonism on hPXR, but has no agonistic or antagonistic activities of MI891 on human VDR, FXR, LXRβ, LXRα, PPARα, PPARγ, AhR, or ERα/β receptors^[1].
MI891 (24 h) demonstrates no effects on viability in various cell lines (up to 30 μM), including COS-1, HepG2, and HK-2^[1].
MI891 (5-10 μM, 48 h) suppresses the expression of CYP3A4, CYP7A1, HMGCS2, PCK1, and MKI67 mRNA in primary human hepatocytes^[1].

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