LXRα agonist 1

LXRα agonist 1 (Compound 40) (48 h) potently activates LXRα in LXRβ-knockout Hep3B hepatocellular carcinoma cells with an EC₅₀ of 27 nM; in cell-based GFP reporter assays, it exhibits over 23-fold higher selectivity for LXRα over LXRβ (EC₅₀ = 631 nM)^[1].
LXRα agonist 1 (5 d) alone does not reduce the viability of Hep3B hepatocellular carcinoma cells, but when combined with 2 μM Sorafenib, its EC₅₀ for reducing Hep3B cell viability is 1.7 μM. In contrast, untransformed AML12 and BNL CL.2 hepatocytes exhibit only extremely low sensitivity to this combination regimen^[1].
LXRα agonist 1 (1-5 μM; 5 d) does not reduce the viability of mouse Akt1^Myr; Myc^OE liver cancer organoids, but it exerts significant anti-tumor activity when combined with 4 μM Sorafenib^[1].
LXRα agonist 1 (3 μM; 3 d) alone does not induce significant oxidative stress in Hep3B hepatocellular carcinoma cells, but when combined with 1 μM Sorafenib, it induces strong oxidative stress at a level higher than that induced by the reference LXR agonist^[1].
LXRα agonist 1 (3 d) combined with 2 μM Sorafenib strongly induces the expression of oxidative stress and endoplasmic reticulum stress response factors including SOD1, GADD34 and CHOP in Hep3B hepatocellular carcinoma cells^[1].

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