Fa-Au

Fa-Au (Compound 8) (72 h) potently inhibits the proliferation of HepG2 and Hepa 1-6 hepatocellular carcinoma cells, with IC₅₀ values of 0.48 μM and 0.69 μM respectively after 72 h of incubation^[1].
Fa-Au (0.5-2 μM; 24 h) inhibits TrxR activity in HepG2 hepatocellular carcinoma cells in a concentration-dependent manner in vitro^[1].
Fa-Au (2 μM; 6 h) induces ROS production in HepG2 hepatocellular carcinoma cells, and this effect is reversed by 6 h pretreatment with the ROS scavenger NAC (HY-B0215)^[1].
Fa-Au (0.5-2 μM) induces ROS-mediated endoplasmic reticulum stress in HepG2 hepatocellular carcinoma cells, which is evidenced by concentration-dependent Ca²⁺ release and upregulation of key ERS markers, and this effect is reversed by pretreatment with NAC^[1].
Fa-Au (0-10 μM) induces ferroptosis in HepG2 hepatocellular carcinoma cells via lipid peroxide accumulation, mitochondrial damage, and downregulation of GPX4 and SLC7A11^[1].
Fa-Au (2 μM) induces immunogenic cell death in HepG2 hepatocellular carcinoma cells, which is characterized by CRT exposure, HMGB1 release, reduced intracellular ATP levels, and altered expression of ICD-related proteins^[1].
Treatment of HepG2 hepatocellular carcinoma cells with Fa-Au (2 μM; 24 h) induces significant changes in the expression of genes associated with oxidative stress and immune response pathways^[1].
IFN-γ enhances Fa-Au-induced ferroptosis in HepG2 hepatocellular carcinoma cells via the IFN-γ/STAT1/SLC7A11 axis^[1].

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