PAA4

PAA4 (0-4.0 μM; 24 h) exerts selective cytotoxicity against human bladder cancer EJ cells (IC₅₀ = 0.8 μM), compared with normal HUVEC cells (IC₅₀ = 2.1 μM) and SV-HUC-1 cells (IC₅₀ = 2.3 μM)^[1].
PAA4 (1-4 μM; 6-8 h) induces ferroptosis in human bladder cancer EJ cells, as evidenced by increased PTGS2 expression, elevated lipid peroxidation levels, and other changes^[1].
PAA4 (1.5 μM; 4-24 h) is efficiently internalized by human bladder cancer EJ cells, with an uptake rate of 30%, and approximately 10% of the gold localizes to mitochondria; at the same or lower concentrations, its cellular uptake rate is higher than that of the mononuclear gold (I) complex PA1^[1].
PAA4 (1.5 μM; 4 h) releases active Au^I ions in human bladder cancer EJ cells^[1].
PAA4 (1.5 μM; 4 h) potently inhibits the activities of cytosolic TrxR1 and mitochondrial TrxR2 in human bladder cancer EJ cells, reducing their activities to 21% and 22% of that in the control group, respectively^[1].
PAA4 (1.5-2.0 μM; 4 h) increases the intracellular ROS level in human bladder cancer EJ cells by 3.4-fold^[1].
PAA4 (1-4 μM; 1-6 h) upregulates the pro-oxidative genes CYBA and CYBB, and induces DNA damage in human bladder cancer EJ cells^[1].
PAA4 (1.5 μM; 4 h) induces loss of mitochondrial membrane potential in human bladder cancer EJ cells^[1].

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