GCLCi0

GCLCi0 (72 h) potently and selectively inhibits the viability of SMARCB1-deficient rhabdoid tumor cells (JMU-RTK-2, G401, G402) with significantly lower IC₅₀ values than in SMARCB1-proficient renal cancer cells, displaying a selective index superior to approved EZH2 inhibitors^[1].
GCLCi0 (0.1-10 μM; 24-48 h) selectively depletes the GSH/GSSG ratio in SMARCB1-deficient rhabdoid tumor cells (JMU-RTK-2, G401, G402) in a concentration-dependent manner, with minimal effect on SMARCB1-proficient renal cancer cells^[1].
GCLCi0 (0.1-4 μM; 72 h) selectively induces concentration-dependent lipid peroxidation in SMARCB1-deficient rhabdoid tumor cells (JMU-RTK-2, G401), an effect that is suppressed by the ferroptosis inhibitor Ferrostatin-1 (HY-100579)^[1].
GCLCi0 (72 h) antiproliferative effect on SMARCB1-deficient JMU-RTK-2 rhabdoid tumor cells is rescued by the ferroptosis inhibitor ferrostatin-1 but not by the apoptosis inhibitor Z-VAD-FMK, confirming ferroptosis as the mechanism of cell death^[1].

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