GPX4-IN-19

GPX4-IN-19 (Compound Y19) (72 h) exhibits effective anti-proliferative activity to six cancer cell lines (MCF-7, MDA-MB-231, PC-3, MDA-MB-468, PANC-1, and ASPC-1) (IC₅₀: 0.021-0.094 μM)^[1].
GPX4-IN-19 (12.5-50 nM, 2 weeks) can effectively inhibit cell proliferation, and the addition of the inhibitor Ferrostatin-1 (HY-100579) (Fer-1) reversed the inhibition of cell proliferation in MDA-MB-231 cells^[1].
GPX4-IN-19 (50 nM, 8 h) can cause mitochondria in the cells to show typical morphological changes, such as rupture of the outer mitochondrial membrane, smaller mitochondrial volume, and reduction or absence of inner mitochondrial crista in MDA-MB-231 cells^[1].
GPX4-IN-19 (12.5-50 nM, 8 h) induces dose-dependent increases in intracellular Fe²⁺ concentration, LPOs accumulation, MDA content, and ROS level in MDA-MB-231 cells^[1].
GPX4-IN-19 (12.5-50 nM, 8 h) causes DNA damage in MDA-MB-231 cells by increasing the expression of γH2AX, and this DNA damage is significantly attenuated by the addition of inhibitors such as Fer-1^[1].
GPX4-IN-19 (1 μM, 2 h) reduces the degradation temperature of GPX4 protein at the same temperature in MDA-MB-231 cells, indicating that GPX4-IN-19 reduced the thermal stability of GPX4 protein^[1].
GPX4-IN-19 (12.5 nM, 25 nM, 50 nM, 8 h) exhibits significant resistance in the MDA-MB-231 cell lines that are resistant to GPX4 inhibitors RSL3 or ML162 (MDA-MB-231-RSL3 and MDA-MB-231-ML162)^[1].
GPX4-IN-19 (12.5-50 nM, 4-12 h) reduces GPX4 levels in a concentration-dependent manner in MDA-MB-231 cells. However, time-course analysis reveals that GPX4 expression initially increases at 4 hours, with minimal change in xCT levels at this early time point, but subsequently decreases at 8 hours accompanied by a significant increase in xCT expression^[1].

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