EGFR-IN-178

EGFR-IN-178 (Compound 14a) (1-100 nM, pretreated for 72 hours, followed by culturing for 10–14 days) with IC₅₀ values of 18.5 nM for H1975-EGFR^L858R/T790M and 15.4 nM for PC9-EGFR^Del19, showing significant efficacy at 5 nM on PC9-EGFR^Del19 cells, at approximately 10 nM on H1975-EGFR^L858R/T790M cells, and no inhibition even at 100 nM on A549-EGFR^WT cells^[1].
EGFR-IN-178 (50-100 nM, 24 h) can enhance green fluorescence of H1975-EGFR^L858R/T790M cells, indicating that EGFR-IN-178 can lead to an increase in intracellular ROS^[1].
EGFR-IN-178 (10-100 nM) inhibits the phosphorylation of EGFR without reducing its total protein content in H1975-EGFR^L858R/T790M cells. It concurrently suppresses the JAK2-STAT3 signaling pathway by significantly decreasing p-JAK2 levels at 100 nM and p-STAT3 levels at 50 nM, which is consistent with its inhibitory effect on JAK2-3 kinase activity^[1].
EGFR-IN-178 (5-100 nM, 24 h) induces ferroptosis in H1975-EGFR^L858R/T790M cells, as evidenced by increased levels of lipid peroxides (MDA), iron ions (Fe²⁺), and oxidized lipids (green fluorescence), alongside decreased glutathione (GSH) and GPX4 levels, while it also promotes apoptosis by increasing cleaved caspase-3 expression^[1].
EGFR-IN-178 (10-50 nM, 12-24 h) can effectively inhibit the invasion and migration of H1975-EGFR^L858R/T790M cells in a concentration-dependent manner^[1].
EGFR-IN-178 shows no significant toxicity to HUVECs, HK-2, Hacat, and mouse-derived C2C12 (muscle tissue) and NIH3T3 (embryonic fibroblasts)^[1].

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