CS47

CS47 (48 h) selectively reduces viability of KRAS-WT and EGFR-MUT human lung cancer cells in 2D culture with IC₅₀ values of 6.74 µM and 6.78 µM, respectively, while showing much lower potency against KM lung cancer cells (IC₅₀ = 24.22 µM) and normal IMR90 fibroblasts (IC₅₀ = 54.85 µM)^[1].
CS47 (48 h) induces potent cell death in 3D spheroids of KRAS-WT (H661, H522) and EGFR-MUT (HCC827) human lung cancer cells, but not in KM (H460) or KRAS-WT H522 cells with KM overexpression^[1].
CS47 (2 μM; 24 h) induces significant lipid peroxidation in KRAS-WT human lung cancer cells (H1993, H1395), but not in KRAS^G12C human lung cancer cells (H157, A549)^[1].
CS47 (2 μM; 24 h) alters lipid homeostasis in KRAS-WT H522 human lung cancer cells, inducing enrichment of ferroptosis-associated PUFA-containing phospholipids and accumulation of LPC and PUFA-containing TG^[1].
CS47 (24 h) induces transcriptomic reprogramming in KRAS-WT and EGFR-MUT human lung cancer cells, downregulating lipid biosynthesis and selenoprotein genes while upregulating ferroptosis-related genes involved in antioxidant response, iron metabolism, and GSH homeostasis; HMOX1 is universally upregulated across all genotypes^[1].

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