NCO-141

NCO-141 (0.1-100 μM; 72 h) inhibits the growth of S1T, MT-2, Jurkat, and HL60 leukemic cell lines in a dose-dependent manner, with GI₅₀ values of 34.9 μM, 26.4 μM, 36.7 μM, and 12.1 μM, respectively^[1].
NCO-141 (0.1-100 μM; 72 h) induces dose-dependent apoptosis in S1T, MT-2, Jurkat, and HL60 leukemic cell lines, with 100 μM treatment resulting in 85.3%, 39.0%, 85.9%, and 86.7% specific annexin V-positive cells, respectively^[1].
NCO-141 (10-50 μM; 6 h) induces mitochondrial superoxide generation in S1T, MT-2, Jurkat, and HL60 leukemic cell lines^[1].
NCO-141 (50-100 μM; 72 h) activates caspase-3, -8, and -9 in S1T, MT-2, Jurkat, and HL60 leukemic cell lines, but induces caspase-independent cell death as pan-caspase inhibition does not prevent cell death or caspase-associated markers^[1].
NCO-141 (72 h) increases acetylated histone H4 levels and promotes nuclear p53 degradation in S1T, MT-2, Jurkat, and HL60 leukemic cell lines^[1].
NCO-141 (25-100 μM; 24-48 h) induces autophagy in S1T, MT-2, Jurkat, and HL60 leukemic cell lines by increasing LC3-II levels, promoting autophagosome accumulation, and inhibiting autophagosome degradation^[1].

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