Apoptosis inducer 49

Apoptosis inducer 49 (Compound 16j) exhibits potent cytotoxicity against CCRF-CEM cells (IC₅₀ = 2.68 μM), shows no significant activity against other cancer cell lines and non-cancer cell lines (IC₅₀ > 50 μM), and the therapeutic index (TI) is 18.66^[1].
Apoptosis inducer 49 (2.68-13.4 μM, 24 h) demonstrates a dose-dependent increase in the proportion of apoptotic cells and induces significant S-phase arrest in CCRF-CEM cells, where at 2.68 μM, early apoptotic (annexin V+/PI-) cells significantly increase concurrently with a rise in S-phase cells and a decrease in G1 and G2/M populations, while at 13.4 μM, late apoptotic (annexin V+/PI+) cells further accumulate and the S-phase arrest effect becomes more pronounced^[1].
Apoptosis inducer 49 (2.68-13.4 μM, 24 h) shows dose-dependent inhibition of DNA replication (nearly complete inhibition at 13.4 μM), but RNA synthesis is enhanced, especially at 13.4 μM in CCRF-CEM cells^[1].
Apoptosis inducer 49 (2.68-13.4 μM, 24 h) shifts the cell population toward the P3 region (high red/green fluorescence) in CCRF-CEM cells, indicating mitochondrial hyperpolarization (increased ΔΨm) rather than typical apoptosis-associated depolarization^[1].
Apoptosis inducer 49 (2.68-13.4 μM, 24 h) induces DNA damage and replication stress, activates the Chk1-p21 axis leading to S-phase arrest, and triggers apoptosis via the mitochondrial pathway (Bcl-2 inhibition and caspase-3 activation) in CCRF-CEM cells^[1].

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