Entadamide A-CO-C12

Entadamide A-CO-C12 (compound 3u) (48 h) exhibits antiproliferative activity against a panel of human cancer cells (MDA MB-231, DU-145, MCF-7, 4T1, NCI-H460, HepG2 and HEK-293), with IC₅₀s of 19.11, 3.04, 2.82, 3.26, 20.98, 18.89, and 77.69 μM, respectively, showing selective anti-cancer activity in breast caner cells (MCF-7 and 4T1)^[1].
Entadamide A-CO-C12 (1.5-3 μM; 48 h-5 days) suppresses migration and downregulate EMT-associated transcription factors in MCF-7 cells^[1].
Entadamide A-CO-C12 (1.5-3 μM; 7 days) inhibits spheroid formation and reduces cancer stemness in MCF-7 cells^[1].
Entadamide A-CO-C12 (1.5-3 μM; 24-48 h) promotes apoptosis by modulating the balance between anti-apoptotic (BCL-2, survivin) and pro-apoptotic (BAX) regulators at both the transcriptional and translational levels in MCF-7 cells, and triggers mitochondrial depolarization and activation of the intrinsic apoptotic pathway^[1].
Entadamide A-CO-C12 (1.5-3 μM; 8-24 h) induces a pronounced, dose-dependent elevation in ROS production in MCF-7 cells^[1].
Entadamide A-CO-C12 (1.5-3 μM; 48 h) attenuates the CD90 and CD133 levels, causes DNA damage, and triggers apoptotic nuclear condensation in MCF-7 cells in a dose-dependent manner^[1].
Entadamide A-CO-C12 (1.5-3 μM; 48 h) potentiates Doxorubicin (HY-15142A) sensitivity through modulation of the ABCG2-mediated efflux pathway in MCF-7 cells^[1].
Entadamide A-CO-C12 shows partial interaction with ABCB1/ABCG2 and BMI1, contributing to the modulation of drug resistance and stemness^[1].

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