AH-26

AH-26 (0.1-20 μM; 72 h) potently inhibits the proliferation of NB4, K562, HL-60, U937, SKOV3, HGC-27, MKN45 and PANC-1 cancer cells, with corresponding IC₅₀ values of 0.16, 0.42, 0.21, 0.36, 0.04, 0.01, 0.49 and 0.10 μM, respectively; meanwhile, it shows low cytotoxicity against normal HK-2 cells^[1].
AH-26 (0.1-0.4 μM; 48 h) inhibits the proliferation of SKOV3 and HL-60 cells in a dose-dependent manner^[1].
AH-26 (0.05-0.4 μM; 6-12 h) inhibits the migration of SKOV3 and HGC-27 cells in a dose-dependent and time-dependent manner^[1].
AH-26 (0.025-0.075 μM; 72 h) upregulates the expression of differentiation markers CD11b and CD14 in NB4 and HL-60 leukemia cells in a dose-dependent manner, and induces cell differentiation^[1].
AH-26 (0.05-0.4 μM; 48 h) downregulates Bcl-2, Bcl-XL, c-Myc, pro-caspase-3 and p-STAT3 and upregulates cleaved caspase-3 in SKOV3 cells at concentrations of 0.1-0.4 μM. At concentrations of 0.05-0.1 μM, it downregulates Bcl-2, Bcl-XL, c-Myc, pro-caspase-9 and p-STAT3 and upregulates cleaved caspase-9 in HGC-27 cells, with no significant effect on total STAT3 levels^[1].
AH-26 (0.05-0.2 μM; 48 h) induces apoptosis in NB4, K562, HL-60, U937, SKOV3 and HGC-27 cells in a dose-dependent manner^[1].
AH-26 (0.05-0.2 μM; 48 h) reduces the mitochondrial membrane potential of NB4, K562, HL-60, U937, SKOV3 and HGC-27 cells in a dose-dependent manner, and triggers mitochondria-mediated apoptosis^[1].
AH-26 (0.025-0.5 μM; 48 h) arrests the cell cycle of NB4, HL-60, SKOV3 and HGC-27 cells at the G1 phase in a dose-dependent manner^[1].
AH-26 (0.1-0.4 μM; 48 h) increases intracellular ROS levels in HL-60 cells in a dose-dependent manner, and this effect is inhibited by the antioxidant NAC^[1].
AH-26 (10 μM; 1 h) increases the thermal stability of STAT3 in SKOV3 and HL-60 cell lysates at 40-49 °C in CETSA, supporting the intracellular interaction between AH-26 and STAT3^[1].

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