Amsacrine isethionate

Amsacrine (1 μM; 4 h) isethionate induces downregulation of phosphorylated and total AKT in acute myeloid leukemia U937 cells via a proteasome-dependent pathway, and this effect is abolished by pretreatment with MG132 (5 μM; 1 h)^[1].
Amsacrine (0.01-100 μM) isethionate potently blocks wild-type HERG potassium channels heterologously expressed in Xenopus oocytes, with an IC₅₀ of 2.0 μM, and exhibits partial reversibility after washout^[2].
The inhibitory effect of Amsacrine (10 μM) isethionate on HERG potassium channels heterologously expressed in Xenopus oocytes is attenuated in the HERG^Y652A mutant, and completely abolished in the HERG^F656A and HERG^Y652A/F656A mutants, indicating that this effect depends on the aromatic residues in the S6 segment of the pore region^[2].
Isethionate salt of Amsacrine (at different concentrations; perfused to achieve steady-state block) potently blocks wild-type HERG potassium channels stably expressed in 293 cells, with an IC₅₀ of 209.4 nM^[2].
Amsacrine isethionate induces chromosome aberrations, sister chromatid exchanges and micronucleus formation in vitro in a variety of mammalian cells^[3].
Amsacrine (0.005-0.25 μg/mL) isethionate induces a dose-dependent increase in chromosome aberrations and sister chromatid exchanges in cultured normal peripheral blood lymphocytes in vitro, with 0.005 μg/mL increasing SCE by 1.5-fold and 0.25 μg/mL increasing SCE by 12-fold^[4].
Amsacrine (5.0 μg/mL; 36 h) isethionate inhibits 80% of RNA synthesis and 60% of DNA synthesis in cultured human peripheral blood lymphocytes in vitro, and exerts no significant effect on protein synthesis after 36 h of incubation^[4].

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