Cerivastatin-d₃ sodium

Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs^[1].
Cerivastatin sodium (5-50 ng/mL; 3 days; MDA-MB-231 cells) treatment induces a dose-dependent decrease in cell proliferation of MDA-MB-231 cells (up to 40% inhibition at 25 ng/mL)^[2].
Cerivastatin sodium (25 ng/mL; 18-36 hours; MDA-MB-231 cells) treatment induces an arrest of the cell cycle in G 1/S phase after 36 h treatment. This arrest is not observed for a shorter incubation time (18 h)^[2].
Cerivastatin sodium (25 ng/mL; 18 hours; MDA-MB-231 cells) treatment induces a marked increase in the level of p21^Waf1/Cip1[2].
Cerivastatin sodium (25 ng/mL; 12 hours; MDA-MB-231 cells) treatment increases the p21 transcript in MDA-MB-231 cells^[2].
Cerivastatin sodium (10-25 ng/mL; 18 hours) inhibits invasion of MDA-MB-231 cells through Matrigel^[2].
Cerivastatin sodium (25 ng/mL; 18-36 hours) delocalizes RhoA and Ras from the membrane to the cytosol and induces morphological changes^[2].
Cerivastatin sodium (25 ng/mL; 4-36 hours) induces inactivation of NFκB, in a RhoA inhibition-dependent manner, resulting in a decrease in urokinase and metalloproteinase-9 expression, and concomitantly increases IκB^[2].

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