Cerivastatin is a highly potent, well-tolerated, and orally active HMG-CoA reductase inhibitor (Ki: 1.3 nM/L). Cerivastatin also inhibits proliferation and invasiveness of MDA-MB-231 cells, mainly by RhoA inhibition with anti-cancer effect. Cerivastatin reduces low-density lipoprotein cholesterol levels.

Cerivastatin (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). Cerivastatin (10-25 ng/mL; 18 hours) inhibits invasion of MDA-MB-231 cells through Matrigel. Cerivastatin (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. Cerivastatin (25 ng/mL; 18-36 hours; MDA-MB-231 cells) treatment induces an arrest of the cell cycle in the G 1/S phase after 36 h treatment. Cerivastatin (25 ng/mL; 18-36 hours) delocalizes RhoA and Ras from the membrane to the cytosol and induces morphological changes. Cerivastatin (25 ng/mL; 18 hours; MDA-MB-231 cells) treatment induces a marked increase in the level of p21Waf1/Cip1. Cerivastatin (25 ng/mL; 12 hours; MDA-MB-231 cells) treatment increases the p21 transcript in MDA-MB-231 cells. This arrest is not observed for a shorter incubation time (18 h) [1].

Cerivastatin is highly bound to plasma proteins (99.5%), with an elimination half-life of 2-4 hours. Cerivastatin is well absorbed, reaching maximal plasma levels in 1-3 hours following oral dosing. Cerivastatin is metabolized predominantly in the liver to three polar metabolites. Plasma concentrations of all metabolites are substantially lower than those of the parent drug. Elimination of metabolites is via the urine (20-25%) and feces (66-73%), while essentially no parent compound is excreted [2].

145599-86-6

C26H34FNO5

459.55

Cerivastatin

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years