Cerivastatin sodium (BAY W 6228 sodium) is an orally active and highly potent HMG-CoA reductase inhibitor with lipid-lowering activity that can reduce low-density lipoprotein cholesterol levels. Cerivastatin sodium has anticancer effects and can be used to study primary hyperlipidemia.

HMG-CoA reductase:ki:1.3 nM/L

Cerivastatin sodium 5-50 ng/mL treatment induces a dose-dependent decrease in cell proliferation of MDA-MB-231 cells (up to 40% inhibition at 25 ng/mL), and 10-25 ng/mL Cerivastatin sodium inhibits invasion of MDA-MB-231 cells through Matrigel. [1]
25 ng/mL Cerivastatin sodium delocalizes RhoA and Ras from the membrane to the cytosol and induces morphological changes, and induces a marked increase in the level of p21Waf1/Cip1. This treatment increases the p21 transcript in MDA-MB-231 cells, and induces inactivation of NFκB, in a RhoA inhibition-dependent manner, resulting in a decrease in urokinase and metalloproteinase-9 expression, and concomitantly increases IκB. [1]

Cerivastatin sodium is well absorbed, reaching maximum plasma concentrations within 1-3 hours after oral administration. In the circulation, it is highly bound to plasma proteins (99.5%) and has an elimination half-life of 2-4 h. Cerivastatin sodium is metabolized primarily by the liver to three polar metabolites. Two of these metabolites are somewhat active, but much less so than the prodrug, while the third metabolite is inactive. Plasma concentrations of these metabolites are much lower than those of the prodrug. The metabolites are excreted primarily in the urine (20-25%) and feces (66-73%), with little detectable excretion of the unchanged prodrug. [2]