Cerivastatin is an orally active and highly effective HMG-CoA reductase inhibitor with anticancer and lipid-lowering effects. Cerivastatin can reduce low-density lipoprotein cholesterol levels, inhibit the proliferation and invasion of MDA-MB-231 cells, and can be used to study primary hyperlipidemia.

HMG-CoA reductase:1.3 nM/L (Ki)

Cerivastatin induced a dose-dependent decrease in cell proliferation of MDA-MB-231 cells (up to 40% inhibition at 25 ng/ml). In contrast, Cerivastatin treatment did not significantly modify MCF-7 cell proliferation. Flow cytometry analysis showed that Cerivastatin induced an arrest of the cell cycle in G 1 /S phase (67.1% in Cerivastatin -treated cells) after 36 h treatment. [1]

Trametinib and Cerivastatin were initially dissolved in DMSO and diluted into an aqueous pooled dose containing a final concentration of 0.5% hypromellose and 0.05% Tween-80, in saline. Generated xenografts of a primary monosomic BAP1-mutated human UM cell line, UPMM3, in highly immunodeficient NOD.Cg-Prkdcscid Il2rgtm1wjl/SzJ mice to validate the effects of trametinib and Cerivastatin combination on UM cells in vivo. One week after subcutaneous injection of UPMM3 cells, when the tumour was palpable, four mice per group were treated with vehicle, trametinib (1 mg/kg, per os, three days/week), Cerivastatin (2 mg/kg per os, three days/week) or trametinib and Cerivastatin for 57 days (until day 64). The end of treatment was followed by 15 days of observation. The addition of Cerivastatin determined a significantly stronger inhibition of tumour growth compared with mice treated with trametinib alone (p = 0.03). [4]