In intact HepG2 cells14C]acetate into free cholesterol and cholesteryl ester, with IC ₅₀ s of 4.9 and 8.0 nM, respectively. FR194738 induces intracellular [ ¹⁴ C]squalene accumulation. It increases the incorporation of [ ¹⁴ C]acetate into squalene, an intermediate of cholesterol synthesis. FR194738 potently inhibits squalene epoxidase (SE) in HepG2 cell homogenate and liver microsomes in dogs and rats . The inhibitory effect of FR194738 in comparison to the HMG-CoA reductase inhibitors, Simvastatin, Fluvastatin and Pravastatin, on cholesterol biosynthesis in HepG2 cells is examined. Among these compounds, FR194738 is the most potent, with an IC _{50 of 2.1 nM. The IC 50 s of Simvastatin, Fluvastatin and Pravastatin are 40, 28 and 5100 nM, respectively. FR194738 inhibits hamster liver microsomal squalene epoxidase activity in a concentration-dependent manner with an IC 50 of 14 nM.}

Serum lipid levels in hamsters after daily administration of FR194738 and Pravastatin for 10 d are measured. It reduces the serum levels of total, non high density lipoprotein (HDL) and HDL cholesterol, and triglyceride. Treatment of hamsters with FR194738 increases HMG-CoA reductase activity by 1.3-fold at 32 mg/kg compared to the control group and does not significantly change that at 100 mg/kg.

IC50: 9.8 nM (squalene epoxidase, in HepG2 cell homogenates)