Animal experiment:

Rats[1]Rats are given a single oral administration of YM-53601 at the concentration of 50 mg/kg, followed 1 h later by intraperitoneal injection of [14C] acetate (40.5 μCi per animal). The rats and the hamsters are anaesthetized with diethyl ether and killed 1 h after the [14C]-acetate injection. Cholesterol biosynthesis is assayed[1].

YM-53601 free base is a squalene synthetase inhibitor which suppresses lipogenic biosynthesis and lipid secretion in rodents.

YM-53601 inhibits cholesterol biosynthesis from acetate in a dose-dependent manner in the plasma of rats. At the same time, YM-53601 inhibits both FFA and triglyceride biosynthesis in rats treated with cholestyramine over the same dose range at which it inhibits cholesterol biosynthesis. YM-53601 by single oral administration decreases the enhanced plasma triglyceride levels in hamsters induced by an injection of protamine sulfate, which inhibits lipoprotein lipase (LPL) and consequently increases plasma very low-density lipoprotein (VLDL) triglyceride levels. YM-53601 also decreases the enhanced plasma triglyceride and cholesterol levels in hamsters treated with Triton WR1339, which also inhibits the degradation of VLDL. Plasma cholesterol was significantly decreased as soon as 1 h after single administration of YM-53601 in hamsters fed a normal diet[1].

[1]. Ugawa T, et al. YM-53601, a novel squalene synthase inhibitor, suppresses lipogenic biosynthesis and lipid secretion in rodents. Br J Pharmacol. 2003 May;139(1):140-6.