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Plasma cholesterol which is one of risk factors for the development of coronary heart disease is derived both from dietry fat and de novo synthesis by the liver1}. There are two main therapeutical approaches to lower plasma cholesterol. The first is to stimulate removal of cholesterol by using an ion exchanger like cholestyramine, which absorbs bile acids synthesized from cholesterol and results in excretion of it from the body as an ion complex. The second is a newer approach to use inhibitory effect on cholesterol biosynthesis of the liver because it is a major site of lipoprotein synthesis. In this pathway, 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase is a rate-limiting enzyme to convert HMG-CoA to mevalonate. As a function of this enzyme is inhibited, incorporation of cholesterol by the hepatocyte is increased by upregulation of low density lipoprotein-receptor (LDL-R). Compactin was discovered first as HMG-CoAreductase inhibitor from culture broth of fungi2). There were also effective agents including pravastatin, lovastatin, simbastatin and fluvastatin, which were developed by modification of compactin to produce moreeffective derivatives2). In the course of our screen for LDL-Rupregulators, we found that PC-766B, bafiloniycin (16-membered macrolide

Elevation of low density lipoprotein-receptor mRNA concentration in human hepatoma HepG2 cells by macrolide antibiotics.