Lovastatin is a hexahydro naphthalene ester isolated from Aspergillus terreus broth. It is an inactive lactone only yielding activity upon hydrolysis after oral administration. It has a strong competitive inhibition on the HMG-CoA reductase in the liver. HMG-CoA reductase is rate-limiting enzyme for de novo cholesterol synthesis in vivo. The inhibition of the enzyme can block the conversion of HMG-CoA to methacrylic acid, causing significant reduction in cholesterol synthesis, and leading to increased expression of the liver LDL receptor which promotes the plasma LDL-C clearance. The reduction of cholesterol synthesis can also cause reduced synthesis of liver ApoB100, thus causing that reduction of VLDL synthesis. Clinical observations show that it has a good effect of lowering of plasma total cholesterol and LDLC on hypercholesterolemia caused by various kinds of reasons such as heterozygous familial hypercholesterolemia, polygenic hypercholesterolemia, and diabetes or kidney disease syndrome.Statins are the secondary metabolites of filamentous fungi. It is capable of selectively inhibiting the activity of HMG coenzyme A (HMG-CoA) reductase and blocking cholesterol biosynthesis, which is due to the similarity of its acid structure with HMG-CoA. These drugs currently used in humans (statin drugs, statins) are mainly either natural or synthetic statins. Natural statins include lovastatin, mevastatin, Pravastatin and simvastatin. Lovastatin is produced by the fermentation of Aspergillus terreus); mevastatin is produced through the fermentation of penicillium citrinum and further conversion by streptomyces carbophilus; Simvastatin is made by semi-synthesis (chemically modified side chains) through lovastatin. Synthetic statins include fluvastatin, cerivastatin and atorvastatin.
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