Pravastatin sodium

Trade Name(s): Pravachol, Selektine, Lipostat

Systematic Name: Sodium (3R,5R)-3,5-dihydroxy-7-[(1S,2S,6S,8S,8aR)-6-hydroxy-2-methyl-8-[[(2S)-methylbutanoyl]oxy]-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]heptanoate

Molecular Formula: C23H35NaO7

Molecular Weight: 446.5 g/mol (anhydrous)

Physical Properties: White/off-white crystalline powder

The API expertise for producing Pravastatin sodium is Fermentation

For more information about Fermentation please click here.

Pravastatin belongs to the family of lipid-lowering compounds known as 'statins'. Broadly, statins work to reduce the level of low-density lipoprotein (LDL) cholesterol in the blood by inhibiting the liver enzyme responsible for its production.

High blood cholesterol levels are associated with cardiovascular diseases such as dyslipidemia (abnormal blood lipid level) and atherosclerosis (narrowing of the artery walls by accumulation of fatty deposits, or 'plaques').

Statins are thus primarily indicated for the prevention and treatment of such diseases. Pravastatin is typically indicated as an adjunct to a cholesterol-reduced diet.

Originally disclosed and claimed in U.S Pat. No. 4.410.629, pravastatin is marketed by Sankyo Pharma Inc. (Japan) and Bristol-Myers-Squibb (outside Japan) under the trade name Pravachol.

As of April 2006, Pravas-tatin Sodium is available in several generic formulations. Pravastatin is presently manufactured by large-scale fermentation, a well-established industrial method using microorganisms to convert raw materials to valuable commercial product through chemical transformations. Through careful strain selection and continuous strain improvement, the process has been streamlined for maximum productivity and yield.

There are two pathways by which pravastatin is thought to lower lipid levels. First, the drug is a reversible inhibitor of the liver enzyme 3-hydroxy-3-methylglutaryl-Co-A reductase (HMG-CoA); this action causes the disruption an early rate-limiting step of the cholesterol biosynthetic pathway in which HMG-CoA is converted to mevalonate.

The overall result is an increase the number of cellular LDL receptors, which help to remove excess LDL from the bloodstream. Second, pravastatin is thought to inhibit very-low-density lipoprotein (VLDL) synthesis, the precursor to LDL.