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Simvastatin Research Paper

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Simvastatin is from a group of drugs called HMG CoA reductase inhibitors, also collectively called statins. A decline in the levels of low-density lipoprotein is caused by this drug. A rise in the levels high-density lipoprotein also occurs when using this drug. Those at a high risk of heart problems may also take this drug to reduce the chances of stroke, heart attack, coronary heart diseases etc. It is usually taken orally. It comes under the brand name of Zocor.
Simvastatin is a strong competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (hydroxymethylglutaryl COA reductases). 3-hydroxy-3-methylglutaryl coenzyme A reductase is the rate-limiting enzyme important in cholesterol biosynthesis. Possible drug interactions …show more content…

PHARMACODYNAMICS:
Simvastatin is a methylated form of lovastatin. HCG-CoA reductase is hindered by this oral antilipemic agent. It is used to treat primary hypercholesterolemia and reduces plasma triglycerides and apolipoprotein B along with LDL-cholesterol.
Mechanism of action: Simvastatin is a prodrug- a compound that is metabolized into an active drug only after administration in the body. Hydrolysis of the 6-membered lactone ring of simvastatin occurs in vivo and this produces the beta,delta-dihydroxy acid which is an active metabolite structurally alike to HMG-CoA. After hydrolyzation, simvastatin competes with HMG-CoA for HMG-CoA reductase, which is a hepatic microsomal enzyme. This reaction is a rate limiting step in the biosynthetic pathway for cholesterol. The quantity of mevalonic acid, a precursor of cholesterol, is decreased by the hindrance with the activity of this enzyme.
High levels of total-C, LDL-C and reduced levels of HDL-C have been shown by epidemiological studies to be linked with the progression of atherosclerosis and elevated cardiovascular risk. Reducing the levels of LDL-C reduces this …show more content…

When Simvastatin was studied in animals, it was found that it reached higher concentrations in liver than in non-targeted tissues. The availability of the drug is low since Simvastatin has a wide-spread first pass metabolism. 1.3 - 2.4 hours after administration is when the peak plasma concentration is achieved in the body. Even though Simvastatin is absorbed well in the gastrointestinal tract, it is greatly removed by the liver and the general circulation only gets about 7% of the dose. Simvastatin can easily cross the blood-brain-barrier. Simvastatin is also greatly bound to human plasma protein (approximately 95%). Its plasma half-life accounts to about 2 to 3 hours.
In a study by the Department of Internal Medicine, University Hospital, Nijmegen, The Netherlands, Simvastatin was given to 38 patients with heterozygous familial hypercholesterolaemia for 24 weeks. A mean decrease in LDL-cholesterol of 43-45% and in triglycerides of 21-31% was shown by a dose of 40 mg per/day. The mean HDL-cholesterol increased noticeably by 10-13%. No significant difference was noted in response to whether the drug was given in one dose or two. When the dose is increased from 5 to 120 mg, the pharmacological activity increases in a linear

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