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  1. 1. PRESENTATION ON: HMG COA Reductase inhibitor Presented by: Under the guidence of Dr.Mohd Mujahid SirMohammad Muztaba M.pharm, Pharmacology 1st year INTEGRAL UNIVERSITY,lucknow session: 2016-2017
  2. 2. INTRODUCTION Hyperlipidemia Hyperlipoproteinemia means abnormally increased plasma lipoproteins-one of the risk factors for atherosclerosis (deposition of fats at walls of arteries, forming plaque) Other risk factors-Cigarette smoking, Diabetes, another source of oxidative stress. Also, obesity and, hypertension. Hyperlipemia denotes increased levels of triglycerides
  3. 3. HMG-CoA Reductase Inhibitors • Prototype drug: Atorvastatin
  4. 4. Pharmacologic class: HMG-CoA reductase inhibitors Therapeutic class: Lipid-lowering agents/statin Pregnancy risk: Pregnancy Category X Contraindicated with pregnancy and lactation due to its potential for adverse reactions on the fetus or neonate
  5. 5. Examples include: Atorvastatin (Lipitor) (Prototype) Fluvastatin (Lescol) Lovastatin (Mevacor) Pitavastatin (Livalo) Pravastatin (Pravachol) Rosuvastatin (Crestor) Simvastatin (Zocor) HMG-CoA Reductase Inhibitors
  6. 6.  HMG-CoA reductase is an enzyme responsible for cholesterol synthesis. Inhibiting this enzyme will lower the levels of serum cholesterol and LDL levels, an important element of developing atherosclerosis, and slightly increase HDL levels, the “good cholesterol,” due to the fat metabolism shift (Karch, 2013, p. 788).  This drug class is typically used for treatment of hyperlipidemia/hypercholester olemia and to slow progression of CAD
  7. 7. A- HMG –COA reductase inhibitors (statins): • Inhibit the first enzymatic step in cholesterol synthesis. • Production of this enzyme and of LDL receptors is transcriptionally regulated by the content of cholesterol in the cell. • -Simvastatin, lovastatin (prodrugs). Atorvastatin &Rosuvastatin are the most potent. • In 2009 the world statins market generated over $27bn in revenues • 2010 onwards, there will be major patent expires – most notably for Lipitor-mfg by Pfizer, and rising competition from generic alternatives.
  8. 8. Mechanism of action:(statins) • Structural analogues of HMG –COA reductase (the rate limiting enzyme in cholesterol synthesis) → reduction of cholesterol synthesis in liver → compensatory ↑ in synthesis of LDL receptors on hepatic and extra hepatic tissues →Increase in hepatic uptake of circulating LDL which decreases plasma LDL cholesterol . • - Decrease TGs to some extent and ↑ HDL. • - Cardio protective: vasodilators and decrease atherosclerosis (stabilize plaque). • Therapeutic uses: • - Effective in all types of hyperlipidemia except those who are homozygous for familial hypercholesterolemia (lack of LDL receptors). • Usually combined with other drugs.
  9. 9. Adverse effects • 1- Increase in liver enzymes (serum transaminases should be monitored continuously ,CI in hepatic dysfunction). • 2-Myopathy and muscle damageInhibits the production of CoQ10, which is essential for the creation of ATP (energy a cell uses). • Muscle fatigue and weakness is caused by the disruption of CoQ10 production(95% source of ATP) and resulting lack of ATP production-esp in heart, liver and kidney which have the highest CoQ10 concentrations. • 3- Cataract and GIT upset. • 4- Increase in warfarin levels. • 5- CI in pregnancy and nursing mothers (safety in pregnancy is not established), lactation, children and teenagers.
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  11. 11. We hope you liked our presentation. Thank you! 

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