Description
1. HMG CoA Reductase Inhibitors Lovastatin, Simvastatin, Metastatin, Pravastatin, Fluvastatin, Atorvastatin,
Pitavastatin, Rosuvastatin
2. Fibrates Clofibrate, Fenofibrate, Gemfibrozil,
Ciprofibrate, benzafibrate, Fluvestatin.
3. Bile acid sequestrants Cholestyramine, Colestipol
4. LDL oxidation inhibitor Probucol
5. Pyridine derivatives Nicotinic acid, Nicotinamide
6. Cholesterol absorption inhibitors Ezetimibe
7. Miscellaneous agents β-Sitosterol, Dextrothyroxine
1. HMG- CoA Reductase inhibitors (STATINS):
• 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA).
• The enzyme that catalyzes the conversion of HMG-CoA to mevanolate.
• This reaction is the rate determining step in the synthetic pathway of cholesterol.
Statins:
• Lovastatin was isolated from Aspergillus terreus.
There are two classes of statins:
o Natural Statins: Lovastatin(mevacor), Pravastatin (pravachol), Simvastatin (Zocor).
o Synthetic Statins: Atorvastatin (Lipitor), Fluvastatin (Lescol).
• Statins are competitive inhibitors of HMG-CoA reductase. They are bulky and “stuck”
in the active site.
• Statins prevents the binding of enzyme with its substrate, HMG CoA.
Drug ADR Uses Lovastatin Increased creatinine phosphor-kinase, Flatulence, Nausea. Antihyperlipoproteinemic agent. Simvastatin Headache, nausea, flatulence, heartburn, abdominal pain. Antihyperlipdemic agent. Pravastatin GI disturbances, headache, insomnia, chest pain, rash. Antihyperlipoproteinemic agent.
Atorvastatin Headache, flatulence, diarrhea. Primmary hyperlipidemia and
secondary hyper cholesterolemia. Rosuvastatin Headache, dizziness, constipation, nausea, vomiting.
High LDL, total cholesterol, TGs.
2. Fibrates:
• Fibrates are antihyperlipidemic agents, these are used in the treatment of various forms of hyperlipidemia and hypercholesterolemia.
• These are 2-phenoxy-2-methyl propanoic acid derivatives.
• These drugs stimulate β-oxidation of fatty acids in mitochondria.
• These are specially using for decreasing plasma levels of fatty acid and
triacylglycerol.
MOA:
• Fibrates are decreasing plasma TGs levels.
• This class of drugs acting through lowering of the blood triglyceride levels by
decreasing the production of liver’s VLDL (the triglyceride-carrying particle that circulates in the blood) by activation of lipoprotein lipase and enhances the removal of TGs from the blood. It is due to activation of PPAR-α.
• These drugs are acts by increasing blood HDL cholesterol and not effective in lowering LDL cholesterol
1. Classify hypolipidemic agents with examples, write the pharmacology of Atorvastatin.
2. Write the classification of hypolipidemics. Explain the complications of dyslipidemia.
3. Write the classification of hypolipidemics with examples. Describe the mechanism of Niacin.
