Antihyperlipidaemic Agents

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Chapter: Medicinal Chemistry : Antihyperlipidaemic Agents

The lipids of human plasma are transported into the macromolecular complex and termed as lipoproteins.

Antihyperlipidaemic Agents


The lipids of human plasma are transported into the macromolecular complex and termed as lipoproteins. A number of metabolic disorders that involve the elevation of any lipoprotein series are termed as hyper lipoproteinaemias or hyperlipidaemias. The two major clinical sequelae of the hyperlipoproteinaemia are the acute pancreatitis and atherosclerosis. Lipoproteins contain alipoprotein (apo). Blood conveys lipids into the artery wall that have low-density lipoprotein.

The pharmacological agents that reduce the concentration of plasma lipids are called hypocholestrolaemic agents. An increase in the plasma lipids, particularly cholesterol is a common feature of atherosclerosis, a condition involving arterial damage, which may lead to ischaemic heart diseases, myocardial infarction, and cerebrovascular accidents.

Lipids are insoluble in water, and they are transported into the plasma as lipoproteins, an increase

in the plasma concentration of these substances is called hyperlipidaemia or hyperlipoproteinaemia. Lipoproteins consists of central core of hydrophobic lipids (triglycerides or cholesterylesters) encased in a more hydrophilic coat of polar substances—phospholipids, free cholesterol, and associated proteins, that is, apoproteins.

Lipoproteins are classified into four types: high-density lipoprotein (HDL), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), and chylomicrons.

Hyperlipoproteinaemias can be the following:


  1. Due to a single gene defect: It is familial and called monogenic or genetic.

  2. Multiple gene: Dietary and physical activity related causes ‘polygene’ or multifactorial.


These are associated with diabetes, myxoedema, nephritic syndrome, chronic alcoholism, and drugs (corticosteroids, oral contraceptives, β blockers), etc. Globally, in blood, the primary carrier of plasma is cholesterol esters and very low-density lipoproteins. The current pharmacotherapy includes the following:

  1. HMG CoA reductase (or 3-hydroxy-3-methyl-glutaryl-CoA reductase or HMGR) inhibitors (statins).

  2. Bile acid sequestrants (resins).

  3. Drugs that activates lipoprotein lipase (fibric acid derivatives).

  4. Drugs that inhibit lipolysis and triglyceride synthesis (nicotinic acid). 

Combined therapeutic regimen is useful in the following cases:

  • When LDL levels are insignificantly increased during treatment of hypercholesterolaemia with a resin.

  • When LDL and VLDL levels are both elevated initially.

  • When LDL and VLDL levels are normalized with a single agent.

  • When elevated level of lipoprotein or HDL deficiency coexist with other hyperlipidaemias.

Fibric acid and bile acid sequestrants are useful in the treatment of familial hyperlipidaemia of which some are intolerant of niacin. HMG CoA reductase inhibitors and bile acid sequestrants synergistically control the familial hypercholesterolaemia, but they may not control the levels of VLDL in some patients with familial combined hyperlipoproteinaemia. Niacin and bile acid sequestrants effectively control LDL levels during resin therapy of familial combined hyperlipoproteinaemia or other disorders involving both increased VLDL and LDL levels. Reductase inhibitors and Ezetimibe are used in treating primary hypercholesterolaemia and has some use in the treatment of homozygous familial hypercholesterolaemia.

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