Classes of hypolipidemic drugs
There are several classes of hypolipidemic drugs. They may differ in both their impact on the cholesterol profile and adverse effects. For example, some may lower the "bad cholesterol" low density lipoprotein (LDL) more so than others, while others may preferentially increase high density lipoprotein (HDL), "the good cholesterol". Clinically, the choice of an agent will depend on the patient's cholesterol profile, cardiovascular risk, and the liver and kidney functions of the patient, evaluated against the balancing of risks and benefits of the medications. In the United States, this is guided by the evidence-based guideline from the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATPIII).
- Statins are particularly well-suited for lowering LDL, the cholesterol with the strongest links to vascular diseases. In studies using standard doses, statins have been found to lower LDL-C by 18% to 55%, depending on the specific statin being used. There is a risk of severe muscle damage (myopathy & rhabdomyolysis) with statins. Hypercholesterolemia is not a risk factor for mortality in persons older than 70 years and risks from statin drugs are more increased after age 85.
- Fibrates are indicated for hypertriglyceridemia. Fibrates typically lower triglycerides by 20% to 50%. Level of the good cholesterol HDL is also increased. Fibrates may decrease LDL, though generally to a lesser degree than statins. Similar to statins, there is a risk of severe muscle damage (myopathy & rhabdomyolysis).
- niacin, like fibrates, is also well-suited for lowering triglycerides by 20–50%. It may also lower LDL by 5–25% and increase HDL by 15–35%. Niacin may cause hyperglycemia, and may also cause liver damage. The niacin derivative acipimox is also associated with a modest decrease in LDL.
- Bile acid sequestrants (resins, e.g. cholestyramine) are particularly effective for lowering LDL-C by sequestering the cholesterol-containing bile acids released into the intestine and preventing their reabsorption from the intestine. It decreases LDL by 15–30% and raises HDL by 3–5%, with little effect on triglycerides but can cause a slight increase. Bile acid sequestrants may cause gastrointestinal problems, and may also reduce the absorption of other drugs and vitamins from the gut.
- ezetimibe (Zetia) is a selective inhibitor of dietary cholesterol absorption.
- lomitapide (Juxtapid) is a microsomal triglyceride transfer protein (MTP) inhibitor.
- phytosterols may be found naturally in plants. Similar to ezetimibe, phytosterols reduce the absorption of cholesterol in the gut. Hence, they are most effective when consumed with meals. However, the precise mechanism of action of phytosterols differs from ezetimibe.
- orlistat (Xenical): Its primary function is to prevent the absorption of about 30% of fats from the human diet; thereby reducing caloric intake (a drug designed to treat obesity) is by inhibiting Pancreatic lipase- an enzyme that breaks down triglycerides in the intestine.
Investigational classes of hypolipidemic agents:
- CETP inhibitors (cholesteryl ester transfer protein), 2 candidates are in trials. It is expected that these drugs will mainly increase HDL while lowering LDL;
- Squalene synthase inhibitor;
- ApoA-1 Milano
- succinobucol(AGI-1067), a novel antioxidant, failed aphase 3 trial
- Apoprotein-B inhibitor Mipomersen (approved by the FDA in 2013 homozygous familial hypercholesterolemia.).
- PCSK9 Monoclonal antibody inhibitors 
- AMDA – The Society for Post-Acute and Long-Term Care Medicine (February 2014), "Ten Things Physicians and Patients Should Question", Choosing Wisely: an initiative of the ABIM Foundation (AMDA – The Society for Post-Acute and Long-Term Care Medicine), retrieved 20 April 2015.
- Pollack, Andrew (29 January 2013) F.D.A. Approves Genetic Drug to Treat Rare Disease The New York Times, Retrieved 31 January 2013
- Staff (29 January 2013) FDA approves new orphan drug Kynamro to treat inherited cholesterol disorder U.S. Food and Drug Administration, Retrieved 31 January 2013
- Koren MJ, Scott R, Kim JB et al Lancet 2012; 380:1995-2006
- Gugliano RP, Desai NR, Kohli P et al Lancet 2012; 380:2007-17