Niacin (also known as vitamin B3 and nicotinic acid) is bio converted to nicotinamide which is further converted to nicotinamide adenine dinucleotide (NAD+) and the hydride equivalent (NADH) which are coenzymes necessary for tissue metabolism, lipid metabolism, and glycogenolysis. Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and TC, and increases HDL-C. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). The mechanism by which niacin alters lipid profiles is not completely understood and may involve several actions, including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity (which may increase the rate of chylomicron triglyceride removal from plasma). Niacin decreases the rate of hepatic synthesis of VLDL-C and LDL-C, and does not appear to affect fecal excretion of fats, sterols, or bile acids. As an adjunct to diet, the efficacy of niacin and lovastatin in improving lipid profiles (either individually, or in combination with each other, or niacin in combination with other statins) for the treatment of dyslipidemia has been well documented. The effect of combined therapy with niacin and lovastatin on cardiovascular morbidity and mortality has not been determined. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect is not yet clear. April 15, 2016: Based on several large cardiovascular outcome trials including AIM-HIGH, ACCORD, and HPS2-THRIVE, the FDA decided that "scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events" Consistent with this conclusion, the FDA has determined that the benefits of niacin ER tablets for coadministration with statins no longer outweigh the risks, and the approval for this indication should be withdrawn.

Probucol is used to lower levels of cholesterol (a fat-like substance) in the blood. Probucol is a drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. This may help prevent medical problems caused by cholesterol clogging the blood vessels. Probucol was voluntarily removed from the market in the United States during 1995. The withdrawal from the market was due to safety concern. robucol lowers serum cholesterol by increasing the fractional rate of low-density lipoprotein (LDL) catabolism in the final metabolic pathway for cholesterol elimination from the body. Additionally, probucol may inhibit early stages of cholesterol biosynthesis and slightly inhibit dietary cholesterol absorption. Recent information suggests that probucol may inhibit the oxidation and tissue deposition of LDL cholesterol, thereby inhibiting atherogenesis. It appears to inhibits ABCA1-mediated cellular lipid efflux.

Dextrothyroxine is the dextrorotary isomer of the synthetic thyroxine. It is an antihyperlipidemic agent. The mechanism of action is not completely understood, but dextrothyroxine apparently acts in the liver to stimulate formation of low-density lipoprotein (LDL) and, to a much greater extent, to increase catabolism of LDL. This leads to increased excretion of cholesterol and bile acids via the biliary route into the feces, with a resulting reduction in serum cholesterol and LDL. Dextrothyroxine has no significant effect on high-density lipoproteins (HDL). Inherently, it will also bind to thyroid receptors and as it is a prohormone, it will bind as a substrate to iodide peroxidase.

Nicotinyl alcohol is a direct-acting vasolidator, that may decrease the blood pressure and it is a cholesterol-lowering agent. Nicotinyl alcohol as a tartrate salt led to the efficiency improvements in patients with intermittent claudication. In addition, nicotinyl alcohol alone or associated with other drugs was studied in the treatment of radicular syndromes; and was shown, that the effect had not been due to mechanical compression.

Tiadenol (2,2'-(decamethylenedithio)-diethanol) exrets hepatic peroxisome proliferative activity, it induces peroxisomal enzymes and peroxisome proliferation. Tiadenol is known for its hypolipidemic properties.

Ciprofibrate is an orally active phenoxyisobutyrate hypolipidemic compound. It acts by activating peroxisome proliferator activated receptor alpha. Ciprofibrate is efficacious for the correction of hyperlipidaemias.

Clofibride is a hypolipaemic drug of p-chlorophenoxyisobutyric type. Clofibride hypolipaemic effects could be due, partially, to a reduction of hormono-dependent lipolysis. Clofibride decreased blood cholesterol and total lipids, increased liver weight and liver catalase content, and decreased biliary excretion of cholesterol in normolipidemic rats after a 7 day treatment.

Bezafibrate is a lipid-lowering fibric acid derivative. Bezafibrate directly bound to and activated all three peroxisome proliferator-activated receptor (PPAR) subtypes respectively in PPAR binding and transactivation assays. However, from a biochemical point of view, bezafibrate is a PPAR ligand with a relatively low potency. Bezafibrate leads to considerable raising of HDL cholesterol and reduces triglycerides, improves insulin sensitivity and reduces blood glucose level, significantly lowering the incidence of cardiovascular events and new diabetes in patients with features of metabolic syndrome. It is the only pan-PPAR activator with more than a quarter of a century of therapeutic experience with a good safety profile.

Simfibrate, a derivative of clofibrate, is a hypolipidemic drug, that lowers serum chlolesterol and triglycerids. Under the brand name Cholesolvin it is indicated for hyperlipidaemia associated with arteriosclerosis, cerebral atherosclerosis, coronary arteriosclerosis, hypertension, diabetes.

Etofibrate is an ethylene glycol diester of clofibrate and nicotinic acid. The drug was used under the names Tricerol and Lipo-Merz, among the others, for the treatment of severe hypertriglyceridemia and mixed hyperlipidemia. The mechanism of etofibrate action implies activation of PPAR-alpha receptors.