The World Health Organization's ATC classification organizes medical drugs based on therapeutic properties, chemical composition, and anatomy. It helps make essential medicines readily available globally and is widely used in the pharmaceutical industry.
Acipimox inhibits the release of fatty acids from adipose tissue and reduces the blood concentrations of very low density lipoproteins (VLDL or Pre-beta) and low density lipoproteins (LDL or beta) with a subsequent overall reduction in triglyceride and cholesterol levels.
Alipogene tiparvovec contains the human lipoprotein lipase (LPL) gene variant LPLS447X in a vector. The human LPL gene variant LPLS447X in an adeno-associated virus serotype 1 (AAV1) vector intended to target the muscle. Alipogene tiparvovec is injected as a one-time series into the muscle of the lower extremities where it is taken up by myocytes.
Alirocumab is a fully human IgG1 monoclonal antibody that binds with high affinity and specificity to proprotein convertase subtilisin kexin type 9 (PCSK9). PCSK9 binds to the low-density lipoprotein receptors (LDLR) on the surface of hepatocytes to promote LDLR degradation within the liver. LDLR is the primary receptor that clears circulating LDL, therefore the decrease in LDLR levels by PCSK9 results in higher blood levels of LDL-C. By inhibiting the binding of PCSK9 to LDLR, alirocumab increases the number of LDLRs available to clear LDL, thereby lowering LDL-C levels.
Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase. Atorvastatin lowers plasma cholesterol and lipoprotein serum concentrations by inhibiting HMG-CoA reductase and subsequently cholesterol biosynthesis in the liver and increases the number of hepatic LDL receptors on the cell surface for enhanced uptake and catabolism of LDL.
Bempedoic acid is an adenosine triphosphate-citrate lyase (ACL) inhibitor that lowers low-density lipoprotein cholesterol (LDL-C) by inhibition of cholesterol synthesis in the liver.
Bezafibrate lowers elevated blood lipids (triglycerides and cholesterol). Elevated VLDL and LDL are reduced by treatment with bezafibrate, whilst HDL-levels are increased. Furthermore, cholesterol biosynthesis is reduced by bezafibrate, which is accompanied by a stimulation of the LDL receptor-mediated lipoprotein catabolism.
Ciprofibrate is a new derivative of phenoxyisobutyric acid which has a marked hypolipidaemic action. It reduces both LDL and VLDL and hence the levels of triglyceride and cholesterol associated with these lipoprotein fractions. It also increases levels of HDL cholesterol.
Colesevelam is a non-absorbed, lipid-lowering polymer that binds bile acids in the intestine, impeding their reabsorption.
Colestipol is an ion exchange resin which lowers plasma cholesterol through binding with bile acids in the intestinal lumen. It is indicated as adjunctive therapy to diet in the management of patients with elevated cholesterol levels who have not responded adequately to diet.
Colestyramine resin absorbs and combines with the bile acids in the intestine to form an insoluble complex which is excreted in the faeces. This results in an increased faecal loss of bile acids which leads to an increased oxidation of cholesterol to bile acids and a decrease in serum cholesterol levels and low density lipoprotein serum levels.
Docosahexaenoic acid (DHA) is an omega-3 fatty acid that is a primary structural component of the human brain, cerebral cortex, skin, and retina. It can be synthesized from alpha-linolenic acid or obtained directly from maternal milk (breast milk), fish oil, or algae oil.
Eicosapentaenoic acid (EPA; also icosapentaenoic acid) is an omega-3 fatty acid. It also has the trivial name timnodonic acid. Eicosapentaenoic acid is a polyunsaturated fatty acid (PUFA) that acts as a precursor for prostaglandin-3 (which inhibits platelet aggregation), thromboxane-3, and leukotriene-5 eicosanoids. Eicosapentaenoic acid is both a precursor and the hydrolytic breakdown product of eicosapentaenoyl ethanolamide (EPEA: C22H35NO2; 20:5,n-3).
Evolocumab binds selectively to PCSK9 and prevents circulating PCSK9 from binding to the low density lipoprotein receptor (LDLR) on the liver cell surface, thus preventing PCSK9-mediated LDLR degradation. Increasing liver LDLR levels results in associated reductions in serum LDL-cholesterol (LDL-C).
Ezetimibe is in a new class of lipid-lowering compounds that selectively inhibit the intestinal absorption of cholesterol. The molecular target of ezetimibe is the sterol transporter, Niemann-Pick C1-Like 1 (NPC1L1), which is responsible for the intestinal uptake of cholesterol.
The lipid-lowering properties of fenofibrate have been explained in vivo by activation of Peroxisome Proliferator Activated Receptor α (PPARα). Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of Apoprotein C-III.
Fluvastatin, a fully synthetic cholesterol-lowering agent, is a competitive inhibitor of HMG-CoA reductase, which is responsible for the conversion of HMG-CoA to mevalonate, a precursor of sterols, including cholesterol. Fluvastatin reduces total-C, LDL-C, Apo B, and triglycerides, and increases HDL-C in patients with hypercholesterolaemia and mixed dyslipidaemia.
Gemfibrozil is a lipid regulating agent which regulates lipid fractions. Gemfibrozil stimulates the peripheral lipolysis of triglyceride rich lipoproteins such as VLDL and cholymicrons by stimulation of LPL. Gemfibrozil also inhibits synthesis of VLDL in the liver.
Inclisiran is a cholesterol-lowering, double-stranded, small interfering ribonucleic acid (siRNA), conjugated on the sense strand with triantennary N-acetylgalactosamine (GalNAc) to facilitate uptake by hepatocytes. It is indicated in adults with primary hypercholesterolaemia (heterozygous familial and non-familial) or mixed dyslipidaemia, as an adjunct to diet.
Lomitapide directly binds and inhibits microsomal triglyceride transfer protein (MTP), which resides in the lumen of the endoplasmic reticulum, thereby preventing the assembly of apo B-containing lipoproteins in enterocytes and hepatocytes. This inhibits the synthesis of chylomicrons and VLDL. The inhibition of the synthesis of VLDL leads to reduced levels of plasma LDL-C.
Lovastatin, which is an inactive lactone, is hydrolysed after oral administration to the corresponding β-hydroxyacid. This is the major metabolite and an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, an enzyme that catalyses an early and rate-limiting step in the biosynthesis of cholesterol.
Pitavastatin competitively inhibits HMG-CoA reductase, the rate-limiting enzyme in the biosynthesis of cholesterol, and inhibits cholesterol synthesis in the liver.
Pravastatin is a competitive inhibitor of 3-hydroxy–3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme catalyzing the early rate limiting step in cholesterol biosynthesis, and produces its lipid lowering effect in two ways.
Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase. Rosuvastatin increases the number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
Simvastatin has a potent activity in inhibiting HMG-CoA reductase (3-hydroxy–3-ethylglutaryl-CoA-reductase). Simvastatin has been shown to reduce both normal and elevated LDL-C concentrations.
Niacin (nicotinic acid) is an essential B complex Vitamin (B3), whose deficiency results in the clinical syndrome known as pellagra. Nicotinamide (niacinamide), the active ingredient, is the physiologically active form of niacin and is the chemical form of Vitamin B3 found in virtually all multivitamin products. Though nicotinic acid and nicotinamide are so closely related chemically, they differ somewhat in pharmacological properties.