Statins represent the most efficient drugs for the treatment of hypercholesterolemia. They competitively inhibit the enzyme HMG-CoA {3-hydroxy-3-methylglutaryl-coenzyme A) reductase, a rate-limiting enzyme, which catalyzes the conversion of hydroxymethylglutarate to mevalonate, an early and rate limiting step in the biosynthesis of cholesterol. The statin class of cholesterol-lowering drugs has been introduced since 1987. Lovastatin is derived from Aspergillus terreus. Whereas simvastatin and pravastatin are produced by semi-synthetic ptocesses, fluvastatin, atorvastatin, pitavastatin and rosuvastatin are completely synthetic compounds. Statins are now among the most frequently prescribed drugs. Although ali statins share a cornrnon rnechanism of action, they differ in terrns of their chernical structures, pharrnacokinetics profiles, and lipid-rnodifying efficacy. Lipid-modifying interventions have been shown to decrease the risk of coronary disease both in patients with hypercholesterolemia and in those with relatively norma! levels of low-density lipoprotein cholesterol. This review surnrnarizes the differences of chemical structures and pharmacokinetic properties of statins and emphasizes their clinically irnportant drug interactions and analytical methods for the determination of statins in biological fluids and pharrnaceutical dosage forms.