Central Research Laboratory, Department of Biotechnology,  Era’s Lucknow Medical College & Hospital, Era University, Lucknow, Uttar Pradesh, India- 226003.

Central Research Laboratory, Department of Biotechnology,  Era’s Lucknow Medical College & Hospital, Era University, Lucknow, Uttar Pradesh, India- 226003.

Central Research Laboratory, Department of Biotechnology,  Era’s Lucknow Medical College & Hospital, Era University, Lucknow, Uttar Pradesh, India- 226003.

Central Research Laboratory, Department of Biotechnology,  Era’s Lucknow Medical College & Hospital, Era University, Lucknow, Uttar Pradesh, India- 226003.

Department of Medicine, Era’s Lucknow Medical College & Hospital, Era University, Lucknow, Uttar Pradesh, India- 226003.

Statins are one of the most widely prescribed drugs globally. The group of medicines is meant to reduce high levels of serum cholesterol and prevent the occurrence of cardiovascular events in future. However, they have the potential to bring LDL cholesterol to normal levels and, therefore, diminish the menace of heart attack or stroke, patients individually show significantly different responses. Hence, in some patients (responders), statin treatment may result in very obvious good effects. Those who are on the same medication as these patients, however, may experience little or no change in their conditions at all (non-responders). This difference was increasingly blamed on genetics, which not only influence the effectiveness but also the safety of statin therapy. Pharmacogenomics has made several strides and discovered that many genetic polymorphisms exist in the genes for drug-metabolizing enzymes and protein membrane transporters that regulate statin pharmacokinetics and pharmacodynamics. The different cytochrome P450 enzymes, like CYP3A4, CYP3A5, CYP2C9, and CYP2C19, determine the metabolism of statins, while the gene variations coding for hepatic acceptance and efflux transporters, e. g., SLCO1B1, ABCB1, and ABCG2, influence the absorption, distribution, and elimination of statins. These genetic variants result in changes in plasma drug concentrations, drug therapeutic effectiveness, and drug-related side effects, specifically, statin-induced myopathy. This review consolidates recent evidence regarding pharmacogenetic factors that lead to the identification of responder and non-responder phenotypes, mainly dealing with essential metabolizing enzymes and transport proteins. These genetic influences clarify a great deal of the variability between individuals in their response to statins and point to the potential of statin dosage personalization to be one of the main tools of precision medicine in the prevention of cardiovascular diseases.