Escitalopram Use in Depression & the Influence of Genetic Variations on Its Safety & Efficacy

Abstract

Major depressive disorder (MDD) is a common debilitating mental illness marked by sad feelings, depressed mood, and lack of interest in routine chores that persists daily or for a minimum of two weeks.  Serotonin-norepinephrine inhibitors, selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors, and atypical antidepressants are some of the common classes of drugs used for the treatment of MDD. Despite strenuous efforts by the researchers, hardly any new antidepressant agent has entered the market. Escitalopram, a highly selective serotonin reuptake inhibitor, is the drug of choice for the treatment of MDD. However, although escitalopram is one of the most frequently prescribed antidepressant agents, a large percentage of MDD patients show variable remission and response to escitalopram.  Scientists spent decades finding the underlying mechanism responsible for the significant variations in drug response and incidence of adverse effects. These inter-individual variations in therapeutic response serve as a foundation for the inception of the pharmacogenomic. Pharmacogenomics is a field of research that expounds on the impact of gene variation on altered clinical outcomes of drugs. There has been substantial hope and potential that pharmacogenomics will ameliorate the current therapies for MDD and aid in finding novel targets for new drug discoveries. Currently, numerous candidate genes have been identified, implicated in changing drug response, whether at the receptor, transporter, or drug-metabolizing enzyme. In this review, we attempt to compile the studies on the genetic variations that have been found to be associated with escitalopram efficacy and adverse effects and briefly discuss the pathophysiology and currently available treatment options for MDD