Abstract
Escitalopram, the S-enantiomer of citalopram is a novel antidepressant drug. Its predecessor, citalopram, makes a racemate of S (-) and R (+) enantiomers in a 1:1 ratio. Only S-enantiomer of citalopram shows high affinity for serotonin transporter with resulting therapeutic activity, and R-enantiomer is devoid of such properties. Escitalopram produces a unique action on serotonin transporter. Serotonin transporter possesses two binding sites: primary one that mediates the inhibition of serotonin reuptake, and a low affinity allosteric site that modulates a binding of ligand at the primary site. Additional binding of escitalopram to allosteric site stabilizes its binding at the primary site. R-citalopram competing for allosteric site, reduces this effect of escitalopram and thereby attenuates its pharmacological and clinical effects. The clinical trials support these theoretical assumptions. Depressed patients taking escitalopram showed faster and better antidepressant response than patients taking citalopram in comparable doses.