Escitalopram has a low potential for clinically signiﬁcant medicine interactions. In vitro studies have shown that the biotransformation of Escitalopram to its demethylated metabolites depends on three parallel pathways (cytochrome P450 (CYP) 2C19, 3A4 and 2D6). Escitalopram is a very weak inhibitor of isoenzyme CYP1A2, 2C9, 2C19, 2E1 and 3A and weak inhibitor of 2D6.
Eﬀects of other medicinal products on Escitalopram in vivo.
The pharmacokinetics of single doses of Escitalopram were not changed by coadministration with a single dose of ritonavir (CYP3A4 inhibitor). Furthermore coadministration with ketoconazole (potent CYP3A4 inhibitor) did not change the pharmacokinetics of racemic citalopram.
Coadministration of racemic citalopram with cimetidine (potent CYP2D6, 3A4 and 1A2 inhibitor) resulted in increased plasma concentrations of the racemate (43% increase in AUC, 39% increase in Cmax). Thus, caution should be exercised at the upper end of the dose range of Escitalopram when used concomitantly with high doses of cimetidine.