Abstract
Citalopram is a serotonin-selective reuptake inhibitor (SSRI) widely used in the treatment of major depression and sometimes also anxiety--associated conditions, obsessive compulsive disorder and behavior disturbances associated with dementia [1, 2]. Citalopram is relatively well tolerated and has been considered to have compa -ratively low potential for drug–drug interactions and anti-adrenergic and anti-cholinergic effects, making it an attractive treatment option for elderly patients [1, 2]. The drug is chiral and the serotonin reuptake inhibitory activity of citalopram resides in the S(+) enantiomer (available as escitalopram) with no therapeutic benefit of the R(–) enantiomer. There is limited evidence that at equivalent doses (i.e. matched concentrations of the S(+) enantio-mer), escitalopram is more effective clinically than citalopram is, raising the possibility of a potential inhibitory effect of the R(–) enantiomer [3–5]. Data from studies, in which serotonin reuptake transporter (SERT) occupancy has been examined in humans, suggest that on repeated dosing with racemic citalopram, R(–) citalopram levels may exceed those of the S(+) enantiomer, leading to reduced S(+) citalopram occupancy of SERT [6].
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