Cipram Mechanism of Action

A selective and potent serotonin re-uptake inhibitor (SSRI).
Pharmacology: Citalopram is a potent selective and inhibitor of serotonin uptake with antidepressant effect.
Cipram has no or very low affinity for a series of receptors including muscarine cholinergic receptors, histamine receptors and adrenoceptors. This absence of effects on receptors could explain why citalopram produces fewer of the traditional adverse effects of tricyclic antidepressants eg, dry mouth, blurred vision, sedation, cardiotoxicity and orthostatic hypotension. Unlike other available SSRIs, Cipram is only a very weak inhibitor of the cytochrome P-450 II D6 metabolic pathway with a consequent reduction in potential for adverse events and interactions.
The antidepressant effect usually sets in after 2-4 weeks.
Cipram does not affect the cardiac conduction system or blood pressure. This is particularly important for elderly patients. In addition, Cipram does not affect the haematological, hepatic or renal systems. The low frequency of side effects and the minimal sedative properties of Cipram make it especially useful in long-term treatment. Moreover, Cipram neither causes weight gain nor potentiates the effect of alcohol.
Pharmacokinetics: The oral bioavailability of citalopram is about 80%. Maximum citalopram plasma levels are reached 2-4 hrs after dosing. The protein-binding is <80%. Metabolism proceeds by demethylation, deamination and oxidation. Unchanged citalopram is the predominant compound in plasma. The kinetics is linear. Steady-state conditions are achieved in 1-2 weeks. The biological half-life is about 1½ days. Excretion is via urine and faeces.