Escitalopram: Mechanism of Action
Escitalopram is a selective serotonin reuptake inhibitor (SSRI) used as a first-line treatment for depression, anxiety disorders, OCD, and PTSD.
SSRIs block the serotonin transporter (SERT), increasing serotonin availability in the synaptic cleft.
How It Works
Selective serotonin reuptake inhibitors (SSRIs) competitively inhibit the serotonin transporter (SERT/SLC6A4) on presynaptic neurons, preventing reuptake of serotonin (5-HT) back into the presynaptic terminal. This increases the concentration of serotonin in the synaptic cleft, enhancing serotonergic neurotransmission in limbic, prefrontal cortex, and raphe nuclei circuits. The therapeutic effect typically emerges over 2–6 weeks due to receptor desensitisation and neuroplasticity changes rather than immediate receptor occupancy.
Receptor / Target Profile
- •SERT (serotonin transporter) — primary target
- •5-HT1A autoreceptors — desensitise over 2–4 weeks, enabling full antidepressant effect
- •5-HT2A/2C receptors — secondary modulation
- •Sigma-1 receptors — implicated in anxiolytic effects (especially sertraline, fluvoxamine)
Pharmacokinetics
Onset of Action
2–6 weeks for antidepressant effect; partial anxiety relief within 1–2 weeks
Half-Life (t½)
Varies: fluoxetine 1–4 days (active metabolite norfluoxetine 4–16 days); sertraline ~26 hours; escitalopram ~27–32 hours; paroxetine ~21 hours; citalopram ~35 hours
Well absorbed orally (60–80% bioavailability). Extensively protein-bound (>95%). Hepatic metabolism via CYP2D6, CYP2C19, and CYP3A4. Renal excretion of metabolites. Fluoxetine has the longest half-life and most forgiving missed-dose profile.
Conditions Treated with Escitalopram
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