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Systematic (IUPAC) name
CAS number 128196-01-0
ATC code N06AB10
PubChem 146570
DrugBank APRD00683
Chemical data
Formula C20H21FN2O 
Mol. mass 324.392 g/mol
(414.40 as oxalate)
Pharmacokinetic data
Bioavailability 80%
Protein binding ~56%
Metabolism Liver, specifically the enzymes CYP3A4 and CYP2C19
Half life 27–32 hours
Excretion  ?
Therapeutic considerations
Pregnancy cat.


Legal status

Prescription only

Routes Oral

   Escitalopram (Lexapro by Forest Laboratories in the United States and elsewhere by Lundbeck as Lexaprin, Cipralex, Sipralexa, Entact and Seroplex)[1] is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. It is approved for the treatment of major depressive disorder and generalized anxiety disorder; other indications include social anxiety disorder, panic disorder and obsessive-compulsive disorder. Escitalopram is the S-stereoisomer (enantiomer) of the earlier Lundbeck drug citalopram (Celexa), hence the name escitalopram. Escitalopram is noted for its high selectivity of serotonin reuptake inhibition and, as a result has fewer side effects not related to its serotonergic activity.[2]



Escitalopram was developed in a close cooperation between Lundbeck and Forest Laboratories. Its development was initiated in the summer of 1997, and the resulting new drug application was submitted to the FDA in March 2001. The short time (3.5 years) it took to develop escitalopram can be attributed to the previous extensive experience of Lundbeck and Forest with citalopram, which has similar pharmacology.[3] The FDA issued the approval of escitalopram for major depression in August 2002 and for generalized anxiety disorder in December 2003. Escitalopram can be considered an example of "lifecycle management"[4] - the strategy pharmaceutical companies use in order to extend the lifetime of a drug, in this case of the citalopram franchise. Escitalopram is an enantiomer of citalopram, used for the same indication, and for that reason it required less investment and less time to develop. Two years after escitalopram's launch, when the patent on citalopram expired, the escitalopram sales successfully made up for the loss. On May 23 2006, the FDA approved a generic version of escitalopram by Teva.[5] However, on July 14 of that year, the U.S. District Court of Delaware decided in favor of Lundbeck regarding the patent infringement dispute and ruled the patent on escitalopram valid.[6]

Despite the drug's similarity, preclinical as well as various clinical studies (including double-blinded studies—considered the gold standard of clinical evidence) have shown differentiated effects of citalopram and escitalopram,[7] as well as a clinical superiority compared to a variety of other SSRIs, such as paroxetine,[8] especially in severely depressed patients and sertraline. Compared to newer serotonin-norepinephrine reuptake inhibitors such as venlafaxine[9] and duloxetine[10] escitalopram was shown to be at least as effective.


Escitalopram acts by increasing intrasynaptic levels of the neurotransmitter serotonin by blocking the re-uptake of the neurotransmitter into the neuron. Of the SSRIs currently on the market escitalopram has the highest affinity for the human serotonin transporter (SERT). Remarkably, another enantiomer of citalopram (R-citalopram) counteracts to a certain degree the serotonin enhancing action of escitalopram. As a result, escitalopram is a more potent antidepressant than citalopram, which is a mixture of escitalopram and R-citalopram. In order to explain this phenomenon, Sanchez proposed that escitalopram enhances its own binding via an additional interaction with another allosteric site on the transporter.[11] Further research by the same group showed that R-citalopram also enhances binding of escitalopram,[12] and therefore the allosteric interaction cannot explain the observed counteracting effect. However, in the most recent paper the same authors again reversed their findings and reported that R-citalopram decreases binding of escitalopram to the transporter.[13] Although allosteric binding of escitalopram to the serotonin transporter is of unquestionable research interest, its clinical relevance is unclear since binding of escitalopram to the allosteric site is at least 1000 times weaker than to the primary binding site.

In vitro studies using human liver microsomes indicated that CYP3A4 and CYP2C19 are the primary isozymes involved in the N-demethylation of escitalopram. lexapro


The recommended dosage of Lexapro is 10–40 mg a day, averaging between 10 and 20. Exceptions include the elderly, who should only take up to 10 mg a day, and pregnant women in their third trimester should not use Lexapro at all.[14] As both Generalized Anxiety Disorder (GAD) and Depression are both considered chronic conditions, treatment is recommended for several months. However, the efficacy of Lexapro over long periods of time has not been studied, therefore consistent re-evaluation of the treatment is recommended for longer periods of treatment.[14]

Side effects and drug interactions

The side effect profile of escitalopram is close to that of other SSRIs, with nausea, somnolence, and gastrointestinal side effects reported as relatively common. Escitalopram, like other SSRIs, has been shown to cause sexual side effects in many patients.[15] Escitalopram is not associated with significant weight gain. For example, 0.6 kg mean weight change after 6 months of treatment with escitalopram for depression was insignificant and similar to that with placebo (0.2 kg).[16] 1.4-1.8 kg mean weight gain was reported in 8-month trials of escitalopram for depression,[17] and generalized anxiety disorder.[18] A 52-week trial of escitalopram for the long-term treatment of depression in elderly also found insignificant 0.6 kg mean weight gain.[19] Escitalopram may help reduce weight in those treated for binge eating associated obesity.[20] It may also cause dizziness after exercise in children.[citation needed]

A meta-analysis of clinical trials database conducted by the escitalopram manufacturer Lundbeck found no indication that escitalopram would provoke suicidal behaviour compared to placebo in patients with major depressive disorder and anxiety disorders, on the contrary, suicidal thoughts in the escitalopram group were significantly decreased.[21] An analysis conducted by the FDA found a statistically insignificant 1.5 to 2.4-fold, depending on the statistical technique used, increase of suicidality among the adults treated with escitalopram for psychiatric indications.[22][23][24] Similarly, the UK MHRA data indicate an 80% increase of suicide-related events, not reaching statistical significance, in the escitalopram vs placebo patients.[25] The authors of a related study note the general problem with statistical approaches—due to the rarity of suicidal events in clinical trials, it is hard to draw firm conclusions with a sample smaller than two million patients.[26] A single case report described a patient developing suicidal ideation after beginning treatment with escitalopram, and suicidal ideation disappearing after stopping the treatment.[27]

Escitalopram should be taken with caution when using St John's wort.[28]

Discontinuation symptoms

Lexapro discontinuation, particularly abruptly, may cause certain withdrawal symptoms such as paresthesia (for example, electric shock sensations also known as "brain shivers" or "brain zaps"), dizziness and irritability.[29]

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Escitalopram". A list of authors is available in Wikipedia.
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