Escitalopram (trade names Lexapro, Cipralex) is the pure (S) enantiomer of racemic citalopram and is a selective serotonin reuptake inhibitor (SSRI). Escitalopram is used in the treatment of depression and anxiety.
According to a meta-analysis of 12 new-generation antidepressants, escitalopram and sertraline are the best in terms of efficacy and acceptability in the acute-phase treatment of adults with unipolar major depression. Reboxetine was significantly worse
WHAT IS LEXAPRO?
WHAT IS LEXAPRO?
Lexapro is an antidepressant in a group of drugs called selective serotonin reuptake inhibitors (SSRIs). It affects chemicals in the brain that may become unbalanced and cause depression or anxiety.
Lexapro is used to treat anxiety and major depressive disorder.
Lexapro may also be used for purposes other than those listed in this medication guide.
Escitalopram (Lexapro by Forest Laboratories in the United States and elsewhere by Lundbeck as Cipralex, Sipralexa, Seroplex and also as Lexapro)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.Escitalopram acts by increasing intrasynaptic levels of the neurotransmitter serotonin by blocking the reuptake of the neurotransmitter into the neuron. Of the SSRIs currently on the market escitalopram has the highest affinity for the human serotonin transporter (SERT). 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, researchers from Lundbeck proposed that escitalopram enhances its own binding via an additional interaction with another allosteric site on the transporter.Further research by the same group showed that R-citalopram also enhances binding of escitalopram,and therefore the allosteric interaction cannot explain the observed counteracting effect. In the most recent paper, however, the same authors again reversed their findings and reported that R-citalopram decreases binding of escitalopram to the transporter. Although allosteric binding of escitalopram to the serotonin transporter is of unquestionable research interest, its clinical relevance is unclear since the binding of escitalopram to the allosteric site is at least 1000 times weaker than to the primary binding site.
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, researchers from Lundbeck proposed that escitalopram enhances its own binding via an additional interaction with another allosteric site on the transporter.Further research by the same group showed that R-citalopram also enhances binding of escitalopram,and therefore the allosteric interaction cannot explain the observed counteracting effect. In the most recent paper, however, the same authors again reversed their findings and reported that R-citalopram decreases binding of escitalopram to the transporter. Although allosteric binding of escitalopram to the serotonin transporter is of unquestionable research interest, its clinical relevance is unclear since the 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 - WHAT IS LEXEPRO?
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