What is escitalopram

Therapy for depression and anxiety: Escitalopram leaves the sun faster than

The neurotransmitters norepinephrine and serotonin play a central role in the treatment of depression and anxiety, as it is known that a decrease in these two substances in the CNS is associated with corresponding symptoms.

Almost all antidepressants intervene in the synaptic communication of the neurotransmitters serotonin and noradrenaline in the CNS - however, they use different biochemical pathways. The most important way goes back to the classic tricyclic antidepressants: They inhibit the transport proteins that are responsible for the return transport of neurotransmitters from the synaptic cleft to the presynapse.

SSRIs have a favorable effect / side effect profile

The selective serotonin reuptake inhibitors also work by inhibiting these transport proteins. What they all have in common is a more or less pronounced selectivity for serotonin receptors. Norepinephrine receptors are hardly influenced, and additional receptor profiles are almost completely absent.

The antidepressant and anxiolytic effectiveness of SSRIs is comparable to that of tricyclic or tetracyclic antidepressants, but due to the selectivity for serotonin, the substances have no cardiotoxic properties. However, they are of course not free from side effects. By blocking the absorption of serotonin, they can lead to nausea, vomiting, sleep disorders, restlessness, weight loss and sexual dysfunction. Overall, however, they have such a favorable effect / side effect profile that they are widely used as first-line therapeutic agents for depression. They are considered the gold standard in the therapy of anxiety disorders.

Escitalopram: The active "part" of citalopram

The selective serotonin reuptake inhibitors currently approved in Germany include citalopram, fluoxetine, fluvoxamine, paroxetine and sertraline. Another substance - escitalopram - is to be added to the spectrum soon. Strictly speaking, it is a further development of Citalopram.

Citalopram, which was synthesized in 1972, is a racemate consisting of the levorotatory (S) and dextrorotatory (R) enantiomer. However, its effect is only mediated by the levorotatory part, the R enantiomer is actually unnecessary ballast. This fact had been known for a long time, in 1988 it was possible for the first time to separate the two enantiomers in the laboratory and to examine their effects.

However, separation on an industrial scale was impossible at the time. It was not until the mid-1990s, with the development of the so-called "Simulated Moving Bed" technology, that large quantities of the S-enantiomer were released from the racemate and that it was now also being tested in clinical studies.

Escitalopram works faster

Various studies have shown that escitalopram is characterized by a faster onset of action compared to citalopram. For example, in a study with around 1300 participants, the antidepressant effect of escitalopram in concentrations of 10, 20 and 40 mg per day was compared with 20 mg / d citalopram and placebo over a period of eight weeks.

While both citalopram and escitalopram were superior to placebo at the end of the study, only escitalopram in the two higher doses had a clear effect after just one week. After two weeks, the 10 mg dose was also clearly superior to the placebo. The side effect profile and the extent of the side effects of escitalopram corresponded to those of citalopram in the study.