Essobel (escitalopram) coated tablets 20 mg. №28

Description

Essobel Storage
active substance: escitalopram;

1 tablet contains escitalopram oxalate equivalent to escitalopram 10 mg or 20 mg;

Excipients: copovidone, lactose monohydrate, corn starch, microcrystalline cellulose, croscarmellose sodium, magnesium stearate, Sepifilm LP 770 coating: hydroxypropylmethylcellulose, microcrystalline cellulose, stearic acid, titanium dioxide.

Essobel Dosage form
Coated tablets.

Basic physical and chemical properties:

10 mg tablets: oval, coated tablets, white, with a break line on one side and engraved with “10” on the other;

20 mg tablets: Oval, coated tablets, white, with a break line on one side and engraved with “20” on the other.

Pharmacotherapeutic group
Antidepressants. Selective serotonin reuptake inhibitors.

ATX code N06A B10.

Pharmacological properties

Pharmacodynamics.

Essobel® is an antidepressant, a selective serotonin reuptake inhibitor (SSRI), which determines the clinical and pharmacological effects of the drug. It has a high affinity for the main binding element and the adjacent allosteric element of the serotonin transporter and has no or very weak ability to bind to a number of receptors, including serotonin 5 ‑ HT1A-, 5 ‑ HT2-receptors, dopamine D1- and D2-receptors, a1‑, a2‑, β ‑ adrenergic receptors, histamine H1, muscarinic cholinergic, benzodiazepine and opiate receptors.

Escitalopram is the S-enantiomer of racemic citalopram with its own therapeutic activity. It is proved that the R-enantiomer is not inert, but counteracts the serotonergic properties and the corresponding pharmacological effects of the S-enantiomer.

Essobel Pharmacokinetics.

Absorption is almost complete and does not depend on food intake. The maximum concentration in blood plasma is reached in 4 hours after reception. The bioavailability of escitalopram is approximately 80%.

Escitalopram and its major metabolites are less than 80% bound to blood proteins.

Metabolism occurs in the liver to demethylated and didemethylated metabolites. Both of them are pharmacologically active. The biotransformation of escitalopram to the demethylated metabolite is via cytochrome CYP2C19. Insignificant participation in the process of isoenzymes CYP3A4 and CYP2D6 is possible. The half-life of the drug is approximately 30 hours. The creatinine clearance when taken orally is approximately 0.6 l / min. In major metabolites, the half-life is longer. Escitalopram and its major metabolites are excreted by the liver (metabolic pathway) and kidneys. Most of the dose is excreted as metabolites in the urine. The kinetics of escitalopram are linear. Equilibrium concentration is reached in about 1 week. In elderly patients (over 65 years) escitalopram is excreted more slowly than in young patients.

In patients with mild to moderate hepatic impairment (Child-Pugh classes A and B), the half-life was twice as long and the exposure was 60% higher than in subjects with normal hepatic function.

Patients with renal impairment had a longer half-life and slightly higher exposure with racemic citalopram. The concentration of metabolites in blood plasma has not been studied, but may be elevated.

Patients with poor CYP2C19 metabolic function had twice the plasma concentrations of escitalopram than patients with normal CYP2C19 function. No significant changes in exposure with reduced CYP2D6 function were observed.

Indication
Treatment of major depressive episodes, panic disorders with or without agoraphobia, social anxiety disorders (social phobia), generalized anxiety disorders, obsessive-compulsive disorders.

Contraindication
Hypersensitivity to escitalopram or to other components of the drug;
concomitant treatment with non-selective irreversible monoamine oxidase inhibitors (MAOIs), as there is a risk of serotonin syndrome, manifested by agitation, tremor, hyperthermia;
combination with reversible MAO-A inhibitors (eg moclobemide) or reversible non-selective MAO inhibitor linezolid, as there is a risk of serotonin syndrome;
QT prolongation or congenital long QT syndrome;
concomitant use with drugs that prolong the QT interval;
concomitant treatment with pimozide.