Treatment: major depressive episodes; panic disorders with or without agoraphobia; social anxiety disorders (social phobia); generalized anxiety disorders; obsessive-compulsive disorders.
Ezopram 10 mg Composition
active substance: escitalopram;
1 tablet contains escitalopram oxalate equivalent to escitalopram 10 mg;
excipients: microcrystalline cellulose, colloidal silicon, talc, croscarmellose sodium, magnesium stearate
sheath: Opandry 03F2846 White: hypromellose 6cP, titanium dioxide (E 171), macrogol 600.
Ezopram 10 mg Dosage form
Basic physical and chemical properties:
Esopram 10 mg – white, oval, double-lumpy tablets, film-coated with an “E” marking on one side and a distribution notch on the other and on both sides.
Ezopram 10 mg Pharmacotherapeutic group
Antidepressants. Selective serotonin reuptake inhibitors (SSRIs). ATX code N06A B10.
Escitalopram is a selective serotonin reuptake inhibitor (5-HT) with high affinity for the primary binding site. It also binds to the allosteric site of the serotonin transporter with a 1000-fold lower affinity.
Escitalopram has no or very weak ability to bind to receptors such as 5-HT1A, 5-HT2, dopamine D1 and D2 receptors, α1-, α2-, β-adrenergic receptors, histamine H1, muscarinic cholinergic, benzodiazepine and opiate receptors. Inhibition of 5-HT serotonin reuptake is only a probable mechanism of action that can explain the pharmacological and clinical effects of escitalopram.
Absorption. Absorption is almost complete and does not depend on food intake. The average time to reach the maximum concentration (mean Tmax) is about 4 hours. The bioavailability of escitalopram is expected to be 80%.
Distribution. The volume of distribution (Vd, β / F) after oral administration ranges from 12 to 26 l / kg. The binding of escitalopram and its main metabolites with blood plasma proteins is less than 80%.
Metabolism. Escitalopram is metabolized in the liver to biologically active demethylated and didemethylated metabolites. Nitrogen can also be oxidized to form an N-oxide metabolite. Both the metabolites and the parent compound are partially excreted in the form of glucuronides. After repeated use, the average concentration of demethyl- and didemethylmetabolite is usually 28-31% and <5% of the escitalopram concentration, respectively. The metabolism of escitalopram to the demethylated metabolite occurs primarily via cytochrome CYP2C19. Certain participation of CYP3A4 and CYP2D6 enzymes is also possible.
Allocations. The half-life (t½β) after repeated use is about 30 hours. Oral clearance is 0.6 l / min. In the main metabolites of escitalopram, the elimination half-life is longer. It is believed that escitalopram and its major metabolites are excreted through the liver (metabolic pathway) and kidneys. Most of it is excreted in the form of metabolites in the urine.
The kinetics of escitalopram is linear. Equilibrium concentration is achieved in 1 week. The average equilibrium concentration of 50 nmol / l (from 20 to 125 nmol / l) is achieved with a daily dose of 10 mg.
Elderly patients (over 65 years old)
Withdrawal of escitalopram in elderly patients occurs more slowly than in younger patients. Systemic exposure (AUC) in the elderly is about 50% higher than in young healthy volunteers.
In patients with moderate or mild hepatic impairment (Child-Pugh class A and B), the half-life of escitalopram was almost doubled and the exposure was approximately 60% higher than in those with normal liver function.
Impaired renal function
In patients with impaired renal function (CLcr 10-53 ml / min), an increase in the half-life of racemic citalopram and a slight increase in exposure were observed. Plasma concentrations of metabolites have not been studied, but an increase can be assumed.
Polymorphism. With insufficient activity of the CYP2C19 enzyme, double plasma concentrations of the drug were observed compared to the normal metabolism of escitalopram. No significant changes in exposure were observed with CYP2D6 enzyme deficiency.