Monotherapy (first-choice drug) for: partial seizures with or without secondary generalization in adults and adolescents aged 16 and older who were first diagnosed with epilepsy. As an additional therapy for: partial seizures with or without secondary generalization in adults and children aged 1 month and older with epilepsy; myoclonic seizures in adults and adolescents aged 12 years and older, with juvenile myoclonic epilepsy; primary generalized tonic-clonic seizures in adults and adolescents aged 12 years and older, patients with idiopathic generalized epilepsy.
1 tablet contains 250 mg or 500 mg, or 750 mg, or 1000 mg of levetiracetam;
excipients: crospovidone, povidone, colloidal anhydrous silica, magnesium stearate;
250 mg tablets: hypromellose, macrogol, titanium dioxide (E 171), talc, indigo carmine (E 132);
500 mg tablets: hypromellose, macrogol, titanium dioxide (E 171), talc, iron oxide yellow (E 172);
750 mg tablets: hypromellose, macrogol, titanium dioxide (E 171), talc, yellow FCF (E 110), iron oxide red (E 172);
tablets of 1000 mg: hypromellose, macrogol, titanium dioxide (E 171), talc.
Levetiracetam Dosage form. Film-coated tablets.
Basic physical and chemical properties:
250 mg tablets: oval tablets, coated with a blue film, with a line on one side;
500 mg tablets: oval tablets, coated with a yellow film, with a line on one side;
750 mg tablets: oval tablets, film-coated orange, with a line on one side;
1000 mg tablets: Oval tablets, white film-coated, scored on one side.
Pharmacotherapeutic group. Antiepileptic drugs. Levetiracetam.
Code ATX N03A X14.
It is a derivative of pyrrolidone (S-enantiomer of alpha-ethyl-2-oxo-1-pyrrolidine-acetamide), chemically different from known antiepileptic drugs.
The mechanism of action of levetiracetam is insufficiently studied, but it is established that it differs from the mechanism of action of known antiepileptic drugs. Based on in vitro and in vivo studies, it is assumed that levetiracetam does not alter the basic characteristics of the nerve cell and normal neurotransmission. In vitro studies have shown that levetiracetam affects internal neuronal Ca2 + levels by partially suppressing current through N-type Ca2 + channels and reducing Ca2 + release from intraneuronal depots. It also partially counteracts the inhibition of gamma-aminobutyric acid (GABA) and glycine-regulated current, which is due to the action of zinc and beta-carbolines. In addition, in vitro studies, levetiracetam has been associated with specific areas in rodent brain tissue. The binding site is the protein of synaptic vesicles 2A, which is involved in the fusion of vesicles and the release of neurotransmitters. The affinity of levetiracetam and the corresponding analogues with the protein of synaptic vesicles 2A correlated with the strength of their anticonvulsant action in models of audiogenic epilepsy in mice. These results suggest that the interaction between levetiracetam and synaptic vesicle protein 2A may partly explain the mechanism of antiepileptic action of the drug.
Provides protection against seizures in a wide range of models of partial and primary generalized seizures in animals without causing a seizure effect. The major metabolite is inactive.