Monotherapy (first choice drug) for treatment: partial seizures with or without secondary generalization in adults and children over 16 years of age who were first diagnosed with epilepsy. As an additional therapy for treatment: partial seizures with or without secondary generalization in adults and children aged 6 years and older with epilepsy; myoclonic seizures in adults and children over 12 years of age with juvenile myoclonic epilepsy; primary generalized tonic-clonic seizures in adults and children older than 12 years, patients with idiopathic generalized epilepsy.
Levenium tablets Composition
active substance: levetiracetam;
1 coated tablet contains levetiracetam 500 mg;
Levenium tablets Excipients:
500 mg tablets: corn starch, croscarmellose sodium, colloidal silicon dioxide, talc, magnesium stearate, Opadry Yellow 03F52321 coating: hypromellose, titanium dioxide (E 171), macrogol 6000, talc, iron oxide yellow (E 172).
Levenium tablets Dosage form
Basic physical and chemical properties:
500 mg tablets: oval, biconvex film-coated tablets of light yellow color, smooth on one side and with a break line on the other.
Levenium tablets Pharmacotherapeutic group
Antiepileptic drugs. Levetiracetam. ATX code N03A X14.
Levetiracetam is a derivative of pyrrolidone (S-enantiomer of alpha-ethyl-2-oxo-1-pyrrolidine-acetamide), differs in chemical structure from known antiepileptic drugs.
Mechanism of action.
The mechanism of action of levetiracetam is not well understood. 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 intra-neuronal Ca 2+ levels by partially suppressing the current through N-type Ca 2+ channels and decreasing Ca2 + release from intra-neuronal stores. It also partially neutralizes the inhibition of GABA and glycine-regulated current caused by the action of zinc and β-carboline. In addition, in in vitro studies, levetiracetam binds to specific sites in rodent brain tissues. The binding site is the synaptic vesicle protein 2A, which is involved in vesicle fusion and neurotransmitter release. The relationship (in rank order) of levetiracetam and the corresponding analogs with the synaptic vesicle protein 2A correlated with the potency 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 partially explain the mechanism of antiepileptic action of the drug.
Levetiracetam provides protection against seizures in a wide range of animal models of partial and primary generalized attacks, without causing a prodome effect. The main metabolite is inactive.
In humans, the activity of the drug has been confirmed for both partial and generalized epileptic seizures (epileptiform manifestations / photoparoxysmal reaction), which indicates a wide spectrum of the pharmacological profile of levetiracetam.
Levetiracetam is characterized by high solubility and permeability. Pharmacokinetics is linear, does not depend on time and is characterized by low inter- and intrasubject variability. After repeated use of the drug, the clearance does not change. There were no signs of influence of gender, race or circadian rhythm on pharmacokinetics. The pharmacokinetic profile was similar in healthy volunteers and patients with epilepsy.
Due to complete and linear absorption, the plasma level of the drug can be predicted from the oral dose of levetiracetam, expressed in mg / kg body weight. Therefore, it is not necessary to monitor plasma levels for levetiracetam.
In adults and children, there was a significant correlation between the concentration of the drug in saliva and blood plasma (the concentration ratio in saliva / plasma ranged from 1 to 1.7 after taking oral tablets and 4 hours after taking oral solution).
Adults and adolescents.
Levetiracetam is rapidly absorbed after oral administration. The absolute oral bioavailability is close to 100%. The maximum concentration in blood plasma (Cmax) is reached 1.3 hours after taking the drug. The equilibrium state is achieved after 2 days of using the drug twice a day. The maximum concentration (Cmax) is usually 31 and 43 μg / ml after a single dose of 1000 mg and a repeated dose of 1000 mg twice a day, respectively. The degree of absorption does not depend on the dose and does not change with food.