Levit Mechanism of Action

Pharmacology: Pharmacodynamics: The active substance, levetiracetam, is a pyrrolidone derivative (S-enantiomer of a-ethyl-2-oxo-1-pyrrolidine acetamide), chemically unrelated to existing antiepileptic active substance.
The mechanism of action of levetiracetam still remains to be fully elucidated but appears to be different from the mechanisms of current antiepileptic medicinal products. In vitro and in vivo experiments suggest that levetiracetam does not alter basic cell characteristics and normal neurotransmission. In vitro studies show that levetiracetam affects intraneuronal Ca2+ levels by partial inhibition of N-type Ca2+ currents and by reducing the release of Ca2+ from intraneuronal stores. In addition, it partially reverses the reductions in GABA-and -glycine-gated currents induced by zinc and B-carbolines. Furthermore, levetiracetam has been shown in vitro studies to bind to a specific site in rodent brain tissue. This binding site is the synaptic vesicle protein 2A, believed to be involved in vesicle fusion and neurotransmitter exocytosis.
Levetiracetam and related analogs show a rank order of affinity for binding to the synaptic vesicle protein 2A which correlates with the potency of their anti-seizure protection in the mouse audiogenic model of epilepsy. This finding suggests that the interaction between levetiracetam and the synaptic vesicle protein 2A seems to contribute to the antiepileptic mechanism of action of the medicinal product.
Pharmacokinetics: Levetiracetam is readily absorbed from the gastrointestinal tract and peak plasma concentration are usually achieved within 1.3 hours of oral administration and steady-state achieved after 2 days. Levetiracetam is not extensively metabolized; approximately 25% of the dose is metabolized by hydroxylation to inactive metabolites. About 95% of a dose is excreted as unchanged drug and metabolites in the urine. Plasma protein binding is minimal. The plasma elimination half-life has been reported to be about 7 hours.