or K+ currents. Selectracetam has been demonstrated to not significantly affect currents gated by NMDA, AMPA, GABA, glycine, or kainic acid. The dual effect of seletracetam is an overall decrease in the amount of Ca2+ influx in the cell during an action potential due to binding at N-type channels, which prevents over-excitation of the neuron, as well as a decrease in neurotransmitter release as a product of cellular excitation due to the interaction of the drug with SV2A, which reduces the spread of excitation to nearby cells. Compared to levetiracetam, which binds at the same site, seletracetam binds to SV2A with ten times higher affinity. The nature of why the seletracetam molecule binds so specifically to SV2A and how SV2A affects exocytosis is unclear. Pharmacodynamics and pharmacokinetics The oral bioavailability of seletracetam is >90% and its half-life is approximately 8 hours. 25% of ingested seletracetam is metabolized and excreted unchanged and about 53% is excreted in the form of an inactive carboxylic acid metabolite. The main metabolic mechanism is the hydrolysis of an acetamide to a carboxylic acid. Seletracetam exhibits first-order mono-compartmental pharmacokinetics, in which there is a simple linear relationship between the amount of drug that was administered, the time that has passed, and the amount of drug subsequently remaining in the body. This contrasts the nonlinear pharmacokinetics typical of previously available anticonvulsants such as phenobarbital, phenytolin, valproate and carbamazepine. The benefit of linear kinetics is that the steady-state concentration of the drug is directly and reliably related to the dose of the drug that is administered; this allows for simple and reliable dose adjustments. In vitro studies In vitro studies performed in rodent hippocampal slices found that seletracetam causes a complete reversal of the increases in activity of population spike amplitude in epilepsy models. These reductions in in vitro epilepsy symptoms were present at extracellular concentrations of 3.2 μM. This is approximately 10% of the most effective concentration of levetiracetam in similar tests. Animal studies Seletracetam has been tested on various animal models for epilepsy, with mixed results. Unlike drugs that act on voltage-gated sodium channels, seletracetam was demonstrated to have no significant effect on the maximal electroshock seizure test results in mice. It similarly had no relieving effects in mice of the other most common acute seizure model, the pentylenetetrazol convulsion-induction model. Seletracetam did, however, show promising results in acquired and genetic epilepsy models. In the mouse