Seletracetam

[7] Seletracetam was in Phase II clinical trials under the supervision of the U.S. Food and Drug Administration (FDA) but its production is on hold.

[3] Seletracetam's molecular structure contains elements common to other anticonvulsants, including levetiracetam and brivaracetam, such as a nitrogen heterocyclic system.

[1] Seletracetam's anti-epileptic effects are due to its high affinity binding to synaptic vesicle glycoprotein 2A (SV2A)[1][2][3]—part of a calcium ion regulator.

[4] Selectracetam has been demonstrated to not significantly affect currents gated by NMDA, AMPA, GABA, glycine, or kainic acid.

[15] 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.

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.

Unlike drugs that act on voltage-gated sodium channels,[19] seletracetam was demonstrated to have no significant effect on the maximal electroshock seizure test results in mice.

[2][7] In the mouse model of corneal kindling, which exhibits the anticonvulsant capability of generalized motor seizures, doses as low as 0.07 mg/kg intraperitoneal injection (i.p.

[11][14][24] This drug neither inhibits nor unnecessarily induces the action of any major human metabolizing enzymes, which further reduces adverse effects.

[25] In phase II trials side effects were limited to the CNS in origin, were of mild to moderate severity, and most were resolved within 24 hours[2] and with no medical intervention.

(twice daily) doses of 200 mg.[11] Toxicology studies have shown that this drug has low acute oral toxicity and no significant negative effects on the CNS, cardiac, or respiratory systems.

[11] Phase II clinical trials of seletracetam were ongoing but in July 2007 the company stated that the drug's development has been put on hold.