Anatomical Therapeutic Chemical Classification System
Brivaracetam displays a high and selective affinity for synaptic vesicle protein 2A (SV2A), a transmembrane glycoprotein found at presynaptic level in neurons and in endocrine cells. Although the exact role of this protein remains to be elucidated it has been shown to modulate exocytosis of neurotransmitters.
Cannabidiol is indicated for the treatment of seizures associated with Lennox‑Gastaut syndrome (LGS), Dravet syndrome (DS), or tuberous sclerosis complex (TSC) in patients 1 year of age and older.
Cenobamate is a small molecule with a dual mechanism of action. It is a positive allosteric modulator of subtypes of the γ-aminobutyric acid (GABAA) ion channel, that does not bind to the benzodiazepine binding site. Cenobamate has also been shown to reduce repetitive neuronal firing by enhancing the inactivation of sodium channels and by inhibiting the persistent component of the sodium current.
Lacosamide is a functionalised amino acid. The precise mechanism by which lacosamide exerts its antiepileptic effect in humans remains to be fully elucidated.
Lamotrigine is a use and voltage dependent blocker of voltage gated sodium channels. It inhibits sustained repetitive firing of neurons and inhibits release of glutamate (the neurotransmitter which plays a key role in the generation of epileptic seizures).
Levetiracetam, is a pyrrolidone derivative, chemically unrelated to existing antiepileptic active substances. Levetiracetam induces seizure protection in a broad range of animal models of partial and primary generalised seizures without having a pro-convulsant effect. The primary metabolite is inactive.
Perampanel is a first-in-class selective, non-competitive antagonist of the ionotropic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor on post-synaptic neurons. Glutamate is the primary excitatory neurotransmitter in the central nervous system and is implicated in a number of neurological disorders caused by neuronal overexcitation. The precise mechanism by which perampanel exerts its antiepileptic effects in humans remains to be fully elucidated.
In vitro studies indicate that retigabine acts primarily through opening neuronal potassium channels. This stabilises the resting membrane potential and controls the sub-threshold electrical excitability in neurons, thus preventing the initiation of epileptiform action potential bursts. The mechanism of action of retigabine on potassium channels has been well documented, however other mechanisms by which retigabine may assert an antiepileptic effect have yet to be fully elucidated.
Stiripentol potentiates the efficacy of other anticonvulsants, such as carbamazepine, sodium valproate, phenytoin, phenobarbital and many benzodiazepines, as the result of pharmacokinetic interactions. The second effect of stiripentol is mainly based on metabolic inhibition of several isoenzymes, in particular CYP450 3A4 and 2C19, involved in the hepatic metabolism of other anti-epileptic medicines.
Sultiame is indicated as an anticonvulsant for behavioural disorders associated with epilepsy; hyperkinetic behaviour; temporal lobe epilepsy; myoclonic seizures; grand mal attacks; Jacksonian seizures.
Topiramate is classified as a sulfamate-substituted monosaccharide. The precise mechanism by which topiramate exerts its antiseizure and migraine prophylaxis effects are unknown.
Zonisamide is a benzisoxazole derivative with antiepileptic and anticonvulsant activity. The mechanism of action of zonisamide is not fully elucidated, but it appears to act on voltage-sensitive sodium and calcium channels, thereby disrupting synchronised neuronal firing, reducing the spread of seizure discharges and disrupting subsequent epileptic activity.