Ezogabine (U.S. adopted name) or retigabine (international nonproprietary name) is one of a family of aminopyrroles with anticonvulsant activity. It is used as an adjunctive treatment for partial epilepsies in treatment-experienced adult patients. The drug was approved by the European Medicines Agency under the trade name Trobalt and by the United States Food and Drug Administration (FDA), under the trade name Potiga. The mechanism by which ezogabine exerts its therapeutic effects has not been fully elucidated. In vitro studies indicate that ezogabine enhances transmembrane potassium currents mediated by the KCNQ (Kv7.2 to 7.5) family of ion channels. By activating KCNQ channels, ezogabine is thought to stabilize the resting membrane potential and reduce brain excitability. This mechanism of action is unique among antiepileptic drugs, and may hold promise for the treatment of other neurologic conditions, including migraine, tinnitus and neuropathic pain. In vitro studies suggest that ezogabine may also exert therapeutic effects through augmentation of GABA-mediated currents.

Ethotoin is a hydantoin derivative and anticonvulsant. Ethotoin exerts an antiepileptic effect without causing general central nervous system depression. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. Ethotoin inhibits nerve impulses in the motor cortex by lowering sodium ion influx, limiting tetanic stimulation. Ethotoin is used for the control of tonic-clonic (grand mal) and complex partial (psychomotor) seizures. Ethotoin is marketed as Peganone by Ovation.

Phensuximide is an anticonvulsant in the succinimide class. For the treatment of epilepsy. Phensuximide suppresses the paroxysmal three cycle per second spike and wave EEG pattern associated with lapses of consciousness in absence (petit mal) seizures. The frequency of attacks is reduced by depression of nerve transmission in the motor cortex. Phensuximide's mechanism of action not understood, but may act in inhibitory neuronal systems that are important in the generation of the three per second rhythm. It's effects may be related to its ability to inhibit depolarization-induced accumulation of cyclic AMP and cyclic GMP in brain tissue.

Methbarbital is a barbiturate anticonvulsant, discovered by Merck in 1905. It was introduced to market for treatment of epolepsy by Abbott in 1952, and discontinued in 1990.

Beclamide (N-benzyl-B-chloropropionamide) is a drug that possesses anticonvulsant activity. It is no longer used. It has been used as a sedative and as an anticonvulsant. Beclamide has been used in the management of both epilepsy and behavioral disorders associated with epilepsy. It was introduced into clinical practice in 1952 under the brand names Hibicon, Lederle and later it was withdrawn. This agent was shown to be effective in grand mal but not absence seizures. Early claims emphasized its safety, and it is not entirely clear why it was withdrawn from therapy for epilepsy. Interest in the drug was rekindled in the 1990s as an adjunct in the treatment of schizophrenia.

Phenacemide, also known as phenylacetylurea, is an anticonvulsant of the ureide (acetylurea) class. Phenacemide was introduced in 1949 for the treatment of epilepsy, but was eventually withdrawn from the market because of its severe side effects, which includes personality changes, blood, renal and skin disorders.

Paramethadione is an anticonvulsant in the oxazolidinedione class developed by the Abbott Laboratories, approved by the Food and Drug Administration in 1949 for the treatment of absence seizures, also called partial seizures. Paramethadione acts to reduce T-type calcium currents in thalamic neurons which has been proposed to underlie the 3-Hz spike-and-wave discharge seen on electroencephalogram (EEG) during absence seizures.

Mephenytoin is an antiepileptic drug which can be useful in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, mephenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Mephenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures. The mechanism of action of mephenytoin is not definitely known, but extensive research strongly suggests that its main mechanism is to block frequency-, use- and voltage-dependent neuronal sodium channels, and therefore limit repetitive firing of action potentials. Mephenytoin is no longer available in the US or the UK. It is still studied largely because of its interesting hydroxylation polymorphism.

Trimethadione (brand name is TRIDIONE) is an oxazolidinedione compound that was developed as an antiepileptic agent for control of petit mal seizures that are refractory to treatment with other drugs. Tridione does not modify the maximal seizure pattern in patients undergoing electroconvulsive therapy and has a sedative effect that may increase to the point of ataxia when excessive doses are used. Trimethadione acts as a voltage-activated T-type Ca2+ channel blocker. Trimethadione is rapidly absorbed from the gastrointestinal tract. It is demethylated by liver microsomes to the active metabolite, dimethadione. Approximately 3% of a daily dose of tridione is recovered in the urine as the unchanged drug. The majority of trimethadione is excreted slowly by the kidney in the form of dimethadione.

Mephobarbital us a barbiturate derivative used primary as an anticonvulsant, but also as a sedative and anxiolytic. Marketing of mephobarbital was discontinued in 2012.