Ethopropazine is an anticholinergic drug. Ethopropazine is an inhibitor of butyrylcholinesterase and non-selective muscarinic acetylcholine receptor antagonist. Ethopropazine has been used for the treatment of parkinsonism and drug-induced extrapyramidal reactions. Also It used for the symptomatic treatment of hepatolenticular degeneration and congenital athetosis.

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 It was introduced into clinical practice in 1952 under the brand names Hibicon, Lederle and later it was withdrawn.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 Early claims emphasized its safety, and it is not entirely clear why it was withdrawn from therapy for epilepsy.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.

Nalorphine has a mixed opioid agonist-antagonist properties. Nalorphine inhibits the cholinesterases of mouse brain, bovine erythrocytes and horse serum. It acts on mu-, k- and sigma-opioid receptors. Nalorfin by virtue of the agonistic effect has an analgesic effect but to a much lesser extent than morphine. Initially, before the appearance of a "pure" morphine-naloxone antagonist, nalorphine was used as an antidote for severe respiratory depression and other body function disorders caused by acute poisoning in case of an overdose of morphine, promedol, fentanyl or other narcotic analgesics, or with increased sensitivity to them. At present, nalorphine is practically not used for this purpose. It was replaced by naloxone. Large doses of nalorphine can cause nausea, cramps, drowsiness, headache, mental stimulation.

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 Phenacemide was introduced in 1949 for the treatment of epilepsy, but was eventually withdrawn from the market because of its severe side effects, which includes personality changes, blood, renal and skin disorders.

Dihydroergocornine is an ergot alkaloid, one of the three components of ergoloid (trade name Hydergine). Dihydroergocornine (as the component of Ergoloid mesylates) has been used to treat dementia and age-related cognitive impairment (such as in Alzheimer disease), as well as to aid in recovery after stroke. There is no specific evidence which clearly establishes the mechanism by which Hydergine® (ergoloid mesylates) preparations produce mental effects, nor is there conclusive evidence that the drug particularly affects cerebral arteriosclerosis or cerebrovascular insufficiency. Hydergine may stimulates dopaminergic and serotonergic receptors and blocks alpha-adrenoreceptors.

Dihydroergocristine is an ergot alkaloid that has an partial agonist activity on dopaminergic and alpha-adrenergic receptors and antagonist activity on serotonin receptors. The drug was approved by FDA in combination with other alkaloids (dihydroergocornine, dihydro-alpha-ergocryptine and dihydro-beta-ergocryptine mesylate salts) under the name Hydergine for the treatment of dimentia and cerebrovascular insufficiency.

Dihydro-alpha-ergocryptine is an ergot alkaloid that has an agonist activity on D2 dopaminergic receptors and a partial agonist activity on D1 receptors. It also demonstrated antagonistic activity towards alpha-adrenergic receptors. The drug was approved by FDA in combination with other alkaloids (dihydroergocornine, dihydroergocristine and dihydro-beta-ergocryptine mesylate salts) under the name Hydergine for the treatment of dimentia and cerebrovascular insufficiency.

Pregnenolone sulfate is an endogenous neurosteroid with excitatory effects in the brain, acting as a potent negative allosteric modulator of the GABAA receptor, a positive allosteric modulator of the NMDA receptor, and activator of transient receptor potential cation channel TRPM1 and TRPM3. In the model of schizophrenia, treatment with pregnenolone sulfate normalized the hyperlocomotion and stereotypic bouts, and rescued the PPI deficits of dopamine transporter knockout mice. Promnesic properties of pregnenolone sulfate were demonstrated in rat models of spatial memory performance.

Cyclamic acid (Cyclamate) is banned in the United States but it is used in many other Western countries without safety concerns. Cyclamate interacts with the sweet taste receptor subunit T1R3 transmembrane domain. Initially it was recommended for use in treatment of obese patients and by individuals with diabetes but in August 27, 1970 FDA concluded that there was no substantial evidence of effectiveness of cyclamate compounds at any level for treatment of obese patients and individuals with diabetes and therefore prohibited continued sale of cyclamate containing products with drug labeling. cyclamate is the putative carcinogenic agent. Cyclamate was tested in the Maximal Electroshock Seizure model (mice, ip), showing moderate anticonvulsant activity.