Chloral is a chlorinated aldehyde that found extensive use, beginning in the 1940s, as a precursor in the production of the insecticide DDT and, to a lesser extent, of other insecticides and pharmaceuticals. This use of chloral has declined steadily since the 1960s, especially in those countries where the use of DDT has been restricted. Chloral is readily converted to chloral hydrate in the presence of water. Chloral hydrate is used as a sedative before medical procedures and to reduce anxiety related to withdrawal from drugs. Wider exposure to chloral hydrate occurs at microgram-per-liter levels in drinking water and swimming pools as a result of chlorination. Chloral hydrate is a well-established aneuploidogenic agent that also has some mutagenic activity. In human cells in vitro, chloral hydrate induced aneuploidy, micronuclei and gene mutations. Chloral hydrate clearly induced micronuclei in Chinese hamster cells, whereas findings in mouse lymphoma cells were conflicting. Induction of somatic mutation (but not sex-linked mutation) by chloral hydrate was demonstrated in insects. Chloral hydrate is metabolized in vivo to trichloroethanol, which is responsible for its physiological and psychological effects. The metabolite of chloral hydrate exerts its pharmacological properties via enhancing the GABA receptor complex and therefore is similar in action to benzodiazepines, nonbenzodiazepines, and barbiturates. In clinical studies, oral chloral hydrate appears to have a lower sedation failure rate when compared with oral promethazine for children undergoing pediatric neurodiagnostic procedures. The sedation failure was similar for other comparisons such as oral dexmedetomidine, oral hydroxyzine hydrochloride, and oral midazolam. When compared with intravenous pentobarbital and music therapy, oral chloral hydrate had a higher sedation failure rate. Compared to dexmedetomidine, chloral hydrate was associated with a higher risk of nausea and vomiting.

Chloral is a chlorinated aldehyde that found extensive use, beginning in the 1940s, as a precursor in the production of the insecticide DDT and, to a lesser extent, of other insecticides and pharmaceuticals. This use of chloral has declined steadily since the 1960s, especially in those countries where the use of DDT has been restricted. Chloral is readily converted to chloral hydrate in the presence of water. Chloral hydrate is used as a sedative before medical procedures and to reduce anxiety related to withdrawal from drugs. Wider exposure to chloral hydrate occurs at microgram-per-liter levels in drinking water and swimming pools as a result of chlorination. Chloral hydrate is a well-established aneuploidogenic agent that also has some mutagenic activity. In human cells in vitro, chloral hydrate induced aneuploidy, micronuclei and gene mutations. Chloral hydrate clearly induced micronuclei in Chinese hamster cells, whereas findings in mouse lymphoma cells were conflicting. Induction of somatic mutation (but not sex-linked mutation) by chloral hydrate was demonstrated in insects. Chloral hydrate is metabolized in vivo to trichloroethanol, which is responsible for its physiological and psychological effects. The metabolite of chloral hydrate exerts its pharmacological properties via enhancing the GABA receptor complex and therefore is similar in action to benzodiazepines, nonbenzodiazepines, and barbiturates. In clinical studies, oral chloral hydrate appears to have a lower sedation failure rate when compared with oral promethazine for children undergoing pediatric neurodiagnostic procedures. The sedation failure was similar for other comparisons such as oral dexmedetomidine, oral hydroxyzine hydrochloride, and oral midazolam. When compared with intravenous pentobarbital and music therapy, oral chloral hydrate had a higher sedation failure rate. Compared to dexmedetomidine, chloral hydrate was associated with a higher risk of nausea and vomiting.

Aprobarbital is a barbiturate derivative. Aprobarbital have been used for the short-term treatment of insomnia and for routine sedation to relieve anxiety, tension, and apprehension however, barbiturates generally have been replaced by benzodiazepines.

Flunitrazepam is an intermediate-acting benzodiazepine with general properties similar to those of diazepam. It is generally intended to be for short-term treatment for chronic or severe insomniacs who are unresponsive to other hypnotics. The main pharmacological effects of Flunitrazepam are the enhancement of GABA at the GABAA receptor. The physical effects of Flunitrazepam include sedation, muscle relaxation, decreased anxiety, and prevention of convulsions. It causes partial amnesia; individuals are unable to remember certain events that they experience while under the influence of the drug. Chronic use of Flunitrazepam can result in physical dependence and the appearance of a withdrawal syndrome when the drug is discontinued. Flunitrazepam impairs cognitive and psychomotor functions affecting reaction time and driving skill. The use of this drug in combination with alcohol is a particular concern as both central nervous system depressants potentiate each other's toxicity.

Vinburnine is a nutritional product, a peripheral vasodilator with cerebral activities that also act as a cerebral metabolic stimulant and appears to be able to relax the smooth muscle cells within the walls of blood vessels. (+/-)-Eburnamonine is the racemate of the alkaloid Vinburnine. Dextrorotatory, levorotatory, and racemic forms of eburnamonine exist in nature. The (-)-form, also known as vincamone (isolated from Vinca minor), is a drug that possesses a stimulating activity for muscle and is used as cerebrotonic, whereas both enantiomers have hypotensive effects.

Etifoxine (etafenoxine, StresamⓇ) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by GABA-A2 receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to 2 or 3 subunits of the GABAA receptor complex. It also modulates GABAA receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines.