Propiomazine is a typical antipsychotic, blocking H1 receptors and is primarily indicated in conditions Insomnia. Propiomazine was also used under brand name largon for the relief of restlessness and apprehension, preoperatively or during surgery. In addition largon was used as an adjunct to analgesics for the relief of restlessness and apprehension during labor. But this drug was discontinued.

Propiomazine is a typical antipsychotic, blocking H1 receptors and is primarily indicated in conditions Insomnia. Propiomazine was also used under brand name largon for the relief of restlessness and apprehension, preoperatively or during surgery. In addition largon was used as an adjunct to analgesics for the relief of restlessness and apprehension during labor. But this drug was discontinued.

Glutethimide is a GABA agonist that was introduced by Ciba in 1954 as a safe alternative to barbiturates to treat insomnia. Before long, however, it had become clear that glutethimide was just as likely to cause addiction and caused similarly severe withdrawal symptoms. Glutethimide was discontinued in the US by manufacturers in 1993. Current production levels in the United States point to it only being used in small-scale research.

Methyprylon (brand name Noludar) is a sedative agent, which used to treat insomnia. But then the drug was replaced in the market by another drugs with less side effects. The precise mechanism of action is not known, but was made suggestion, that methyprylon increases the effects of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the brain.

Methyprylon (brand name Noludar) is a sedative agent, which used to treat insomnia. But then the drug was replaced in the market by another drugs with less side effects. The precise mechanism of action is not known, but was made suggestion, that methyprylon increases the effects of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the brain.

Secobarbital sodium, a barbiturate, is FDA approved for the treatment of insomnia and for pre-anesthetic use. This drug binds at a distinct site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. Adverse reactions are drowsiness, lethargy, hangover, paradoxical excitement in elderly patients, somnolence. Rifampin may decrease secobarbital levels by increasing metabolism.

Butethal is a sedative and a hypnotic drug indicated for the treatment of severe intractable insomnia. It acts on receptors in the brain (GABA A receptors) causing the release of the chemical GABA. This chemical inhibits certain areas of the brain resulting in sleepiness. Common side effects are: drowsiness, sedation, unsteadiness, vertigo and inco- ordination. Also, hangover effect, paradoxical excitement, confusion, memory defects and skin rashes. Interactions may occur with the following: adrenocorticoids (cortisone-like medicine), anticoagulants (blood thinners), carbamazepine, corticotropin (barbiturates may decrease the effects of these medicines), central nervous system (CNS) depressants (using these medicines with barbiturates may result in increased CNS depressant effects), divalproex sodium, valproic acid (using these medicines with barbiturates may change the amount of either medicine that you need to take), and oral contraceptives containing estrogens (barbiturates may decrease the effectiveness of these oral contraceptives, and you may need to change to a different type of birth control).

AMOBARBITAL is a barbiturate derivative with hypnotic and sedative properties. In an in vitro study in rat thalamic slices amobarbital worked by activating GABAA receptors, which decreased input resistance, depressed burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increased both the amplitude and decay time of inhibitory postsynaptic currents. Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high.

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.