| Indication | Used for short-term hypnotic therapy in the management of insomnia for periods of up to one week in duration; however, this medication generally has been replaced by other sedative-hypnotic agents. |
| Pharmacodynamics | Ethchlorvynol is a sedative drug and schedule IV (USA) controlled substance. It produces cerebral depression, however the exact mechanism of action is not known. |
| Mechanism of action | Although the exact mechanism of action is unknown, ethchlorvynol appears to depress the central nervous system in a manner similar to that of barbiturates. Barbiturates bind at a distinct binding sites 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. |
| Absorption | Rapidly absorbed from gastrointestinal tract. |
| Volume of distribution | Not Available |
| Protein binding | 35-50% |
| Metabolism | About 90% of a dose is metabolized in the liver. Some ethchlorvynol may also be metabolized in the kidneys. Ethchlorvynol and metabolites undergo extensive enterohepatic recirculation. |
| Route of elimination | Not Available |
| Half life | Plasma half-life is approximately 10 to 20 hours, terminal half-life is 21-100 hours. |
| Clearance | Not Available |
| Toxicity | Symptoms of overdose include thrombocytopenia. |