| Indication | For the short-term treatment of insomnia (generally 7-10 days). |
| Pharmacodynamics | Temazepam is a benzodiazepine used as a hypnotic agent in the management of insomnia. Temazepam produces CNS depression at limbic, thalamic, and hypothalamic levels of the CNS. Temazepam increases the affinity of the neurotransmitter gamma-aminobutyric acid (GABA) for GABA receptors by binding to benzodiazepine receptors. Results are sedation, hypnosis, skeletal muscle relaxation, anticonvulsant activity, and anxiolytic action. |
| Mechanism of action | Benzodiazepines bind nonspecifically to benzodiazepine receptors, which affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABAA) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of the inhibitory neurotransmitter GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell. |
| Absorption | Well absorbed, minimal first-pass metabolism. |
| Volume of distribution | Not Available |
| Protein binding | 96% |
| Metabolism | Hepatic. Temazepam is completely metabolized through conjugation prior to excretion. The major metabolite is the O-conjugate of temazepam (90%). |
| Route of elimination | Temazepam was completely metabolized through conjugation prior to excretion; 80% to 90% of the dose appeared in the urine. |
| Half life | 10-20 hours |
| Clearance | Not Available |
| Toxicity | Not Available |