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 |