Temazepam (trade name Restoril) is a intermediate-acting psychoactive substance of the benzodiazepine class, which produces anxiolytic, sedative, hypnotic, muscle relaxant, anticonvulsant, and amnesic effects.
Temazepam, like other benzodiazepines, binds to specific sites on the GABAA gamma-amino-butyric acid receptor. Temazepam is commonly used for the short term treatment of insomnia and as a preoperative sedative. Temazepam has a rapid onset of action and symptomatic relief. The hypnotic effects take between 20-90 minutes to take effect. Temazepam is effective for both inducing sleep and maintaining sleep.
It’s worth noting the sudden discontinuation of benzodiazepines can be potentially dangerous or life-threatening for individuals using regularly for extended periods, sometimes resulting in seizures or death. It is highly recommended tapering one’s dose by gradually lowering the amount taken each day for a prolonged period of time, instead of stopping abruptly.
Temazepam is a drug of the benzodiazepine class. Benzodiazepine drugs contain a benzene ring fused to a diazepine ring, which is a seven membered ring with the two nitrogen constituents located at R1 and R4. The benzyl ring of temazepam is substituted at R8 with a chlorine group. Further, the diazepine ring is bonded at R5 to a phenyl ring. Temazepam also has a hydroxyl group bonded to the 3-position of the diazepine ring.
Temazepam is a white, crystalline substance, slightly soluble in water, and sparingly soluble in alcohol.
Benzodiazepines produce various effects by binding to the benzodiazepine receptor site, magnifying the efficiency and effects of the neurotransmitter gamma aminobutyric acid (GABA) by acting on its receptors. As this site is the most prolific inhibitory receptor set within the brain, its modulation results in the sedating (or calming effects) of temazepam on the nervous system. When temazepam binds to the GABAA receptor, it causes the Cl-ion pore to open more frequently. The anticonvulsant properties of benzodiazepines may be, in part or entirely, due to binding to voltage-dependent sodium channels, rather than benzodiazepine receptors.
Its main pharmacological action is to increase the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor. This causes sedation, motor impairment, ataxia, anxiolysis, an anticonvulsant effect, muscle relaxation, and a reinforcing effect. As a medication before surgery, temazepam decreased cortisol in elderly patients. In rats, it triggered the release of vasopressin into the periventricular nucleus of the hypothalamus, and decreased the release of ACTH under stress.
In a single- and multiple-dose absorption, distribution, metabolism, and excretion (ADME) study, using tritium-labeled drug, temazepam was well absorbed and found to have minimal (8%) first-pass drug metabolism. No active metabolites were formed, and the only significant metabolite present in blood was the O-conjugate. The unchanged drug was 96% bound to plasma proteins. The blood-level decline of the parent drug was biphasic, with the short half-life ranging from 0.4-0.6 hours and the terminal half-life from 3.5–18.4 hours (mean 8.8 hours), depending on the study population and method of determination.
