| Indication | For the short-term treatment of insomnia. |
| Pharmacodynamics | A short-acting benzodiazepine used as a hypnotic agent in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries. Triazolam has a shorter half-life than chlordiazepoxide, flurazepam, and prazepam and does not generate active metabolites. |
| Mechanism of action | Benzodiazepines bind nonspecifically to bezodiazepine receptors BNZ1, which mediates sleep, and BNZ2, which affects 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 GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell. |
| Absorption | Bioavailability is 44% (oral) and 53% (sublingual). |
| Volume of distribution | Not Available |
| Protein binding | Not Available |
| Metabolism | Hepatic. Small amounts of unmetabolized triazolam appear in the urine. |
| Route of elimination | Triazolam and its metabolites, principally as conjugated glucuronides, which are presumably inactive, are excreted primarily in the urine. Only small amounts of unmetabolized triazolam appear in the urine. The two primary metabolites accounted for 79.9% of urinary excretion. |
| Half life | 1.5-5.5 hours |
| Clearance | Not Available |
| Toxicity | Symptoms of overdose include drowsiness, slurred speech, motor inco-ordination, coma, and respiratory depression. |