| Indication | For short-term and intermittent use in patients with recurring insomnia and poor sleeping habits |
| Pharmacodynamics | Flurazepam, a benzodiazepine derivative, is a hypnotic agent which does not appear to decrease dream time as measured by rapid eye movements (REM). Furthermore, it decreases sleep latency and number of awakenings for a consequent increase in total sleep time. |
| Mechanism of action | Flurazepam binds to an allosteric site on GABA-A receptors. Binding potentiates the action of GABA on GABA-A receptors by opening the chloride channel within the receptor, causing chloride influx and hyperpolarization. |
| Absorption | Flurazepam hydrochloride is rapidly (30 minutes) absorbed from the gastrointestinal tract |
| Volume of distribution | Not Available |
| Protein binding | 83% |
| Metabolism | Flurazepam is rapidly metabolized and is excreted primarily in the urine. Both hydroxyethyl flurazepam (the major metabolite) and N-desalkyl flurazepam are active. The N-desalkyl metabolite is slowly excreted in the urine as the conjugated form |
| Route of elimination | Flurazepam is rapidly metabolized and is excreted primarily in the urine. Less than 1% of the dose is excreted in the urine as N1-desalkyl-flurazepam. |
| Half life | The mean apparent half-life of flurazepam is 2.3 hours. The half life of elimination of N1-des-alkyl- flurazepam ranged from 47 to 100 hours |
| Clearance | Not Available |
| Toxicity | Coma, confusion, low blood pressure, sleepiness |