Is Brotizolam a sleeping pill?

Brotizolam (marketed under brand name Lendormin) is a sedative-hypnotic thienotriazolodiazepine drug which is a benzodiazepine analog….Brotizolam.

Clinical data
Bioavailability 48–95%
Metabolism Hepatic
Elimination half-life 4.4 hours (range, 2.6–6.9 h)
Excretion Renal

How long does Bondormin last?

Duration of treatment Treatment should be as short as possible. Generally, the duration of treatment varies from a few days to a maximum of two weeks. Treatment should be discontinued by gradual tapering, which should be tailored to the individual (see section 4.4).

How do I stop taking Bondormin?

Treatment should be discontinued by gradual tapering, which should be tailored to the individual (see section 4.4). It should be borne in mind that discontinuation may initially cause rebound insomnia and that, in rare cases, restlessness, anxiety and tension may also occur.

How does brotizolam work as a muscle relaxer?

Brotizolam is a sedative-hypnotic thienodiazepine drug which is a benzodiazepine analog. It demonstrates anxiolytic, anticonvulsant, hypnotic, sedative and skeletal muscle relaxant effects. Brotizolam has similar effects to short-acting benzodiazepines such as triazolam.

Are there any side effects to taking brotizolam?

Dangers are related to CNS (cental nervous system) depression, and include ataxia, headache, dizziness, fatigue, slurred speech, and others. Common side effects are similar to those of other hypnotic benzodiazepines. Bioavailability after an oral dose is approximately 70%.

How is brotizolam used in the treatment of insomnia?

Brotizolam is a benzodiazepine analogue with sedative-hypnotic properties used for short-term treatment of severe or debilitating insomnia. Brotizolam is a sedative-hypnotic thienodiazepine drug which is a benzodiazepine analog.

Why does brotizolam have equal affinity for the BZ receptor?

A series of thienylpyrazoloquinoline derivatives shows that ( 17) and its isostere have equal affinity for the benzodiazepine (BZ) receptor but that they cause opposite behavioral effects. This phenomenon is postulated to result from inverse agonism at the receptor 〈88JMC1738〉.