flubromazepam

Description

buy flubromazepam research chemicals online

Flubromazepam is a long-lasting psychoactive substance of the benzodiazepine class which produces anxiolytic, sedative, muscle relaxant, depressant and amnesic effects.

This compound was first made in 1960, but was never marketed and did not receive any further attention or study until late 2012. It has potential use for the short-term treatment of anxiety, insomnia, acute seizures, and the sedation of hospitalized patients. However, it is currently exclusively sold by online research chemical vendors for use as a recreational psychoactive substance and has not been formally studied. This means that any comments regarding its pharmacology are purely speculation based upon the subjective effects it induces and its structural similarity to triazolam, pyrazolam and other benzodiazepines.

Flubromazepam, or 7-Bromo-5-(2-fluorophenyl)-1,3-dihydro-1,4-benzodiazepin-2-one, is a chemical of the benzodiazepine class. Flubromazepam is named for the fluorine and bromine substitutions on its core benzodiazepine skeleton (FLUorine-BROMine-azepam). Flubromazepam is a member of the benzodiazepine class as it contains a 1,4 diazepine ring fused to a substituted benzene ring. Bromine is bound to this bicyclic structure at R₇. Additionally, a fluorine-substituted phenyl ring is bound to this structure at R₅. Flubromazepam also contains an oxygen group double bonded to R₂ of its diazepine ring to form a ketone. This oxygen substitution at R₂ is shared with other benzodiazepine drugs with the suffix -azepam.

Benzodiazepines produce a variety of effects by binding to the benzodiazepine receptor site and 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 flubromazepam on the nervous system.

The anticonvulsant properties of benzodiazepines may be, in part or entirely, due to binding to voltage-dependent sodium channels rather than benzodiazepine receptors.