|Common names||Clonazepam, Klonopin, “K-Pins”, Rivotril|
clonazepam (trade name klonopin) is a long-acting psychoactive substance of the benzodiazepine class which produces anxiolytic, anticonvulsant, muscle relaxant, amnesic, sedative, depressant and hypnotic effects. it is commonly used and fda approved for the medical treatment of panic disorder, generalized anxiety disorder (gad), and social anxiety disorder (sad).
clonazepam has an elimination half-life of 18 – 50 hours to 19 – 60 hours, and is generally considered to be a long-acting benzodiazepine. clonazepam has an intermediate onset of action, with a peak blood level occurring one to four hours after oral administration.
it’s worth noting that the sudden discontinuation of benzodiazepines can be potentially life-threatening for individuals using regularly for extended periods of time. it is highly recommended to taper one’s dose by gradually lowering the amount taken each day for a prolonged period of time instead of stopping abruptly.
clonazepam 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 clonazepam is substituted at r8 with a nitro group, no2-. further, the diazepine ring is bonded at r5 to a 2-chlorinated phenyl ring. clonazepam 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 clonazepam 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.