Clonazepam Powder | CAS 1622-61-3 | Chlonazepam Powder

Clonazepam is a synthetic benzodiazepine derivative used for myotonic or atonic seizures, absence seizures, and photosensitive epilepsy, anticonvulsant Clonazepam appears to enhance gamma-aminobutyric acid receptor responses, although its mechanism of action is not clearly understood. It is seldom effective in generalized tonic-clonic or partial seizures. (NCI04)

What is Clonazepam?

Common side effects include sleepiness, poor coordination, and agitation. Long-term use may result in tolerance, dependence, and withdrawal symptoms if stopped abruptly. Dependence occurs in one-third of people who take clonazepam for longer than four weeks. There is an increased risk of suicide, particularly in people who are already depressed. If used during pregnancy it may result in harm to the fetus. Clonazepam binds to GABA_A receptors, thus increasing the effect of the chief inhibitory neurotransmitter γ-aminobutyric acid (GABA).

Effects of Chlonazepam?

Clonazepam is 1,3-Dihydro-2H-1,4-benzodiazepin-2-one in which the hydrogens at positions 5 and 7 are substituted by 2-chlorophenyl and nitro groups, respectively. It is used in the treatment of all types of epilepsy and seizures, as well as myoclonus and associated abnormal movements, and panic disorders. However, its use can be limited by the development of tolerance and by sedation. It has a role as an anticonvulsant, a GABA modulator and an anxiolytic drug. It is a 1,4-benzodiazepinone and a member of monochlorobenzenes.

When to take Klonopin?

Clonazepam is lipid-soluble, rapidly crosses the blood–brain barrier, and penetrates the placenta. It is extensively metabolised into pharmacologically inactive metabolites, with only 2% of the unchanged drug excreted in the urine. Clonazepam enhances the activity of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system to give its anticonvulsant, skeletal muscle relaxant, and anxiolytic effects. It acts by binding to the benzodiazepine site of the GABA receptors, which enhances the electric effect of GABA binding on neurons, resulting in an increased influx of chloride ions into the neurons.