Clonazepam pharmacokinetics and molecular data

Pharmacokinetics topics
Pharmacodynamics Pharmacokinetics

Pharmacodynamics
The precise mechanism by which Clonazepam exerts its antiseizure and antipanic effects is unknown, although it is believed to be related to its ability to enhance the activity of gamma aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Convulsions produced in rodents by pentylenetetrazol or, to a lesser extent, electrical stimulation are antagonized, as are convulsions produced by photic stimulation in susceptible baboons. A taming effect in aggressive primates, muscle weakness and hypnosis are also produced. In humans, Clonazepam is capable of suppressing the spike and wave discharge in absence seizures (petit mal) and decreasing the frequency, amplitude, duration and spread of discharge in minor motor seizures. Return to top

Pharmacokinetics
Clonazepam is rapidly and completely absorbed after oral administration. The absolute bioavailability of Clonazepam is about 90%. Maximum plasma concentrations of Clonazepam are reached within 1 to 4 hours after oral administration. Clonazepam is approximately 85% bound to plasma proteins. Clonazepam is highly metabolized, with less than 2% unchanged Clonazepam being excreted in the urine. Biotransformation occurs mainly by reduction of the 7-nitro group to the 4-amino derivative. This derivative can be acetylated, hydroxylated, and glucuronidated. Cytochrome P-450, including CYP3A, may play an important role in Clonazepam reduction and oxidation. The elimination half-life of Clonazepam is typically 30 to 40 hours. Clonazepam pharmacokinetics are dose independent throughout the dosing range. There is no evidence that Clonazepam induces its own metabolism or that of other drugs in humans. Return to top