Clonazepam pharmacokinetics and molecular data
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884
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
The content of this page is taken from the FDA package insert for this drug and should not be edited.
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
