Following oral treatment, clonazepam is quickly and virtually completely absorbed. Clonazepam reaches its peak plasma concentrations in 1 to 4 hours. The half-life of absorption is approximately 25 minutes. 90% of the total bioavailability.

Regarding the degree of clonazepam absorption, clonazepam pills are bioequivalent to an oral solution, however the rate of absorption is a little slower from tablets.

A once-daily dosage schedule results in 3-fold higher steady-state plasma concentrations of clonazepam than a single oral dose; the expected accumulation rates for a two- and three-times-daily schedule are 5 and 7, respectively. The average steady pre-dose plasma concentration of clonazepam after several oral doses of 2 mg three times per day was 55 ng/mL. Clonazepam has a linear connection between plasma levels and dose. As an anticonvulsant, clonazepam’s ideal plasma concentration ranges from 20 to 70 ng/ml. Around 17 ng/ml is the plasma concentration threshold for those with panic disorder.

The body’s organs and tissues rapidly distribute clonazepam, with the brain reabsorbing it preferentially. A half-life for dispersion is between 0.5 and 1 hours. 3 L/kg is the distribution volume. The protein binding rate is 82–86%.

By reduction to 7-amino-clonazepam and by N-acetylation to 7-acetamino-clonazepam, clonazepam is extensively metabolized. The C-3 position also undergoes hydroxylation.

The nitroreduction of clonazepam to pharmacologically inactive metabolites is carried out by hepatic cytochrome P450 3A4.

The metabolites (glucuronide and sulphate) are found in the urine as free and conjugated molecules.

The elimination half-life is typically 30 to 40 hours. 55 ml/min is the clearance. As metabolites, 50–70% of a dosage is eliminated in the urine and 10–30% in the feces.

Typically, less than 2% of the administered dose of unaltered clonazepam is excreted in the urine.

Children’s kinetic elimination is comparable to what is seen in adults.

Pharmaceutical kinetics in unique clinical circumstances:

A kidney condition has no impact on clonazepam’s pharmacokinetics. No dose change is necessary in patients with renal insufficiency based on pharmacokinetic criteria.

Hepatic disease has not been studied for its potential to affect clonazepam’s pharmacokinetics.

Clonazepam’s pharmacokinetics in the elderly have not been determined.

Neonatal clearance and elimination half-lives are in the same order of magnitude as those reported for adults.

The pharmacological characteristics of clonazepam are similar to those of benzodiazepines, and they include anticonvulsant, sedative, muscle relaxant, and anxiolytic actions. Its effects are thought to be predominantly caused by GABA-mediated postsynaptic inhibition, similar to other benzodiazepines, while some animal studies also indicate a serotonin impact.

Clonazepam quickly suppresses many types of paroxysmal activity, including spike-and-wave discharge in absence seizures (petit mal), slow spike waves, slow spike waves, generalized spikes, spikes with temporal or other locations, as well as irregular waves and spikes, according to data from animal models and some electroencephalographic studies in humans.

More often than focal abnormalities, generalized EEG abnormalities are suppressed. This suggests that clonazepam is effective in treating both widespread and focal epilepsies.