Clobazam chemical structure
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Clobazam

Clobazam is a drug which is a benzodiazepine derivative. It has been marketed as an anxiolytic since 1975 and an anticonvulsant since 1984. more...

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Pharmacology

Clobazam is a 1,5-benzodiazepine, meaning that its diazepine ring has nitrogen atoms at the 1 and 5 positions (instead of the usual 1 and 4). Like other 1,5-benzodiazepines (arfendazam, lofendazam, e.g.), it has less affinity for the ω1-allosteric binding site on the GABAA receptor compared to the 1,4-benzodiazepines. It has selective affinity for the ω2 site, where it has agonistic activity.

In a double-blind placebo-controlled trial published in 1990 comparing it to clonazepam, 10mg or 20 mg of clobazam was shown to be much less sedating than either 0.5mg or 1 mg of clonazepam.

The ω1-receptor, which is found on the α1 subtype of the GABAA receptor, was shown to be responsible for the sedative effects of diazepam by McKernan et al in 2000, who also showed that its anxiolytic and anticonvulsant properties could still be seen in mice whose α1 receptors were insensitive to diazepam. It would seem, then, that the anticonvulsant properties of clobazam are due to its selective affinity for ω2.

In 1996, Nakamura et al reported that clobazam and its active metabolite, N-desmethylclobazam (norclobazam), work by enhancing GABA-activated chloride currents at GABAA-receptor-coupled Cl- channels. It was also reported that these effects were inhibited by the GABA antagonist flumazenil, and that clobazam acts most efficiently in GABA-deficient brain tissue.

Nine years earlier, Kilpatrick et al noted that there was a correlation between plasma levels of norclobazam and therapeutic effects, although this was not true with the parent compound.

According to Valli and colleagues in 1984, clobazam lowered prolactin levels elevated by sulpiride, a typical antipsychotic. Hyperprolactinemia (i.e. elevated blood prolactin) occurs occasionally in people using antipsychotics, (particularly the typical ones), and can lead to cardiovascular disease, breast cancer, galactorrhea, infertility, amenorrhea, dysmenorrhea, osteopenia, osteoporosis, loss of libido, impotence, and hypogonadism.

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Severe Myoclonic Epilepsy Responds Well to Stiripentol - Brief Article
From Family Pratice News, 3/15/00 by Sharon Worcester

ORLANDO, FLA. - An investigational antiepilepsy drug was an effective add-on therapy for controlling seizures in children with severe myoclonic epilepsy in infancy, the results of a double-blind, placebo-controlled study have shown.

Stiripentol, which is believed to inhibit the activity of several P-450 cytochromes, resulted in the highest response rate ever reported for severe myoclonic epilepsy, one of the most intractable epilepsy syndromes, Dr. Catherine Chiron reported at the annual meeting of the American Epilepsy Society.

Of 41 refractory patients aged 3-20 years, 15 of 21 treated with stiripentol in addition to clobazam and valproate responded with at least a 50% reduction in clonic seizures. One patient became seizure free during treatment. Only 1 of the 20 patients in the group taking placebo plus clobazam and valproate responded, said Dr. Chiron of St. Vincent de Paul Hospital in Paris.

Those patients treated with stiripentol had an average of 6.4 seizures per month, compared with 13.9 per month in the placebo group. After 2 months of treatment, patients in the stiripentol group had an average 62% reduction in seizures, compared with an 8% increase with placebo.

Side effects occurred in all 21 patients on stiripentol versus 8 patients on placebo. Side effects in the stiripentol group included only drowsiness and loss of appetite. These were moderate in most patients and usually were related to overdose of clobazam; dose reductions led to resolution of the side effects in some patients, and other cases were transient, Dr. Chiron noted.

COPYRIGHT 2000 International Medical News Group
COPYRIGHT 2001 Gale Group

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