| Indication |
For use only in those patients who respond inadequately to
alternative treatments and whose epilepsy is so severe that a
substantial risk of aplastic anemia and/or liver failure is deemed
acceptable in light of the benefits conferred by its use. |
| Pharmacodynamics |
Felbamate is an antiepileptic indicated as monotherapy or as an
adjunct to other anticonvulsants for the treatment of partial seizures
resulting from epilepsy. Receptor-binding studies in vitro
indicate that felbamate has weak inhibitory effects on GABA-receptor
binding, benzodiazepine receptor binding, and is devoid of activity at
the MK-801 receptor binding site of the NMDA receptor-ionophore complex.
However, felbamate does interact as an antagonist at the
strychnine-insensitive glycine recognition site of the NMDA
receptor-ionophore complex. |
| Mechanism of action |
The mechanism by which felbamate exerts its anticonvulsant
activity is unknown, but in animal test systems designed to detect
anticonvulsant activity, felbamate has properties in common with other
marketed anticonvulsants. In vitro receptor binding studies
suggest that felbamate may be an antagonist at the
strychnine-insensitive glycine-recognition site of the
N-methyl-D-aspartate (NMDA) receptor-ionophore complex. Antagonism of
the NMDA receptor glycine binding site may block the effects of the
excitatory amino acids and suppress seizure activity. Animal studies
indicate that felbamate may increase the seizure threshold and may
decrease seizure spread. It is also indicated that felbamate has weak
inhibitory effects on GABA-receptor binding, benzodiazepine receptor
binding. |
| Absorption |
>90% |
| Volume of distribution |
|
| Protein binding |
20-36% |
| Metabolism |
Hepatic |
| Route of elimination |
Not Available |
| Half life |
20-23 hours |
| Clearance |
- 26 +/- 3 mL/hr/kg [single 1200 mg dose]
- 30 +/- 8 mL/hr/kg [multiple daily doses of 3600 mg]
|
| Toxicity |
LD50=5000 mg/kg (Orally in rats) |
