| Indication |
For use as an adjunctive treatment (with other drugs) in treatment
resistant epilepsy, complex partial seizures, secondary generalized
seizures, and for monotherapy use in infantile spasms in West syndrome. |
| Pharmacodynamics |
Vigabatrin, is an anticonvulsant chemically unrelated to other
anticonvulsants. Vigabatrin inhibits the catabolism of GABA. It is an
analog of GABA, but it is not a receptor agonist. Vigabatrin
irreversibly inhibits the enzyme GABA transaminase. |
| Mechanism of action |
It is believed that vigabatrin increases brain concentrations of
gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the
CNS, by irreversibly inhibiting enzymes that catabolize GABA
(gamma-aminobutyric acid transaminase GABA-T) or block the reuptake of
GABA into glia and nerve endings. Vigabatrin may also work by
suppressing repetitive neuronal firing through inhibition of
voltage-sensitive sodium channels. |
| Absorption |
Rapidly absorbed following oral administration. Food may slightly decrease the rate, but not the extent, of absorption. |
| Volume of distribution |
|
| Protein binding |
Little to none |
| Metabolism |
Almost no metabolic transformation. Does not induce the hepatic cytochrome P450 system. |
| Route of elimination |
Vigabatrin is not significantly metabolized; it is eliminated primarily through renal excretion. |
| Half life |
5-8 hours in young adults, 12-13 hours in elderly. |
| Clearance |
- 2.4 +/- 0.8 L/h [Infant]
- 5.7 +/- 2.5 L/h [Children]
|
| Toxicity |
Not Available |
