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Active ingredient: Vigabatrin - Brands, Medical Use, Clinical Data

Brands, Medical Use, Clinical Data

Drug Category

  • Anticonvulsants
  • Enzyme Inhibitors

Dosage Forms

  • Powder (500 mg sachets)
  • Tablet (500 mg)

Brands / Synonyms

4-Amino-5-hexenoic acid; 4-Aminohexenoic acid; gamma-Vinyl GABA ; GVG; Sabril; Sabril (TN); Vigabatrin [USAN:BAN:INN]; Vigabatrina [Spanish]; Vigabatrine; Vigabatrine [French]; Vigabatrinum [Latin]

Indications

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.

Pharmacology

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.

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.

Toxicity

Not Available

Biotrnasformation / Drug Metabolism

Almost no metabolic transformation. Does not induce the hepatic cytochrome P450 system.

Contraindications

In pregnancy and lactation and in patients with a known hypersensitivity to vigabatrin or to any components of the product.

Drug Interactions

A study published in 2002 found that vigabatrin causes a statistically significant increase in plasma clearance of carbamazepine. In 1984, Drs Rimmer and Richens at the University of Wales reported that administering vigabatrin with phenytoin lowered the serum phenytoin concentration in patients with treatment-resistant epilepsy. The concentration of phenytoin falls to 23% within five weeks, according to an experiment published in 1989 by the same two scientists that tried and failed to elucidate the mechanism behind this interaction.

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