Vigabatrin

K K Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.)
Originally released December 18, 1998; last updated September 21, 2017; expires September 21, 2020

This article includes discussion of vigabatrin and gamma-vinyl-GABA. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Historical note and terminology

The era of antiepileptic drugs started with the introduction of bromides in 1857 and was followed by the discovery of the anticonvulsant effect of barbiturates in 1912 as well as the introduction of hydantoins in 1916. Carbamazepine was introduced into clinical practice as an antiepileptic drug in 1963. Carbamazepine and lamotrigine block repetitive firing of neurons by blocking sodium channels. Lamotrigine, unrelated to any previous antiepileptic drug, reduces presynaptic excitatory amino acid release. Like most other antiepileptic drugs, its discovery was serendipitous. Gabapentin, a GABA-receptor agonist, was first studied as an antiepileptic drug in humans in 1987. The synthesis of vigabatrin (gamma-vinyl-GABA) was a result of a rational approach to design compounds to inhibit the major GABA-degrading enzyme, GABA transaminase. It was approved for use in several European countries in 1989. It was approved by the United States Food and Drug Administration in 1997. During the 15 years since the initial clinical trial in humans and 10 years since approval, more than 175,000 patients have been treated with this drug. More than 30 years of history for research and development of vigabatrin has been presented in a clinically relevant review (Tolman and Faulkner 2009).

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