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Vigabatrin
Author(s) -
French Jacqueline A.
Publication year - 1999
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1999.tb00914.x
Subject(s) - vigabatrin , tiagabine , gaba transaminase , anticonvulsant , pharmacology , mechanism of action , neurotransmitter , medicine , reuptake inhibitor , epilepsy , central nervous system , neuroscience , chemistry , serotonin , enzyme , biochemistry , biology , psychiatry , glutamate decarboxylase , receptor , in vitro
Summary: Vigabatrin (VGB) is a structural analogue of the inhibitory neurotransmitter γ‐amino butyric acid (GABA), which produces its antiepileptic effect by irreversibly inhibiting the degradative enzyme GABA‐transaminase. This produces an increase in central nervous system (CNS) GABA levels. VGB is among the few antiepileptic drugs (AEDs) that was synthesized with a specific targeted mechanism in mind and was subsequently demonstrated to function by that mechanism. Tiagabine, a GABA reuptake blocker, is the only other “designer drug” among the currently available AEDs. Therefore, VGB is among the few AEDs for which the mechanism of action is well understood. Recently, safety issues have been raised with regard to the use of vigabatrin. This article reviews the mechanism of action, pharmacokinetics, safety, and efficacy of VGB.