Monitoring Parameters
Seizure frequency, liver function tests , suicidality

History
Tiagabine was discovered at Novo Nordisk in Denmark in 1988 by a team of medicinal chemists and pharmacologists under the general direction of Claus Bræstrup. The drug was co-developed with Abbott Laboratories, in a 40/60 cost sharing deal, with Abbott paying a premium for licensing the IP from the Danish company.U.S. patents on tiagabine listed in the Orange Book expired in April 2016. See also
CI-966
Deramciclane
Nipecotic acid
SKF-89976A

References
External links
Gabitril(manufacturers website)
Iminoglycinuria is an autosomal recessive disorder of renal tubular transport affecting reabsorption of the amino acid glycine, and the imino acids proline and hydroxyproline. This results in excess urinary excretion of all three acids (-uria denotes "in the urine").Iminoglycinuria is a rare and complex disorder, associated with a number of genetic mutations that cause defects in both renal and intestinal transport systems of glycine and imino acids.Imino acids typically contain an imine functional group, instead of the amino group found in amino acids. Proline is considered and usually referred to as an amino acid, but unlike others, it has a secondary amine. This feature, unique to proline, identifies proline also as an imino acid. Hydroxyproline is another imino acid, made from the naturally occurring hydroxylation of proline. Presentation
The primary characteristic of iminoglycinuria is the presence of glycine and imino acids in the urine. Otherwise, it is thought to be a relatively benign disorder, although symptoms associated with disruptions of proline and glycine metabolism caused by malabsorption may be present with iminoglycinuria. These include encephalopathy, mental retardation, deafness, blindness, kidney stones, hypertension and gyrate atrophy.Gyrate atrophy is an inherited degenerative disorder of the retina and choroid, sometimes accompanying the metabolic condition hyperornithinemia. The presence of gyrate atrophy with iminoglycinuria stems from a deficiency of proline in chorioretinal tissues, while processes behind hyperornithinemia disrupt the metabolic pathway from ornithine to proline, which alters the catabolism of ornithine, and also results in reduced levels of proline.