Tiagabine, CAS: 115103-54-3

Solid
Tiagabine is a piperidinemonocarboxylic acid that is (R)-nipecotic acid in which the hydrogen attached to the nitrogen has been replaced by a 1,1-bis(3-methyl-2-thienyl)but-1-en-4-yl group. A GABA reuptake inhibitor, it is used (generally as the hydrochloride salt) for the treatment of epilepsy. It has a role as a GABA reuptake inhibitor and an anticonvulsant. It is a piperidinemonocarboxylic acid, a beta-amino acid, a member of thiophenes and a tertiary amino compound. It derives from a (R)-nipecotic acid. It is a conjugate base of a tiagabine(1+).|Tiagabine is an anti-convulsive medication. It is also used in the treatment for panic disorder as are a few other anticonvulsants. Though the exact mechanism by which tiagabine exerts its effect on the human body is unknown, it does appear to operate as a selective GABA reuptake inhibitor.|Tiagabine is an Anti-epileptic Agent. The physiologic effect of tiagabine is by means of Decreased Central Nervous System Disorganized Electrical Activity.|Tiagabine is a unique anticonvulsant used largely as an adjunctive agent in therapy of partial seizures in adults or children. Therapy with tiagabine is not associated with serum aminotransferase elevations, and clinically apparent liver injury from tiagabine has not been reported and must be rare if it occurs at all.|A nipecotic acid derivative that acts as a GABA uptake inhibitor and anticonvulsant agent. It is used in the treatment of EPILEPSY, for refractory PARTIAL SEIZURES.
Tiagabine is a second- generation antiepileptic drug (AED) known under the proprietary brand name of Gabitril® (Teva, Petah Tikva, Israel) in the UK and USA.
White to Off-White Crystalline Solid
A glance at tiagabine’s structure suggests anuptake inhibitor. Reportedly, it blocks GABA reuptake asa major mode of its anticonvulsant activity. Its use isagainst partial seizures. Inhibitors of GABA transporter-1(GAT-1 inhibitors) increase extracellular GABA concentrationin the hippocampus, striatum, and cortex, therebyprolonging the inhibitory action of GABA released synaptically.Nipecotic acid is a potent inhibitor of GABA reuptakeinto synaptosomal membranes, neurons, and glialcells. However, nipecotic acid fails to cross the blood-brainbarrier following systemic administration because of itshigh degree of ionization. Tiagabine, marketed as thesingle R(-)-enantiomer, a potent GAT-1 inhibitor structurallyrelated to nipecotic acid, has an improved ability tocross the blood-brain barrier, and it has recently receivedFood and Drug Administration (FDA) approval as anAED.It is well absorbed and readily metabolized byCYP3A4 to an inactive metabolite, 5-oxo-tiagabine (oxidationof the thiophen ring) or eliminated as glucuronide ofthe parent molecule.Over 90% of tiagabine is metabolized by CYP3A4isozymes.The primary site of metabolic attack is the oxidationof the thiophen rings leading to 5-oxo-tiagabine thatlacks anticonvulsant activity and the glucuronidation via thecarboxylic function. Thus, the plasma concentrations oftiagabine would be greatly effected by any compound thatinduces or inhibits CYP3A4.