| Indication |
For the treatment of partial seizures |
| Pharmacodynamics |
Tiagabine is used primarily as an anticonvulsant for the
adjunctive treatment of epilepsy. The precise mechanism by which
Tiagabine exerts its antiseizure effect is unknown, although it is
believed to be related to its ability to enhance the activity of gamma
aminobutyric acid (GABA), the major inhibitory neurotransmitter in the
central nervous system. Tiagabine binds to recognition sites associated
with the GABA uptake carrier. It is thought that, by this action,
Tiagabine blocks GABA uptake into presynaptic neurons, permitting more
GABA to be available for receptor binding on the surfaces of
post-synaptic cells. |
| Mechanism of action |
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. |
| Absorption |
Tiagabine is nearly completely absorbed (>95%). |
| Volume of distribution |
Not Available |
| Protein binding |
96% |
| Metabolism |
Tiagabine is likely metabolized primarily by the 3A isoform subfamily of hepatic cytochrome P450. |
| Route of elimination |
Approximately 2% of an oral dose of tiagabine is excreted
unchanged, with 25% and 63% of the remaining dose excreted into the
urine and feces, respectively, primarily as metabolites. |
| Half life |
7-9 hours |
| Clearance |
- 109 mL/min [Healthy subjects]
|
| Toxicity |
mptoms most often accompanying tiagabine overdose, alone or in
combination with other drugs, have included: seizures including status
epilepticus in patients with and without underlying seizure disorders,
nonconvulsive status epilepticus, coma, ataxia, confusion, somnolence,
drowsiness, impaired speech, agitation, lethargy, myoclonus, spike wave
stupor, tremors, disorientation, vomiting, hostility, and temporary
paralysis. Respiratory depression was seen in a number of patients,
including children, in the context of seizures. |
