Тиагабин: Құрамы, қолданылуы және жағымсыз әсерлері

Anticonvulsant medication

Drugbox
| verifiedrevid = 470609936
| IUPAC name = (−) (3R) 1 [4,4 bis(3 methyl 2 thienyl) 3 buten 1 yl] 3 piperidinecarboxylic acid
| image = Tiagabine. svg
| width = 250

| tradename = Gabitril
| Drugs. com =
| pronounce = /t//aɪ/'/æ//ɡ//ə//b//iː//n/
| MedlinePlus = a698014
| pregnancy AU = B3
| pregnancy US = C
| legal AU = S4
| legal BR = C1
| legal BR comment =
| legal CA = Rx only
| legal UK = POM
| legal US = Rx only
| routes of administration = Oral (tablets)

| bioavailability = 90–95%
| protein bound = 96%
| onset = Tmax = 45 min
| excretion = Fecal (63%) and renal (25%) It is effective as monotherapy and combination therapy with other antiepileptic drugs in the treatment of partial seizure. The American Academy of Sleep Medicine's 2017 clinical practice guidelines recommended against the use of tiagabine in the treatment of insomnia due to poor effectiveness and very low quality of evidence.

Side effects of tiagabine are dose related. Other side effects that have been observed with a rate of statistical significance relative to placebo include asthenia, somnolence, nervousness, memory impairment, tremor, headache, diarrhea, and depression. Adverse effects such as confusion, aphasia (difficulty speaking clearly)/stuttering, and paresthesia (a tingling sensation in the body's extremities, particularly the hands and fingers) may occur at higher dosages of the drug (e. g., over 8 mg/day). Tiagabine can also reportedly interfere with visual color perception.

Tiagabine overdose can produce neurological symptoms such as lethargy, single or multiple seizures, status epilepticus, coma, confusion, agitation, tremors, dizziness, dystonias/abnormal posturing, and hallucinations, as well as respiratory depression, tachycardia, hypertension, and hypotension. Overdose may be fatal especially if the victim presents with severe respiratory depression and/or unresponsiveness.

Tiagabine is primarily used as an anticonvulsant in the treatment of epilepsy as a supplement. Although the exact mechanism by which Tiagabine exerts its antiseizure effect is unknown, it is thought to be related to its ability to increase the activity of gamma aminobutyric acid (GABA), the central nervous system's major inhibitory neurotransmitter. Tiagabine attaches to the GABA uptake carrier's recognition sites. Tiagabine is thought to block GABA uptake into presynaptic neurons as a result of this action, allowing more GABA to be available for receptor binding on the surfaces of post synaptic cells.

Tiagabine enhances the power of cortical delta (< 4 Hz) oscillations up to 1000% relative to placebo, which may result in an EEG or MEG signature resembling non rapid eye movement sleep even while the person who has taken tiagabine is awake and conscious. This demonstrates that cortical delta activity and wakeful consciousness are not mutually exclusive, i. e., high amplitude delta oscillations are not always a reliable indicator of unconsciousness.

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.