Tiagabine hydrochloride

• CAT Number: I009803
• CAS Number: 145821-59-6
• Molecular Formula: C20H26ClNO2S2
• Molecular Weight: 412.003
• Purity: ≥95%
• Synonyms: NO-329; NO329; NO 329; NNC-05-0328; NO-05-0328; Tiagabine hydrochloride; brand name Gabitril;(R)-1-(4,4-bis(3-methylthiophen-2-yl)but-3-en-1-yl)piperidine-3-carboxylic acid hydrochloride
• Solubility: Soluble in DMSO, not in water
• Storage: 0 - 4 °C for short term, or -20 °C for long term
• InChI: InChI=1S/C20H25NO2S2.ClH/c1-14-7-11-24-18(14)17(19-15(2)8-12-25-19)6-4-10-21-9-3-5-16(13-21)20(22)23;/h6-8,11-12,16H,3-5,9-10,13H2,1-2H3,(H,22,23);1H/t16-;/m1./s1
• InChIKey: YUKARLAABCGMCN-PKLMIRHRSA-N
• SMILES: CC1=C(SC=C1)C(=CCCN2CCC[C@H](C2)C(=O)O)C3=C(C=CS3)C.Cl

Tiagabine hydrochloride (CAT: I009803) is a pharmaceutical compound primarily used as an antiepileptic drug. It acts as a selective gamma-aminobutyric acid (GABA) reuptake inhibitor, increasing the concentration of GABA in the brain. GABA is an inhibitory neurotransmitter that helps regulate the excitability of neurons. By inhibiting GABA reuptake, tiagabine hydrochloride enhances GABAergic neurotransmission, resulting in reduced neuronal excitability and seizure control. It is commonly prescribed as an adjunctive treatment for partial seizures in patients with epilepsy who have not responded adequately to other antiepileptic medications.

Reference

1:Brain Res. 1997 Apr 11;753(2):260-8. Tigabine hydrochloride, an inhibitor of gamma-aminobutyric acid (GABA) uptake, induces cortical depolarizations in vitro.Hu RQ,Davies JA, PMID: 9125411
Abstract: The effect of the gamma-aminobutyric acid uptake inhibitor tiagabine hydrochloride was studied on electrical responses in cortical wedges prepared from 20-30 day-old, audiogenic seizure-prone DBA/2 mice. Perfusion of tiagabine (50 microM) for 15 min, evoked large, slow depolarizations with a frequency of 6-8/h which persisted for 4-5 h. The GABA(A) receptor antagonists, bicuculline (10 microM) and picrotoxin (100 microM), inhibited established depolarizations. These depolarizations were also calcium-dependent and blocked by tetrodotoxin. The non-opioid antitussive, dextromethorphan, which has been shown to inhibit glutamate release, irreversibly blocked the depolarizations. Conversely, 4-aminopyridine (50 microM), a potassium channel antagonist, markedly potentiated the responses. The NMDA receptor antagonist, 3-((R)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, had no effect on the depolarizations at concentrations up to 100 microM but the AMPA/kainate receptor antagonist, 6,7-dinitroquinoxaline-2.3-dione at high concentrations (100 and 200 microM), reversibly decreased the frequency without affecting the amplitude. It is concluded that the tiagabine-induced depolarizations in this in vitro preparation were initiated through GABA(A) receptors leading, possibly, to a release of excitatory amino acids.