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| Name | Tiagabine | ||||||||||||||||||||||||||||||||||||
| Accession Number | DB00906 (APRD00344) | ||||||||||||||||||||||||||||||||||||
| Type | small molecule | ||||||||||||||||||||||||||||||||||||
| Groups | approved | ||||||||||||||||||||||||||||||||||||
| Description | 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. |
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| Structure |
Download: MOL | SDF | SMILES | InChI Display: 2D Structure | 3D Structure |
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| Synonyms |
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| Brand name mixtures | Not Available | ||||||||||||||||||||||||||||||||||||
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| CAS number | 115103-54-3 | ||||||||||||||||||||||||||||||||||||
| Weight |
Average: 375.548 Monoisotopic: 375.132670429 |
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| Chemical Formula | C20H25NO2S2 | ||||||||||||||||||||||||||||||||||||
| InChI Key | InChIKey=PBJUNZJWGZTSKL-MRXNPFEDSA-N | ||||||||||||||||||||||||||||||||||||
| InChI |
InChI=1S/C20H25NO2S2/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)/t16-/m1/s1
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| IUPAC Name |
(3R)-1-[4,4-bis(3-methylthiophen-2-yl)but-3-en-1-yl]piperidine-3-carboxylic acid
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| SMILES |
CC1=C(SC=C1)C(=CCCN1CCC[C@H](C1)C(O)=O)C1=C(C)C=CS1
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| Mass Spec | Not Available | ||||||||||||||||||||||||||||||||||||
| Taxonomy | |||||||||||||||||||||||||||||||||||||
| Kingdom | Organic | ||||||||||||||||||||||||||||||||||||
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| Pharmacology | |||||||||||||||||||||||||||||||||||||
| 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.
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| 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 | ||||||||||||||||||||||||||||||||||||
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| 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. | ||||||||||||||||||||||||||||||||||||
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| Pathways | Not Available | ||||||||||||||||||||||||||||||||||||
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| Properties | |||||||||||||||||||||||||||||||||||||
| State | solid | ||||||||||||||||||||||||||||||||||||
| Melting point | Not Available | ||||||||||||||||||||||||||||||||||||
| Experimental Properties |
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| Predicted Properties |
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| Synthesis Reference | Not Available | ||||||||||||||||||||||||||||||||||||
| General Reference | Not Available | ||||||||||||||||||||||||||||||||||||
| External Links |
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| ATC Codes |
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| AHFS Codes | Not Available | ||||||||||||||||||||||||||||||||||||
| PDB Entries | Not Available | ||||||||||||||||||||||||||||||||||||
| FDA label | show (251.3 KB) | ||||||||||||||||||||||||||||||||||||
| MSDS | Not Available | ||||||||||||||||||||||||||||||||||||
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| Drug Interactions | Not Available | ||||||||||||||||||||||||||||||||||||
| Food Interactions | Not Available | ||||||||||||||||||||||||||||||||||||
| Targets |
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1. Sodium- and chloride-dependent GABA transporter 1 Pharmacological action: yesActions: inhibitor Terminates the action of GABA by its high affinity sodium-dependent reuptake into presynaptic terminals Organism class: humanUniProt ID: P30531 ![]() Gene: SLC6A1 ![]() Protein Sequence: FASTA Gene Sequence: FASTA SNPs: SNPJam Report ![]() References:
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| Enzymes |
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Actions: substrate
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation reactions (e.g. caffeine 8-oxidation, omeprazole sulphoxidation, midazolam 1'-hydroxylation and midazolam 4- hydroxylation) of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. The enzyme also hydroxylates etoposide UniProt ID: P08684![]() Gene: CYP3A4 Protein Sequence: FASTA Gene Sequence: FASTA SNPs: SNPJam Report ![]() References:
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This project is supported by Genome Alberta & Genome Canada, a not-for-profit organization that is leading Canada's national genomics strategy with $600 million in funding from the federal government. This project is also supported in part by GenomeQuest, Inc., an enterprise genomic information company serving the life science community.