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Revision as of 15:56, 10 January 2012 editBeetstra (talk | contribs)Edit filter managers, Administrators172,031 edits Saving copy of the {{drugbox}} taken from revid 453937451 of page Vigabatrin for the Chem/Drugbox validation project (updated: 'DrugBank').  Latest revision as of 20:40, 16 October 2024 edit MusikBot II (talk | contribs)Bots, Interface administrators, Administrators103,174 editsm Removing protection templates from unprotected page (more info) 
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{{Short description|Epilepsy medication}}
{{ambox | text = This page contains a copy of the infobox ({{tl|drugbox}}) taken from revid of page ] with values updated to verified values.}}
{{Use mdy dates|date=September 2024}}
{{Drugbox
{{cs1 config|name-list-style=vanc|display-authors=6}}
| verifiedrevid = 419002448
{{Infobox drug
| IUPAC_name = (''RS'')-4-aminohex-5-enoic acid
| Watchedfields = changed
| verifiedrevid = 470630102
| image = Vigabatrin.svg | image = Vigabatrin.svg
| width = 200 | alt =
| image2 = Vigabatrin ball-and-stick.png
| imagename = 1 : 1 mixture (racemate)
| drug_name = Vigabatrin | alt2 =


<!--Clinical data--> <!-- Clinical data -->
| pronounce = {{IPAc-en|v|aɪ|ˈ|ɡ|æ|b|ə|t|ɹ|ɪ|n}}<br />{{respell|vy|GAB|ə|trin}}
| tradename = Sabril
| tradename = Sabril, others
| Drugs.com = {{drugs.com|CDI|vigabatrin}}
| Drugs.com = {{drugs.com|monograph|vigabatrin}}
| MedlinePlus = a610016 | MedlinePlus = a610016
| DailyMedID = Vigabatrin
| pregnancy_AU = D | pregnancy_AU = D
| routes_of_administration = ]
| legal_status = Not a controlled substance
| ATC_prefix = N03
| routes_of_administration = Oral
| ATC_suffix = AG04
| ATC_supplemental =

| legal_AU = S4
| legal_BR = C1
| legal_BR_comment = <ref>{{Cite web |author=Anvisa |author-link=Brazilian Health Regulatory Agency |date=March 31, 2023 |title=RDC Nº 784 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial |trans-title=Collegiate Board Resolution No. 784 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control|url=https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-784-de-31-de-marco-de-2023-474904992 |url-status=live |archive-url=https://web.archive.org/web/20230803143925/https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-784-de-31-de-marco-de-2023-474904992 |archive-date=August 3, 2023 |access-date=August 16, 2023 |publisher=] |language=pt-BR |publication-date=April 4, 2023}}</ref>
| legal_CA = Rx-only
| legal_UK = POM
| legal_US = Rx-only
| legal_US_comment = <ref>{{cite web | title=Sabril- vigabatrin tablet, film coated | website=DailyMed | date=October 20, 2021 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a5d389d2-d0e1-4395-a2a2-b552808e7f98 | access-date=September 5, 2024}}</ref><ref>{{cite web | title=Sabril- vigabatrin powder, for solution | website=DailyMed | date=October 20, 2021 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a88ac1b4-e2c9-45c0-b321-4785902172e3 | access-date=September 5, 2024}}</ref><ref name="Vigafyde FDA label">{{cite web | title=Vigafyde- vigabatrin solution | website=DailyMed | date=August 23, 2024 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=8d3d6316-33ab-41e8-9485-4495c218be56 | access-date=September 5, 2024}}</ref><ref>{{cite web | title=Vigadrone- vigabatrin tablet | website=DailyMed | date=July 14, 2023 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=01f7f049-78c2-47c2-a66e-ec662ba48a98 | access-date=September 5, 2024}}</ref><ref name="Vigpoder FDA label">{{cite web | title=Vigpoder- vigabatrin powder, for solution | website=DailyMed | date=March 20, 2024 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1859a632-e98e-4152-b91d-b8aae1107be1 | access-date=September 5, 2024}}</ref>
| legal_EU = Rx-only


<!--Pharmacokinetic data--> <!-- Pharmacokinetic data -->
| bioavailability = 80–90% | bioavailability = 80–90%
| protein_bound = Nil | protein_bound = 0%
| metabolism = Almost no metabolic transformation occurs | metabolism = not metabolized
| elimination_half-life = 5–8 hours in young adults, 12–13 hours in the elderly. | elimination_half-life = 5–8 hours in young adults, 12–13 hours in the elderly.
| excretion = ] | excretion = ]


<!--Identifiers--> <!-- Identifiers -->
| IUPHAR_ligand = 4821
| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number_Ref = {{cascite|correct|CAS}}
| CAS_number = 60643-86-9
| CAS_number = 68506-86-5
| ATC_prefix = N03
| ATC_suffix = AG04
| ATC_supplemental =
| PubChem = 5665 | PubChem = 5665
| DrugBank_Ref = {{drugbankcite|correct|drugbank}} | DrugBank_Ref = {{drugbankcite|correct|drugbank}}
Line 40: Line 53:
| ChEMBL_Ref = {{ebicite|correct|EBI}} | ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 89598 | ChEMBL = 89598
| synonyms = γ-Vinyl-GABA


<!--Chemical data--> <!-- Chemical data -->
| IUPAC_name = (''RS'')-4-aminohex-5-enoic acid
| C=6 | H=11 | N=1 | O=2
| C=6 | H=11 | N=1 | O=2
| molecular_weight = 129.157 g/mol
| smiles = O=C(O)CCC(\C=C)N | smiles = O=C(O)CCC(\C=C)N
| InChI = 1/C6H11NO2/c1-2-5(7)3-4-6(8)9/h2,5H,1,3-4,7H2,(H,8,9)
| InChIKey = PJDFLNIOAUIZSL-UHFFFAOYAL
| StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C6H11NO2/c1-2-5(7)3-4-6(8)9/h2,5H,1,3-4,7H2,(H,8,9) | StdInChI = 1S/C6H11NO2/c1-2-5(7)3-4-6(8)9/h2,5H,1,3-4,7H2,(H,8,9)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = PJDFLNIOAUIZSL-UHFFFAOYSA-N | StdInChIKey = PJDFLNIOAUIZSL-UHFFFAOYSA-N
| melting_point = 171
| melting_high = 177
}} }}

'''Vigabatrin''', sold under the brand name '''Sabril''' among others, is a ] used in the management and treatment of ] and refractory complex partial seizures.

It works by inhibiting the ] of ] (GABA). It is also known as γ-vinyl-GABA, and is a ] of GABA, but does not bind to ]s.<ref name=what_is_vigabatrin>{{cite web | vauthors = Long PW | url = http://www.mentalhealth.com/drug/p30-s07.html | title = Vigabatrin | work = Drug Monograph | archive-url = https://web.archive.org/web/20060423082047/http://www.mentalhealth.com/drug/p30-s07.html | archive-date=April 23, 2006 | publisher = Internet Mental Health | date = 2003 }}</ref>

Vigabatrin is generally used only in cases of treatment-resistant epilepsy due to the risk of permanent vision loss.<ref>{{cite web|title=Sabril (vigabatrin) Tablets for Oral Use, Powder for Oral Solution. Full Prescribing Information|url=http://www.lundbeck.com/upload/us/files/pdf/Products/Sabril_PI_US_EN.pdf|publisher=Lundbeck}}</ref> Although estimates of visual field loss vary substantially, risk appears to be lower among infants with treatment duration less than 12 months and the risk of clinically meaningful vision loss is very low among children treated for infantile spasms.<ref>{{cite journal|title=High vigabatrin dosage is associated with lower risk of infantile spasms relapse among children with tuberous sclerosis complex|date=2018 |pmc=6347124 | vauthors = Hussain SA, Schmid E, Peters JM, Goyal M, Bebin EM, Northrup H, Sahin M, Krueger DA, Wu JY, Williams ME, Hanson E, Bing N, Kent B, o'Kelley S, Filip-Dhima R, Dies K, Bruns S, Scherrer B, Cutter G, Murray DS, Roberds SL | collaboration = Tuberous Sclerosis Complex Autism Center of Excellence Network |journal=Epilepsy Research |volume=148 |pages=1–7 |doi=10.1016/j.eplepsyres.2018.09.016 |pmid=30296632 }}</ref><ref>{{cite journal|title=A lack of clinically apparent vision loss among patients treated with vigabatrin with infantile spasms: The UCLA experience|date=2016 |pmid=26921595 |url=https://pubmed.ncbi.nlm.nih.gov/26921595/ | vauthors = Schwarz MD, Li M, Tsao J, Zhou R, Wu YW, Sankar R, Wu JY, Hussain SA |journal=Epilepsy & Behavior |volume=57 |issue=Pt A |pages=29–33 |doi=10.1016/j.yebeh.2016.01.012 }}</ref>

==Medical uses==

===Epilepsy===
In Canada, vigabatrin is approved for use as an adjunctive treatment (with other drugs) in treatment resistant ], ]s, ], and for monotherapy use in ]s in ].<ref name=what_is_vigabatrin/>

As of 2003, vigabatrin is approved in Mexico for the treatment of epilepsy that is not satisfactorily controlled by conventional therapy (adjunctive or monotherapy) or in recently diagnosed patients who have not tried other agents (monotherapy).<ref name=mexicanuses>{{cite web | url = http://www.facmed.unam.mx/bmnd/plm/mex/productos/10130.htm | title = DEF Mexico: Sabril | archive-url = https://web.archive.org/web/20050914050706/http://www.facmed.unam.mx/bmnd/plm/mex/productos/10130.htm | archive-date=September 14, 2005 | work = Diccionario de Especialdades Farmaceuticas. | edition = 49 | date = 2003 }}</ref>

Vigabatrin is also indicated for monotherapy use in secondarily generalized ]s, ]s, and in infantile spasms due to West syndrome.<ref name=mexicanuses/>

===Others===
Vigabatrin reduced ]-induced symptoms of ], in addition to elevated ] and ] levels, in healthy volunteers.<ref name=vigabatrinpanic>{{cite journal |vauthors=Zwanzger P, Baghai TC, Schuele C, Strohle A, Padberg F, Kathmann N, Schwarz M, Moller HJ, Rupprecht R | title=Vigabatrin decreases cholecystokinin-tetrapeptide (CCK-4) induced panic in healthy volunteers | journal=Neuropsychopharmacology | volume=25 | issue=5 | year=2001 | pages=699&ndash;703 | pmid=11682253 | doi=10.1016/S0893-133X(01)00266-4| doi-access=free }}</ref>

Vigabatrin is also used to treat seizures in ] (SSADHD), which is an inborn GABA metabolism defect that causes ], ], ]s, ], and ] through the accumulation of γ-Hydroxybutyric acid (]). Vigabatrin helps lower GHB levels through GABA transaminase inhibition. However, this is in the brain only; it has no effect on peripheral GABA transaminase, so the GHB keeps building up and eventually reaches the brain.<ref>{{cite book | vauthors = Pearl PL, Wiwattanadittakul N, Roullet JB, Gibson KM | chapter = Succinic Semialdehyde Dehydrogenase Deficiency | veditors = dam MP, Mirzaa GM, Pagon RA, Wallace SE, Bean LJ, Gripp KW, Amemiya A | title = GeneReviews | date = May 5, 2004 | pmid = 20301374 | chapter-url = https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&part=ssadh | access-date = September 6, 2010 | publisher = University of Washington | url-status = live | archive-url = https://web.archive.org/web/20200728224158/https://www.ncbi.nlm.nih.gov/books/NBK1195/ | archive-date = July 28, 2020 }}</ref>

==Adverse effects==

===Central nervous system===
] (12.5%), ] (3.8%), dizziness (3.8%), nervousness (2.7%), ] (2.5%), memory disturbances (2.3%), ] (2.2%), aggression (2.0%), ] (1.9%), ] (1.9%), ] (1.8%), vision loss (1.6%) (See below), ] (1.4%), ] (1.3%), impaired concentration (1.2%), ] (1.1%).<ref name=what_is_vigabatrin /> Out of 299 children, 33 (11%) became hyperactive.<ref name=what_is_vigabatrin/>

Some patients develop ] during the course of vigabatrin therapy,<ref name=psyhosis>{{cite journal |vauthors=Sander JW, Hart YM | title=Vigabatrin and behaviour disturbance | journal=Lancet | volume=335 | issue=8680 | year=1990 | pages=57 | pmid=1967367 | doi=10.1016/0140-6736(90)90190-G| s2cid=34456538 }}</ref> which is more common in adults than in children.<ref name=pediatric_psychosis>{{cite journal |vauthors=Chiaretti A, Castorina M, Tortorolo L, Piastra M, Polidori G | title= | journal= La Pediatria Medica e Chirurgica: Medical and Surgical Pediatrics | volume=16 | issue=5 | year=1994 | pages=489&ndash;90 | pmid = 7885961 | language = it }}</ref> This can happen even in patients with no prior history of psychosis.<ref name=never_before>{{cite journal |vauthors=Sander JW, Hart YM, Trimble MR, Shorvon SD | title=Vigabatrin and psychosis | journal=Journal of Neurology, Neurosurgery, and Psychiatry | volume=54 | issue=5 | year=1991 | pages=435&ndash;9 | pmid=1865207 | doi=10.1136/jnnp.54.5.435 | pmc=488544}}</ref> Other rare CNS side effects include anxiety, ], irritability, tremor, abnormal ], and ].<ref name=what_is_vigabatrin/>

===Gastrointestinal===
Abdominal pain (1.6%), constipation (1.4%), vomiting (1.4%), and nausea (1.4%). ] and increased appetite occurred in less than 1% of subjects in clinical trials.<ref name=what_is_vigabatrin/>

===Body as a whole===
Fatigue (9.2%), weight gain (5.0%), ] (1.1%).<ref name=what_is_vigabatrin/>

===Teratogenicity===
A ] study conducted in rabbits found that a dose of 150&nbsp;mg/kg/day caused ] in 2% of pups and a dose of 200&nbsp;mg/kg/day caused it in 9%.<ref name=what_is_vigabatrin /> This may be due to a decrease in ] levels, according to a study published in March 2001.<ref name=teratogenicity_possible_mechanism>{{cite journal |vauthors=Abdulrazzaq YM, Padmanabhan R, Bastaki SM, Ibrahim A, Bener A | title=Placental transfer of vigabatrin (gamma-vinyl GABA) and its effect on concentration of amino acids in the embryo of TO mice | journal=Teratology | volume=63 | issue=3 | year=2001 | pages=127&ndash;33 | pmid=11283969 | doi=10.1002/tera.1023| doi-access=free }}</ref> In 2005, a study conducted at the ] was published stating that rats whose mothers had consumed 250–1000&nbsp;mg/kg/day had poorer performance in the ] and ]s, rats in the 750&nbsp;mg group were underweight at birth and did not catch up to the control group, and rats in the 1000&nbsp;mg group did not survive pregnancy.<ref name=teratology_rat>{{cite journal | vauthors=Lombardo SA, Leanza G, Meli C, Lombardo ME, Mazzone L, Vincenti I, Cioni M | title=Maternal exposure to the antiepileptic drug vigabatrin affects postnatal development in the rat | journal=Neurological Sciences | volume=26 | issue=2 | year=2005 | pages=89&ndash;94 | pmid=15995825 | doi=10.1007/s10072-005-0441-6 | hdl=2108/194069 | s2cid=25257244 | url=https://art.torvergata.it/bitstream/2108/194069/1/lombardo2005.pdf | hdl-access=free | access-date=September 3, 2019 | archive-date=August 27, 2021 | archive-url=https://web.archive.org/web/20210827182311/https://art.torvergata.it/retrieve/handle/2108/194069/383064/lombardo2005.pdf | url-status=live }}</ref>

There is no controlled teratology data in humans to date.

===Sensory===
In 2003, vigabatrin was shown by Frisén and Malmgren to cause irreversible diffuse ] of the ]l ] layer in a ] study of 25 patients.<ref name=vigabatrinretina>{{cite journal |vauthors=Frisén L, Malmgren K | title=Characterization of vigabatrin-associated optic atrophy | journal=Acta Ophthalmologica Scandinavica | volume=81 | issue=5 | year=2003 | pages=466&ndash;73 | pmid=14510793 | doi=10.1034/j.1600-0420.2003.00125.x| doi-access=free }}</ref> This has the most effect on the outer area (as opposed to the ]r, or central area) of the retina.<ref name=retinalatrophy>{{cite journal |vauthors=Buncic JR, Westall CA, Panton CM, Munn JR, MacKeen LD, Logan WJ | title=Characteristic retinal atrophy with secondary "inverse" optic atrophy identifies vigabatrin toxicity in children | journal=Ophthalmology | volume=111 | issue=10 | year=2004 | pages=1935&ndash;42 | pmid=15465561 | pmc=3880364 | doi=10.1016/j.ophtha.2004.03.036}}</ref>
Visual field defects had been reported as early as 1997 by Tom Eke and others, in the UK. Some authors, including Comaish ''et al''. believe that visual field loss and electrophysiological changes may be demonstrable in up to 50% of Vigabatrin users.

The retinal toxicity of vigabatrin can be attributed to a ] depletion.<ref name="PMID 22476345">{{cite journal | vauthors = Gaucher D, Arnault E, Husson Z, Froger N, Dubus E, Gondouin P, Dherbécourt D, Degardin J, Simonutti M, Fouquet S, Benahmed MA, Elbayed K, Namer IJ, Massin P, Sahel JA, Picaud S | title = Taurine deficiency damages retinal neurones: cone photoreceptors and retinal ganglion cells | journal = Amino Acids | volume = 43 | issue = 5 | pages = 1979–1993 | date = November 2012 | pmid = 22476345 | pmc = 3472058 | doi = 10.1007/s00726-012-1273-3 }}</ref>

Due to safety issues, the Vigabatrin ] Program is required by the FDA to ensure informed decisions before initiating and to ensure appropriate use of this drug.<ref>{{Cite web|url=https://dev.sabril.net/prescribing-sabril|title=Sabril (vigabatrin) tablets, for oral use Sabril (vigabatrin) powder for oral...|website=Sabril.net|language=en|access-date=May 31, 2019}}{{Dead link|date=July 2023 |bot=InternetArchiveBot |fix-attempted=yes }}</ref>

==Interactions==
A study published in 2002 found that vigabatrin causes a ] increase in ] clearance of ].<ref name=vigabatrin_carbamazepine>{{cite journal | vauthors = Sánchez-Alcaraz A, Quintana MB, López E, Rodríguez I, Llopis P | title = Effect of vigabatrin on the pharmacokinetics of carbamazepine | journal = Journal of Clinical Pharmacy and Therapeutics | volume = 27 | issue = 6 | pages = 427–430 | date = December 2002 | pmid = 12472982 | doi = 10.1046/j.1365-2710.2002.00441.x | s2cid = 29986581 | doi-access = free }}</ref>

In 1984, Drs Rimmer and Richens at the University of Wales reported that administering vigabatrin with ] lowered the serum phenytoin concentration in patients with treatment-resistant epilepsy.<ref name=phenytoin>{{cite journal |vauthors=Rimmer EM, Richens A | title=Double-blind study of gamma-vinyl GABA in patients with refractory epilepsy | journal=Lancet | volume=1 | issue=8370 | year=1984 | pages=189&ndash;90 | pmid=6141335 | doi=10.1016/S0140-6736(84)92112-3| s2cid=54336689 }}</ref> Five years later, the same two scientists reported a fall in concentration of phenytoin of 23% within five weeks in a paper describing their failed attempt at elucidating the mechanism behind this interaction.<ref name=phenytoin2>{{cite journal |vauthors=Rimmer EM, Richens A | title=Interaction between vigabatrin and phenytoin | journal=British Journal of Clinical Pharmacology | volume=27 | issue=Suppl 1 | year=1989 | pages=27S–33S | pmid=2757906 | pmc=1379676 | doi=10.1111/j.1365-2125.1989.tb03458.x}}</ref>

==Pharmacology==
Vigabatrin is an irreversible ] of ] (GABA-AT), the ] responsible for the ] of ]. Inhibition of GABA-AT results in increased levels of ] in the brain.<ref name=what_is_vigabatrin /><ref>{{cite journal | vauthors = Rogawski MA, Löscher W | title = The neurobiology of antiepileptic drugs | journal = Nature Reviews. Neuroscience | volume = 5 | issue = 7 | pages = 553–564 | date = July 2004 | pmid = 15208697 | doi = 10.1038/nrn1430 | url = https://zenodo.org/record/1233562 | access-date = June 5, 2020 | url-status = live | s2cid = 2201038 | archive-url = https://web.archive.org/web/20201216114030/https://zenodo.org/record/1233562 | archive-date = December 16, 2020 }}</ref> Vigabatrin is a ] compound, and its -] is pharmacologically active.<ref name=senantiomer>{{cite journal | vauthors = Sheean G, Schramm T, Anderson DS, Eadie MJ | title = Vigabatrin--plasma enantiomer concentrations and clinical effects | journal = Clinical and Experimental Neurology | volume = 29 | pages = 107–116 | year = 1992 | pmid = 1343855 }}</ref><sup>,</sup><ref name=Gram_et_al_1989>{{cite journal | vauthors = Gram L, Larsson OM, Johnsen A, Schousboe A | title = Experimental studies of the influence of vigabatrin on the GABA system | journal = British Journal of Clinical Pharmacology | volume = 27 | issue = Suppl 1 | pages = 13S–17S | year = 1989 | pmid = 2757904 | pmc = 1379673 | doi = 10.1111/j.1365-2125.1989.tb03455.x | author-link1 = Lone Gram }}</ref>
cluster-containing enzyme, complexed with gamma-ethynyl-GABA and with the antiepilepsy drug vigabatrin | journal = The Journal of Biological Chemistry | volume = 279 | issue = 1 | pages = 363–373 | date = January 2004 | pmid = 14534310 | doi = 10.1074/jbc.M305884200 | doi-access = free | url = https://www.openaccessrepository.it/record/94973/files/fulltext.pdf }}</ref>]]

==Pharmacokinetics==
With most drugs, elimination half-life is a useful predictor of dosing schedules and the time needed to reach ]s. In the case of vigabatrin, however, it has been found that the half-life of biologic activity is far longer than the elimination half-life.<ref name=bioactivehalflife>{{cite journal | vauthors = Browne TR | title = Pharmacokinetics of antiepileptic drugs | journal = Neurology | volume = 51 | issue = 5 Suppl 4 | pages = S2–S7 | date = November 1998 | pmid = 9818917 | doi = 10.1212/wnl.51.5_suppl_4.s2 | s2cid = 39231047 }}</ref>

For vigabatrin, there is no range of target concentrations because researchers found no difference between the serum concentration levels of responders and those of non-responders.<ref name=karolinska_no_correlation>{{cite journal |vauthors=Lindberger M, Luhr O, Johannessen SI, Larsson S, Tomson T | title=Serum concentrations and effects of gabapentin and vigabatrin: observations from a dose titration study | journal=Therapeutic Drug Monitoring | volume=25 | issue=4 | year=2003 | pages=457&ndash;62 | pmid=12883229 | doi=10.1097/00007691-200308000-00007| s2cid=35834401 }}</ref> Instead, the duration of action is believed to be more a function of the GABA-T resynthesis rate; levels of GABA-T do not usually return to their normal state until six days after stopping the medication.<ref name=Gram_et_al_1989 />

==History==
Vigabatrin was developed in the 1980s with the specific goal of increasing GABA concentrations in the brain in order to stop an epileptic seizure. To do this, the drug was designed to irreversibly inhibit the GABA transaminase, which degrades the GABA substrate. Although the drug was approved for treatment in the United Kingdom in 1989, the authorized use of Vigabatrin by US Food and Drug Administration was delayed twice in the United States before 2009. It was delayed in 1983 because animal trials produced intramyelinic edema, however, the effects were not apparent in human trials so the drug design continued. In 1997, the trials were temporarily suspended because it was linked to peripheral visual field defects in humans.<ref name=drug_design>{{cite journal | vauthors = Ben-Menachem E | title = Mechanism of action of vigabatrin: correcting misperceptions | journal = Acta Neurologica Scandinavica. Supplementum | volume = 124 | issue = 192 | pages = 5–15 | year = 2011 | pmid = 22061176 | doi = 10.1111/j.1600-0404.2011.01596.x | s2cid = 25347559 | doi-access = free }}</ref>

==Society and culture==

=== Legal status ===
Vigabatrin (Sabril) was approved for medical use in the United States in August 2009.<ref>{{cite web | title=Drug Approval Package: Sabril (Vigabatrin) Tablets NDA #020427 | website=U.S. Food and Drug Administration | date=November 23, 2009 | url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/020427s000TOC.cfm | access-date=September 8, 2024}}</ref><ref>{{cite journal | vauthors = Bresnahan R, Gianatsi M, Maguire MJ, Tudur Smith C, Marson AG | title = Vigabatrin add-on therapy for drug-resistant focal epilepsy | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 7 | pages = CD007302 | date = July 2020 | pmid = 32730657 | pmc = 8211760 | doi = 10.1002/14651858.CD007302.pub3 }}</ref>

In April 2017, the US ] (FDA) approved the first generic powder packets for the oral solution version of vigabatrin.<ref>{{Cite web |title= Sabril (vigabatrin) – First-time generic |url=https://professionals.optumrx.com/content/dam/optum3/professional-optumrx/news/rxnews/new-generics/newgenerics_sabril_2017-0824.pdf |website=OptumRx}}</ref> In January 2019, the FDA approved the first generic tablet version of vigabatrin.<ref name=":0">{{cite journal | vauthors = Kotulska K, Kwiatkowski DJ, Curatolo P, Weschke B, Riney K, Jansen F, Feucht M, Krsek P, Nabbout R, Jansen AC, Wojdan K, Sijko K, Głowacka-Walas J, Borkowska J, Sadowski K, Domańska-Pakieła D, Moavero R, Hertzberg C, Hulshof H, Scholl T, Benova B, Aronica E, de Ridder J, Lagae L, Jóźwiak S | title = Prevention of Epilepsy in Infants with Tuberous Sclerosis Complex in the EPISTOP Trial | journal = Annals of Neurology | volume = 89 | issue = 2 | pages = 304–314 | date = February 2021 | pmid = 33180985 | pmc = 7898885 | doi = 10.1002/ana.25956 }}</ref>

Vigpoder was approved in the United States in June 2022.<ref name="Vigpoder FDA label" />

Vigafyde was approved in the United States in June 2024.<ref name="Vigafyde FDA label" /><ref>{{Cite web |last=PharmD |first=Brian Park |date=June 18, 2024 |title=Ready-to-Use Vigabatrin Oral Solution Approved for Infantile Spasms |url=https://www.empr.com/home/news/ready-to-use-vigabatrin-oral-solution-approved-for-infantile-spasms/ |access-date=June 18, 2024 |website=MPR }}</ref><ref>{{Cite press release |date=June 17, 2024 |title=Pyros Pharmaceuticals Announces FDA Approval of Vigafyde (vigabatrin) as the First and Only Ready-to-Use Vigabatrin Oral Solution |url=https://www.businesswire.com/news/home/20240617159224/en/Pyros-Pharmaceuticals-Announces-FDA-Approval-of-VIGAFYDE%E2%84%A2-vigabatrin-as-the-First-and-Only-Ready-to-Use-Vigabatrin-Oral-Solution |access-date=June 18, 2024 |publisher=Pyros Pharmaceuticals | via=Businesswire}}</ref>

===Brand Names===
Vigabatrin is sold under the brand names Sabril, Vigafyde,<ref name="Vigafyde FDA label" /> and Vigpoder.<ref name="Vigpoder FDA label" />

Vigabatrin is sold as Sabril in Canada,<ref name="Canada">{{Cite web |title=Vigabatrin Drug Information |url=https://www.drugs.com/cons/Vigabatrin.html |url-status=live |archive-url=https://web.archive.org/web/20200728224154/https://www.drugs.com/cons/vigabatrin.html |archive-date=July 28, 2020 |access-date=January 23, 2018 |work=Drugs.com}}</ref> Mexico,<ref name="mexicanuses" />
and the United Kingdom.<ref name="UnitedKingdom">{{cite web |title=Treatments for Epilepsy - Vigabatrin |url=http://www.nmhct.nhs.uk/pharmacy/epi5.htm |url-status=dead |archive-url=https://archive.today/20020211201831/http://www.nmhct.nhs.uk/pharmacy/epi5.htm |archive-date=February 11, 2002 |access-date=March 26, 2017 |work=Norfolk and Waveney Mental Health Partnership NHS Trust}}</ref> The brand name in Denmark is Sabrilex.

== Research ==

=== The PREVeNT Trial ===
The PREVeNT study found that early vigabatrin treatment delayed the onset and reduced the overall prevalence of infantile spasms in TSC infants. However, the seizure prevention was not seen for other seizure types, including focal seizures, that are highly prevalent in this population. PREVeNT, similarly to EPISTOP, reported a reduced incidence of infantile spasms up to 24 months of age.<ref name=":0" />

=== EPISTOP Trial ===
Infantile spasms are seen in 50 to 70% of children with TSC, and are associated with both drug-resistance and intellectual disability. Importantly, in EPISTOP, none of the children who received preventive treatment developed infantile spasms throughout the 2-year course of the study, in contrast to 10 of 25 (40%) receiving conventional treatment.<ref name=":0" />

==References==
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{{Anticonvulsants}}
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