Page last updated: 2024-12-05

vigabatrin

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Cross-References

ID SourceID
PubMed CID5665
CHEMBL ID89598
CHEBI ID63638
SCHEMBL ID26714
MeSH IDM0328364

Synonyms (161)

Synonym
chebi:63638 ,
CHEMBL89598 ,
HY-15399
gvg ,
sabril
.gamma.-vinyl-.gamma.-aminobutyric acid
mdl 71,754
hexenoic acid, 4-amino
4-aminohex-5-enoic acid
.gamma.-vinyl-gaba
rmi-71754
mdl-71754
DIVK1C_006760
cpp-109
sabrilex
m071754 ,
EU-0101277
(+/-)-vigabatrin
SPECTRUM_000368
BPBIO1_000925
BSPBIO_000421
5-hexenoic acid, 4-amino-
gamma-vinyl-gaba
rmi 71754
vigabatrina [spanish]
vigabatrinum [latin]
vigabatrine [french]
c6h11no2
vigabatrine
vigabatrin [usan:inn:ban]
mdl 71754
PRESTWICK_837
PRESTWICK2_000501
LOPAC0_001277
BPBIO1_000465
BIOMOL-NT_000247
PRESTWICK3_000501
AB00053309
C07500
60643-86-9
vigabatrin ,
DB01080
gamma vinyl gaba
4-amino-5-hexenoic acid
vinyl gamma-aminobutyric acid
gamma-vinyl-gamma-aminobutyric acid
gamma-vinyl gaba
sabril (tn)
vigabatrin (jan/usp/inn)
D00535
NCGC00024802-05
NCGC00024802-03
KBIO2_005984
KBIO2_003416
KBIOSS_000848
KBIO1_001704
KBIO2_000848
KBIO3_002973
SPECTRUM3_001825
PRESTWICK1_000501
SPECPLUS_000664
PRESTWICK0_000501
SPBIO_002342
SPECTRUM1502036
BSPBIO_003469
NCGC00024802-06
(?)-gamma-vinyl gaba
NCGC00024802-02
NCGC00024802-04
NCGC00016087-03
HMS2094M21
( inverted question mark)-gamma-vinyl gaba
V 8261 ,
NCGC00016087-08
4-amino-hex-5-enoic acid
bdbm50118886
HMS1569F03
NCGC00016087-06
HMS3263P16
HMS2096F03
cas-68506-86-5
tox21_110301
dtxsid4041153 ,
dtxcid2021153
CCG-205350
NCGC00016087-05
NCGC00016087-09
NCGC00016087-07
NCGC00016087-04
4-aminohexenoic acid
FT-0675812
FT-0675811
68506-86-5
(1)-4-aminohex-5-enoic acid
unii-gr120krt6k
hsdb 8395
cpp109
(+-)-gamma-vinyl gaba
einecs 270-929-6
vigabatrinum
gr120krt6k ,
cpp 109
vigabatrina
LP01277
(+/-)-gamma-vinyl gaba
CS-0791
AKOS015854596
kigabeq
gtpl4821
BRD-A07893380-001-01-6
vigabatrin [usp-rs]
vigabatrin [mi]
vigabatrin [orange book]
vigabatrin [usp monograph]
vigabatrin [who-dd]
vigabatrin [inn]
vigabatrin [ep monograph]
vigabatrin [mart.]
vigabatrin, (+/-)-
vigabatrin [vandf]
vigabatrin [jan]
vigabatrin [usan]
SCHEMBL26714
.gamma.-vinyl gaba
vinyl .gamma.-aminobutyric acid
NCGC00261962-01
tox21_501277
(y)-gamma-vinyl gaba
NCGC00016087-11
Q-201924
gamma-vinyl gaba; 4-amino-5-hexenoic acid
(+/-)-?-vinyl gaba
HB0868
(a+/-)-gamma-vinyl gaba
AB00053309_04
4-aminohex-5-enoic acid/s(+)-gamma-vigabatrin
mfcd00274577
(+/-)-gamma-vinyl-gaba
SR-01000075653-6
sr-01000075653
vigabatrin, united states pharmacopeia (usp) reference standard
EN300-245587
vigabatrin, european pharmacopoeia (ep) reference standard
SR-01000075653-1
SR-01000075653-4
SBI-0051243.P003
FT-0700968
BCP16220
Q421663
s(+)-4-aminohexenoicacid
Z1255431434
AS-11778
(+/-)-4-aminohex-5-enoic acid
SDCCGSBI-0051243.P004
NCGC00016087-22
AMY6474
A853593
4-amino-5-hexenoicacid
SY263247
-vinyl-gaba
rac-vigabatrin

Research Excerpts

Overview

Vigabatrin (VGB) is a first-line drug used for treatment of infantile spasms. Vigaba is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors.

ExcerptReferenceRelevance
"Vigabatrin (VGB) is an effective antiseizure medication for West syndrome. "( Elevation of brain gamma-aminobutyric acid levels is associated with vigabatrin-associated brain abnormalities on magnetic resonance imaging.
Aida, N; Goto, T; Iai, M; Ikeda, A; Kawai, Y; Tanabe, M; Tomiyasu, M; Tsuji, M; Tsuyusaki, Y; Yamamoto, A, 2022
)
2.4
"Vigabatrin (VGB) is an effective antiepileptic that increases concentrations of inhibitory γ-aminobutyric acid (GABA) by inhibiting GABA transaminase. "( Vigabatrin-Induced Retinal Functional Alterations and Second-Order Neuron Plasticity in C57BL/6J Mice.
Chan, K; Gibson, KM; Gloe, S; Hoon, M; Jansen, E; Kiland, JA; McLellan, GJ; Pattnaik, BR; Roullet, JB; Salomons, G; Ver Hoeve, JN; Vogel, KR; Wahlgren, B; Walters, D; Wetherbee, B; Williams, J, 2020
)
3.44
"Vigabatrin (VGB) is a first-line drug used for treatment of infantile spasms. "( Role of Taurine Transporter in the Retinal Uptake of Vigabatrin.
Murthy, SN; Police, A; Shankar, VK, 2020
)
2.25
"Vigabatrin is an antiepileptic drug licensed for use in drug-resistant epilepsy."( Vigabatrin add-on therapy for drug-resistant focal epilepsy.
Bresnahan, R; Gianatsi, M; Maguire, MJ; Marson, AG; Tudur Smith, C, 2020
)
2.72
"Vigabatrin is a preferred drug in patients younger than two years old for both focal (61.7%) and generalized (56.7%) seizures."( Approach to Preventive Epilepsy Treatment in Tuberous Sclerosis Complex and Current Clinical Practice in 23 Countries.
Fladrowski, C; Jóźwiak, S; Kotulska, K; Roberds, SL; Szymańska, S; Słowińska, M, 2021
)
1.34
"Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear."( Depressive effectiveness of vigabatrin (γ-vinyl-GABA), an antiepileptic drug, in intermediate-conductance calcium-activated potassium channels in human glioma cells.
Huang, CW; Huang, HI; Hung, TY; Wu, SN, 2021
)
2.36
"Vigabatrin is an antiepileptic drug indicated as monotherapy in infantile spasms. "( Proposition of a Minimal Effective Dose of Vigabatrin for the Treatment of Infantile Spasms Using Pediatric and Adult Pharmacokinetic Data.
Bienayme, H; Chiron, C; Duhamel, P; Dulac, O; Jullien, V; Nabbout, R; Ounissi, M; Pons, G; Rodrigues, C, 2019
)
2.22
"Vigabatrin is an antiepileptic drug licensed for use in the treatment of refractory epilepsy."( Vigabatrin for refractory partial epilepsy.
Hemming, K; Hutton, JL; Maguire, MJ; Marson, AG, 2013
)
2.55
"Vigabatrin is an antiepileptic drug that results in higher gamma-aminobutyrate levels in the brain and retina. "( Electroretinographic responses in epileptic children treated with vigabatrin.
Ashrafi, MR; Bakhshandeh Bali, MK; Ghofrani, M; Karimzadeh, P; Nasehi, MM; Otaghsara, SM; Sadighi, N; Soltansanjari, M; Taghdiri, MM, 2014
)
2.08
"Vigabatrin is an anti-epileptic drug substance. "( The absorptive flux of the anti-epileptic drug substance vigabatrin is carrier-mediated across Caco-2 cell monolayers.
Brodin, B; Hansen, SH; Holm, R; Nielsen, CU; Nøhr, MK, 2014
)
2.09
"Vigabatrin is an irreversible inhibitor of γ-aminobutyric acid transaminase (GABA-T) and is used as an adjunctive therapy for adult patients with refractory complex partial seizures (rCPS). "( Population dose-response analysis of daily seizure count following vigabatrin therapy in adult and pediatric patients with refractory complex partial seizures.
Hutmacher, MM; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2015
)
2.1
"Vigabatrin is an inhibitor of γ-aminobutyric acid transaminase. "( Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms.
Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014
)
2.11
"Vigabatrin (VGB) is an anti-epileptic medication which has been linked to peripheral constriction of the visual field. "( Does the Swedish Interactive Threshold Algorithm (SITA) accurately map visual field loss attributed to vigabatrin?
Conway, ML; Cubbidge, RP; Hosking, SL; Zhu, H, 2014
)
2.06
"Vigabatrin is an antiepileptic drug used for treatment of infantile spasms. "( Vigabatrin-induced MRI changes associated with extrapyramidal symptoms in a child with infantile spasms.
Schonstedt, V; Silva, C; Stecher, X; Venegas, V, 2015
)
3.3
"Vigabatrin (VGB) is an antiepileptic drug thatincreases brain γ-aminobutyric acid (GABA) levels through irreversible inhibition of GABA transaminase. "( Genotoxic and mutagenic effects of vigabatrin, a γ-aminobutyric acid transaminase inhibitor, in Wistar rats submitted to rotarod task.
Coelho, VR; de Souza, LP; Leal, MB; Papke, D; Pereira, P; Picada, JN; Pires, TR; Schunck, R; Sousa, K; Vieira, CG, 2016
)
2.15
"Vigabatrin is an effective medical therapy for infantile spasm but has pronounced, potentially worrisome imaging findings in patients receiving therapy."( Brain MRI findings with vigabatrin therapy: case report and literature review.
Chazen, JL; Hussain, K; Walsh, TJ,
)
1.16
"Vigabatrin is a clinically approved anti-seizure drug, which acts by increasing brain GABA levels by irreversibly inhibiting GABA-aminotransferase (GABA-T)."( Continuous bilateral infusion of vigabatrin into the subthalamic nucleus: Effects on seizure threshold and GABA metabolism in two rat models.
Gernert, M; Gey, L; Löscher, W, 2016
)
1.44
"Vigabatrin (Sabril®) is an antiepileptic drug (AED) currently indicated in the US as a monotherapy for patients 1month to 2years of age with infantile spasms (IS) and as adjunctive therapy for patients ≥10years of age with refractory complex partial seizures (rCPS) whose seizures have inadequately responded to several alternative treatments and for whom the potential benefits outweigh the risk of vision loss. "( Which children receive vigabatrin? Characteristics of pediatric patients enrolled in the mandatory FDA registry.
Dribinsky, Y; Faught, E; Foroozan, R; Isojarvi, J; Lee, D; Othman, F; Pellock, JM; Sergott, RC; Shields, WD; Torri, S; Ziemann, A, 2016
)
2.19
"Vigabatrin is a highly effective antiseizure medication, but its use is limited due to concerns about retinal toxicity. "( Plasma taurine levels are not affected by vigabatrin in pediatric patients.
Mabud, TS; Porter, BE; Reimer, R; Spelbrink, EM, 2016
)
2.14
"Vigabatrin (VGB) is a drug indicated mostly for the treatment of spasms in childhood and West's syndrome patients. "( Neurobehavioral effects of vigabatrin and its ability to induce DNA damage in brain cells after acute treatment in rats.
Coelho, VR; Decker, N; Papke, DK; Pereira, P; Pflüger, P; Picada, JN; Pires, TR; Sousa, K, 2017
)
2.19
"Vigabatrin (VGB) is a first-line drug for the treatment of infantile spasms. "( [Reversible alterations in the neuroimages associated with vigabatrine treatment in infants with epileptic spasms].
Fernandez-Garcia, MA; Garcia-Esparza, E; Garcia-Penas, JJ; Gomez-Martin, H; Perez-Sebastian, I; Sirvent-Cerda, S, 2017
)
2.14
"Vigabatrin is an antiepileptic drug licensed for use in the treatment of refractory epilepsy."( Vigabatrin for refractory partial epilepsy.
Hemming, K; Hutton, JL; Maguire, MJ; Marson, AG, 2008
)
2.51
"Vigabatrin (VGB) is a structural analogue of gamma-aminobutyric acid (GABA) that irreversibly inhibits GABA-transaminase (GABA-T), increasing brain levels of GABA. "( Vigabatrin: 2008 update.
Abelson, MB; Ben-Menachem, E; Pellock, JM; Shields, WD; Willmore, LJ, 2009
)
3.24
"Vigabatrin is an antiepileptic drug that produces intramyelinic edema in several animal models. "( Transient brain magnetic resonance imaging hyperintensity in basal ganglia and brain stem of epileptic infants treated with vigabatrin.
Bartoli, C; Chabrol, B; Chapon, F; Girard, N; Hugonenq, C; Lamoureux, S; Livet, MO; Mancini, J; Milh, M; Pineau, S; Villeneuve, N, 2009
)
2
"Vigabatrin (VGB) is an effective drug for treatment of epilepsy and has been used in the treatment of West syndrome and epilepsy resistant to other drugs."( [Ophthalmological monitoring protocol for patients treated with long-term antimalarials or vigabatrin].
Ingster-Moati, I; Orssaud, C, 2009
)
1.29
"Vigabatrin is a second generation anticonvulsant drug available in France since 1995. "( [Therapeutic drug monitoring of vigabatrin].
Bentué-Ferrer, D; Tribut, O; Verdier, MC,
)
1.86
"Vigabatrin is a GABA derivative (gamma-vinyl GABA) which inhibits irreversibly the enzyme activity of GABA transaminase and thus increased indirectly brain GABA concentrations. "( Effects of GABA-transaminase inhibitor Vigabatrin on thermoregulation in rats.
Nikolov, RP; Yakimova, KS, 2011
)
2.08
"Vigabatrin is an efficacious antiepileptic drug licensed as add-on therapy in refractory epilepsy and used in infantile spasms. "( Prevalence of visual field loss following exposure to vigabatrin therapy: a systematic review.
Hemming, K; Hutton, JL; Maguire, MJ; Marson, AG; Wild, JM, 2010
)
2.05
"Vigabatrin is an antiepileptic drug used in more than 50 countries as adjunctive therapy for the treatment of refractory complex partial seizures (rCPS) in adults. "( Vigabatrin therapy for refractory complex partial seizures: review of clinical trial experience in the United States.
Faught, E, 2011
)
3.25
"Vigabatrin is a unique AED approved in both Europe and the United States as adjunctive therapy for adult patients with rCPS who have responded inadequately to several alternative treatments."( Vigabatrin therapy for refractory complex partial seizures: review of major European trials.
Ben-Menachem, E; Sander, JW, 2011
)
2.53
"Vigabatrin is an irreversible inhibitor of γ-aminobutyric acid (GABA) transaminase. "( Understanding and interpreting vision safety issues with vigabatrin therapy.
Plant, GT; Sergott, RC, 2011
)
2.06
"Vigabatrin is an effective antiepileptic drug (AED) for the treatment of refractory complex partial seizures (rCPS) and infantile spasms (IS). "( Non-vision adverse events with vigabatrin therapy.
Kälviäinen, R; Walker, SD, 2011
)
2.1
"Vigabatrin is an effective and well-tolerated antiepileptic drug (AED) for the treatment of refractory complex partial seizures (rCPS) and infantile spasms (IS), but its benefits must be evaluated in conjunction with its risk of retinopathy with the development of peripheral visual field defects (pVFDs). "( Balancing clinical benefits of vigabatrin with its associated risk of vision loss.
Pellock, JM, 2011
)
2.1
"Vigabatrin is a rationally developed antiepileptic drug, which acts by increasing GABA levels in the brain by irreversibly inhibiting GABA degradation. "( Vigabatrin for focal drug delivery in epilepsy: bilateral microinfusion into the subthalamic nucleus is more effective than intranigral or systemic administration in a rat seizure model.
Backofen-Wehrhahn, B; Bankstahl, M; Bröer, S; Gernert, M; Gey, L; Löscher, W, 2012
)
3.26
"Vigabatrin (VGB) is a commonly prescribed antiepileptic drug designed to inhibit GABA-transaminase, effectively halting seizures. "( Vigabatrin-induced retinal toxicity is partially mediated by signaling in rod and cone photoreceptors.
Davis, RJ; Erol, D; Lin, CS; Naumann, MC; Tosi, J; Tsai, YT; Tsang, SH; Yang, J, 2012
)
3.26
"Vigabatrin is a GABA (gamma-aminobutyric acid) transaminase inhibitor that elicits an antiepileptic effect by enhancing inhibitory neurotransmission in the brain. "( Neurotoxic effects of GABA-transaminase inhibitors in the treatment of epilepsy: ocular perfusion and visual performance.
Hilton, EJ; Hosking, SL, 2002
)
1.76
"Vigabatrin is an effective, well-tolerated treatment for infantile spasms."( Vigabatrin for infantile spasms.
Mitchell, WG; Shah, NS, 2002
)
2.48
"Vigabatrin is a selective and irreversible GABA-transaminase inhibitor that greatly increases whole-brain levels of GABA."( Novel mechanisms of action of three antiepileptic drugs, vigabatrin, tiagabine, and topiramate.
Angehagen, M; Ben-Menachem, E; Hansson, E; Rönnbäck, L, 2003
)
1.29
"Vigabatrin is an antiepileptic drug and may increase the intraretinal GABA level due to an inhibition of the enzyme GABA-transaminase and may induce an ascending simple optic nerve atrophy. "( [Vigabatrin-associated bilateral simple optic nerve atrophy with visual field constriction. A case report and a survey of the literature].
Mardin, CY; Viestenz, A, 2003
)
2.67
"Vigabatrin is a novel antiepileptic drug, which increases GABA levels by irreversible inhibition of GABA-aminotransferase. "( Influence of vigabatrin, a novel antiepileptic drug, on the anticonvulsant activity of conventional antiepileptics in pentetrazole-induced seizures in mice.
Czuczwar, SJ; Swiader, M; Wielosz, M; Łuszczki, J,
)
1.94
"Vigabatrin (GVG) is an effective antiepileptic drug used for treating partial seizures in adults and children. "( Visual field defects in pediatric patients on vigabatrin monotherapy.
Ascaso, FJ; Cristobal, JA; Lopez, MJ; Mauri, JA, 2003
)
2.02
"Vigabatrin (VGB) is a new antiepileptic drug, that acts by the irreversible inhibition of gamma-aminobutyric acid (GABA) aminotransferase. "( [Influence of vigabatrin on visual fields and electrophysiological tests in patients with epilepsy].
Bakunowicz-Łazarczyk, A; Mrugacz, M, 2003
)
2.12
"Vigabatrin (VGB) is an irreversible inhibitor of gamma-aminobutyric acid (GABA) transaminase. "( Acute vigabatrin retinotoxicity in albino rats depends on light but not GABA.
Benz, AM; Ishikawa, M; Izumi, M; Izumi, Y; Thio, LL; Zorumski, CF, 2004
)
2.25
"Vigabatrin (VGB) is an important treatment option for infantile spasms. "( Ophthalmologic and neurologic findings in two children exposed to vigabatrin in utero.
Heinonen, S; Herrgård, E; Kälviäinen, R; Pääkkönen, A; Sorri, I; Viinikainen, K, 2005
)
2.01
"Vigabatrin is a GABA mimetic antiepileptic agent that has been used for 10 years in cases of epilepsy that resist other treatments. "( [Electrophysiological monitoring of epileptic patients treated with Vigabatrin].
Baulac, M; Nordmann, JP; Rigolet, MH, 2005
)
2.01
"Vigabatrin (VGB) is a relatively new second line antiepileptic drug and was first registered for use in Poland more than ten years ago."( A comparative study of vigabatrin vs. carbamazepine in monotherapy of newly diagnosed partial seizures in children.
Boćkowski, L; Kułak, W; Smigielska-Kuzia, J; Sobaniec, W; Strzelecka, J,
)
1.16
"Vigabatrin seems to be an effective and safe antiepileptic drug as primary monotherapy for epilepsy with fewer cognitive side effects than carbamazepine."( Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study.
Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995
)
3.18
"Vigabatrin (VGB) is an antiepileptic drug (AED) that acts by irreversibly inhibiting gamma-aminobutyric acid transaminase (GABA-T). "( Immunologic aspects of vigabatrin treatment in epileptic children.
Iannetti, P; Imperato, C; Pacifici, R; Raucci, U; Zuccaro, P, 1995
)
2.04
"Vigabatrin (VGB) is a safe and effective antiepileptic drug (AED) that irreversibly inhibits neuronal and glial GABA-transaminase."( Initial observations on effect of vigabatrin on in vivo 1H spectroscopic measurements of gamma-aminobutyric acid, glutamate, and glutamine in human brain.
Behar, KL; Mattson, RH; Petroff, OA; Rothman, DL, 1995
)
1.29
"Vigabatrin is a specific and irreversible inhibitor of the enzyme gamma-amino-butyric-acid (GABA) transferase."( [Vigabatrin and lamotrigin: experiences with 2 new anticonvulsants in the Swiss epilepsy clinic].
Krämer, G; Vogt, H, 1995
)
1.92
"Vigabatrin is an irreversible inhibitor of gamma-aminobutyrate (Gaba) aminotransferase, producing an increase in Gaba concentrations in the brain. "( [Acute psychosis and vigabatrin in childhood].
Castorina, M; Chiaretti, A; Piastra, M; Polidori, G; Tortorolo, L,
)
1.89
"Vigabatrin (VGB, Sabril) is a new antiepileptic drug used for treatment of partial and secondarily generalized tonic-clonic seizures. "( Vigabatrin: effects on human brain GABA levels by nuclear magnetic resonance spectroscopy.
Behar, K; Mattson, RH; Petroff, O; Rothman, D, 1994
)
3.17
"Vigabatrin (Sabril) is a gamma-aminobutyric acid-transaminase (GABA-T) inhibitor that is effective in the treatment of certain types of drug-resistant or uncontrolled epilepsy but is known to cause microscopic vacuolation (intramyelinic edema) in the brains of treated rats, mice, and dogs. "( Sequential neuropathology of dogs treated with vigabatrin, a GABA-transaminase inhibitor.
Dillberger, JE; Gibson, JP; Heydorn, WE; Hurst, G; Lippert, B; Marler, RJ; Sussman, NM; Yarrington, JT,
)
1.83
"Vigabatrin appears to be a useful antiepilepsy drug with little impact upon tests of either cognitive abilities or quality of life."( Evaluation of the effects of vigabatrin on cognitive abilities and quality of life in epilepsy.
Arnett, JL; Dodrill, CB; Sommerville, KW; Sussman, NM, 1993
)
1.3
"Vigabatrin (VGB) is an effective add-on anti-epileptic drug. "( Retrospective study of vigabatrin and psychiatric behavioural disturbances.
Wong, IC, 1995
)
2.04
"Vigabatrin appears to be a reasonable choice for single-drug therapy in the treatment of certain types of seizures."( Newer antiepileptic drugs as monotherapy: data on vigabatrin.
Fisher, R; Kälviäinen, R; Regesta, G; Tanganelli, P, 1996
)
1.27
"Vigabatrin is an anticonvulsant drug with a relatively favourable side-effect profile. "( Vigabatrin and behaviour disorders: a retrospective survey.
Ring, H; Schmitz, B; Thomas, L; Trimble, M, 1996
)
3.18
"Vigabatrin is a novel antiepileptic drug designed to control seizures by raising brain gamma-aminobutyric acid (GABA) concentrations. "( Human brain gamma-aminobutyric acid levels and seizure control following initiation of vigabatrin therapy.
Behar, KL; Mattson, RH; Petroff, OA; Rothman, DL, 1996
)
1.96
"Vigabatrin (VGB) is a recently-released antiepileptic drug which works by a clearly-defined mechanism of action: inhibition of GABA transaminase leading to an elevation of brain GABA concentration. "( Vigabatrin.
Guberman, A, 1996
)
3.18
"Vigabatrin is a safe and effective antiepileptic medication designed to increase brain GABA by irreversibly inhibiting GABA-transaminase. "( Human brain GABA levels rise rapidly after initiation of vigabatrin therapy.
Behar, KL; Collins, TL; Mattson, RH; Petroff, OA; Rothman, DL, 1996
)
1.98
"Vigabatrin is an irreversible inhibitor of GABA transaminase."( [Antiepileptic drugs: mechanism of action].
Mercadé Cerdá, JM, 1996
)
1.02
"Vigabatrin is a relatively new medication used in the treatment of epilepsia. "( Vigabatrin-induced gingival overgrowth.
Chaushu, G; Givol, N; Katz, J; Shemer, J; Taicher, S, 1997
)
3.18
"Vigabatrin is a structural analogue of gamma amino butyric acid (GABA), which binds irreversibly to GABA-transaminase causing increased brain levels of GABA. "( Vigabatrin.
Sankar, R; Shields, WD, 1997
)
3.18
"Vigabatrin is a highly specific enzyme antagonist."( Evidence for both in vivo and in vitro interaction between vigabatrin and alanine transaminase.
Deybach, JC; McEwan, JR; Mumford, JP; Richens, A, 1997
)
1.26
"Vigabatrin (VGB) is a relatively recently introduced antiepileptic drug that enhances the brain levels of gamma aminobutyric acid (GABA). "( Teratogenic effects of vigabatrin in TO mouse fetuses.
Abdulrazzaq, YM; Bastaki, SM; Padmanabhan, R, 1997
)
2.05
"Vigabatrin is an irreversible inhibitor of GABA-transaminase, effective in the treatment of drug-resistant epilepsy and reported to be eliminated unchanged by renal excretion. "( Pharmacokinetics of the S(+) and R(-) enantiomers of vigabatrin during chronic dosing in a patient with renal failure.
Chiron, C; Guillonneau, M; Jacqz-Aigrain, E; Loirat, C; Macher, MA; Montes, C; Rey, E, 1997
)
1.99
"Vigabatrin is an extremely effective antiepileptic drug that selectively increases brain gamma-aminobutyric acid (GABA). "( Vigabatrin-associated retinal cone system dysfunction: electroretinogram and ophthalmologic findings.
Johnson, MA; Krauss, GL; Miller, NR, 1998
)
3.19
"Vigabatrin is a new antiepileptic medication consisting of a racemic mixture of 50% active S enantiomer and 50% inactive R enantiomer. "( Vigabatrin: placental transfer in vivo and excretion into breast milk of the enantiomers.
Mai, J; Mumford, JP; O'Mahoney, T; Olive, G; Rey, E; Tran, A, 1998
)
3.19
"Vigabatrin acts as an inhibitor of gamma-aminobutyric acid (GABA) transaminase. "( Outer retinal dysfunction in patients treated with vigabatrin.
Arndt, CF; Defoort-Dhellemmes, S; Derambure, P; Hache, JC, 1999
)
2
"Vigabatrin is a newly licensed drug for use in patients with epilepsy. "( Safety and efficacy of vigabatrin and carbamazepine in newly diagnosed epilepsy: a multicentre randomised double-blind study. Vigabatrin European Monotherapy Study Group.
Chadwick, D, 1999
)
2.06
"Vigabatrin (VGB) is a structural analogue of the inhibitory neurotransmitter gamma-amino butyric acid (GABA), which produces its antiepileptic effect by irreversibly inhibiting the degradative enzyme GABA-transaminase. "( Vigabatrin.
French, JA, 1999
)
3.19
"Vigabatrin is an antiepileptic drug that, although relatively well tolerated, is associated with visual field constriction and other visual disturbances of unclear origin."( Visual dysfunction in patients receiving vigabatrin: clinical and electrophysiologic findings.
Endres, M; Girkin, CA; Johnson, MA; Krauss, GL; Miller, NR; Paul, SR; Perry, JD, 1999
)
2.01
"Vigabatrin is a selective and irreversible inhibitor of gamma-aminobutyric acid transaminase. "( Vigabatrin: a novel therapy for seizure disorders.
Gidal, BE; Gilman, JT; Privitera, MD; Sheth, RD, 1999
)
3.19
"Vigabatrin is an antiepileptic drug for the treatment of partial seizures. "( Visual electrophysiological effect of a GABA transaminase blocker.
Barnes, P; Edson, AS; Harding, GF; Robertson, KA; Wild, J,
)
1.57
"1. Vigabatrin is a very efficient drug in long-term treatment of patients with intractable focal epilepsies. "( [Vigabatrin in the treatment of intractable focal epilepsy in children and adolescents. Two-year study].
Grotowska, M; Kozik, A; Ujma-Czapska, B, 2000
)
1.84
"Vigabatrin (VGB) is a novel antiepileptic drug effective as adjunctive therapy in patients with partial seizures. "( Vigabatrin as add-on therapy for adult complex partial seizures: a double-blind, placebo-controlled multicentre study. The Canadian Vigabatrin Study Group.
Bruni, J; Desforges, C; Guberman, A; Vachon, L, 2000
)
3.19
"Vigabatrin (VGB) is a new-generation anticonvulsant used in the treatment of partial seizures and West syndrome. "( Acute encephalopathy associated with vigabatrin in a six-month-old girl.
Haas-Lude, K; Krägeloh-Mann, I; Niemann, G; Riethmüller, J; Wolff, M, 2000
)
2.02
"Vigabatrin is an effective antiepileptic drug, but it is known to cause a variety of changes in visual function, including reductions in the visual field, visual acuity, color vision, and in electroretinogram (ERG) and electro-oculogram amplitudes. "( Visual function loss from vigabatrin: effect of stopping the drug.
Johnson, MA; Krauss, GL; Medura, M; Miller, NR; Paul, SR, 2000
)
2.05
"Vigabatrin is an anti-epileptic drug particularly useful for drug-resistant partial seizures and infantile spasms. "( Visual impairment in children with epilepsy treated with vigabatrin.
Banin, E; Gross-Tsur, V; Lahat, E; Shahar, E; Shalev, RS, 2000
)
1.99
"Vigabatrin (VGB) is a new antiepileptic drug useful in refractOry partial seizures. "( [Acute encephalopathy and myoclonic status induced by vigabatrin monotherapy] .
García Pastor, A; García-Zarza, E; Peraita Adrados, R, 2000
)
2
"Vigabatrin is an effective antiepileptic drug for treatment of partial crises with or without generalization. "( [Visual field changes secondary to vigabatrin treatment].
Abad-Alegría, F; Ascaso-Puyuelo, J; Escalza-Cortina, I; Iñiguez, C; Mauri-Llerda, JA; Morales-Asín, F; Santos-Lasaosa, S; Tejero-Juste, C,
)
1.85
"Vigabatrin (VGB) is a new antiepileptic drug that increases the human brain gamma-aminobutyric acid (GABA) level by irreversibly inhibiting GABA transaminase. "( Effects of vigabatrin on brain GABA+/CR signals in patients with epilepsy monitored by 1H-NMR-spectroscopy: responder characteristics.
Boesiger, P; Duc, CO; Meier, D; Mueller, SG; Russ, W; Weber, B; Weber, OM; Wieser, HG, 2001
)
2.14
"Vigabatrin is an enzyme-activated irreversible inhibitor of gamma-aminobutyric acid (GABA) transaminase that increases brain and cerebrospinal GABA concentrations in animals and man."( Increased vigabatrin entry into the brain by polysorbate 80 and sodium caprate.
Dimitrijevic, D; Domin, M; Florence, AT; Welham, K; Whitton, PS, 2001
)
1.43
"Vigabatrin is an antiepileptic drug (AED) that acts as a selective irreversible inhibitor of gamma-aminobutyric acid (GABA) transaminase. "( Visual field defects with vigabatrin: epidemiology and therapeutic implications.
Kälviäinen, R; Nousiainen, I, 2001
)
2.05
"Vigabatrin (VGB) is a novel antiepileptic drug which inhibits GABA-transaminase (GABA-T) and thus increases the level of GABA in the CNS and in its neurons. "( Concentric visual field restriction under vigabatrin therapy: extent depends on the duration of drug intake.
Toggweiler, S; Wieser, HG, 2001
)
2.02
"Vigabatrin (VGB) is a gabaergic anti-epileptic medication (AEM) reported to produce tunnel vision with constricted fields."( Ethical dilemmas of potential adverse events.
Beran, RG, 2001
)
1.03
"Vigabatrin is an effective antiepileptic drug but visual field constriction (VFC) is found to be a severe side-effect. "( Vigabatrin and retinal changes.
Gram, L; Jensen, H; Sjö, O; Uldall, P, 2002
)
3.2
"Vigabatrin is a specific gamma-aminobutyric acid transaminase inhibitor. "( Effect of vigabatrin on striatal dopamine receptors: evidence in humans for interactions of GABA and dopamine systems.
Costa, DC; Ell, PJ; George, MS; Ring, HA; Trimble, MR; Verhoeff, P, 1992
)
2.13
"Vigabatrin is a structural analogue of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). "( Vigabatrin. Clinical pharmacokinetics.
Olive, G; Pons, G; Rey, E, 1992
)
3.17
"Vigabatrin proved to be a potent anticonvulsant drug at acute doses (100-200 mg/kg), but during chronic administration, the anticonvulsant activity of the treatment was lost already in the second week of treatment."( Development of tolerance to the anticonvulsant effect of vigabatrin in amygdala-kindled rats.
Löscher, W; Rundfeldt, C, 1992
)
1.25
"Vigabatrin is a novel antiepileptic agent, whose action is based on the inhibition of gamma-aminobutyric acid (GABA) aminotransferase, the enzyme responsible for the catabolism of the neurotransmitter GABA."( Effect of long-term vigabatrin therapy on selected neurotransmitter concentrations in cerebrospinal fluid.
Ben-Menachem, E; Haegele, KD; Huebert, N; Mumford, J; Persson, LI, 1991
)
1.33
"Vigabatrin is a new antiepileptic drug that acts by the irreversible inhibition of gamma-aminobutyric acid (GABA) aminotransferase. "( Neuropathologic findings in patients receiving long-term vigabatrin therapy for chronic intractable epilepsy.
Butler, WH; Cannon, DJ; Lewis, PJ; Mumford, JP, 1991
)
1.97
"Vigabatrin is an enzyme-activated, irreversible inhibitor of gamma-aminobutyric acid (GABA) aminotransferase, which causes a marked increase in cerebral GABA concentration and a resulting anticonvulsant action. "( Pharmacology and clinical pharmacology of vigabatrin.
Richens, A, 1991
)
1.99
"Vigabatrin seems to be a valuable therapeutic addition for patients with partial seizures resistant to standard anti-epileptic drugs."( Long-term evaluation of once daily vigabatrin in drug-resistant partial epilepsy.
Ben-Menachem, E; Mumford, J; Persson, L, 1990
)
1.28
"Vigabatrin appears to be a promising new anti-epileptic drug."( Evaluation of vigabatrin as an add-on drug in the management of severe epilepsy.
Hart, YM; Sander, JW; Shorvon, SD; Trevisol-Bittencourt, PC, 1990
)
1.36
"Vigabatrin is a selective, irreversible suicide inhibitor of GABA transaminase and thus increases brain and CSF GABA. "( Vigabatrin: rational treatment for chronic epilepsy.
Farr, IN; Heller, AJ; Reynolds, EH; Ring, HA, 1990
)
3.16
"6. Vigabatrin thus appears to be a safe antiepileptic drug that may be effective in the treatment of severe epilepsy in children."( Vigabatrin in the treatment of epilepsy in children.
Aicardi, J; Arzimanoglou, A; Beaumont, D; Livingston, JH, 1989
)
2.23
"1. Vigabatrin has proved to be a very effective antiepileptic in clinical trials, with excellent long term tolerability. "( Effects of long term vigabatrin on somatosensory evoked potentials in epileptic patients.
Beaumont, D; Chauvel, P; Gisselbrecht, D; Liegeois-Chauvel, C; Marquis, P; Pantieri, R, 1989
)
1.22

Effects

Vigabatrin has a definite role to play in the management of persons with intractable complex partial seizures where standard anti-epileptic therapy has failed to achieve control.

Vigabatrin (VGB) has been shown to cause visual field constriction and other forms of mild visual dysfunction. The drug has been considered the drug of choice for infantile spasms secondary to tuberous sclerosis, and possibly, according to many neurologists, for all cases of infantileSpasm.

ExcerptReferenceRelevance
"Vigabatrin has a definite role to play in the management of persons with intractable complex partial seizures where standard anti-epileptic therapy has failed to achieve control."( Vigabatrin use in 72 patients with drug-resistant epilepsy.
Buchanan, N, 1994
)
3.17
"Vigabatrin has a rapid effect on both the photopic ERG and the EOG; however, the changes merely reflect alterations in retinal GABA levels secondary to concomitant blocking of GABA transaminase by existing vigabatrin therapy."( Visual electrophysiological effect of a GABA transaminase blocker.
Barnes, P; Edson, AS; Harding, GF; Robertson, KA; Wild, J,
)
0.85
"The vigabatrin drug registry has documented a relatively large percentage (37%) of preexisting, baseline visual deficits and a paucity (2%) of potential new visual findings."( Vigabatrin: Lessons Learned From the United States Experience.
Foroozan, R, 2018
)
2.4
"Vigabatrin (VGB) has several therapeutic advantages over older antiepileptic drugs (AED), but there is a lack of information about its potential reproductive toxicologic effects. "( Vigabatrin (VGB) administered during late gestation lowers maternal folate concentration and causes pregnancy loss, fetal growth restriction and skeletal hypoplasia in the mouse.
Abdulrazzaq, YM; Bastaki, SM; Nurulain, M; Padmanabhan, R; Shafiullah, M, 2010
)
3.25
"Vigabatrin has been used as first-line treatment of infantile spasms. "( MRI changes associated with vigabatrin treatment mimicking tumor progression.
Geyer, JR; Ojemann, JG; Pruthi, S; Yang, T, 2010
)
2.1
"Vigabatrin has shown efficacy in the treatment of infantile spasms caused by tuberous sclerosis complex, but its effects on focal seizures caused by tuberous sclerosis complex have not been determined."( Vigabatrin and mental retardation in tuberous sclerosis: infantile spasms versus focal seizures.
Ko, TS; Lee, EH; Yum, MS, 2013
)
2.55
"Vigabatrin has been shown to be particularly effective in treating infantile spasms in the setting of tuberous sclerosis."( [The course and treatment of epilepsy in children with tuberose sclerosis].
Belousova, ED; Dorofeeva, MIu, 2012
)
1.1
"Vigabatrin (VGB) has been shown to be particularly effective in the treatment of infantile spasms for those with tuberous sclerosis complex (TSC). "( Vigabatrin for partial-onset seizure treatment in patients with tuberous sclerosis complex.
Bogner, M; Devinsky, O; Friedman, D; Parker-Menzer, K, 2013
)
3.28
"Vigabatrin has been previously associated with concentric peripheral visual field loss and visual electrophysiological abnormalities."( Neurotoxic effects of GABA-transaminase inhibitors in the treatment of epilepsy: ocular perfusion and visual performance.
Hilton, EJ; Hosking, SL, 2002
)
1.04
"Vigabatrin (VGB) has been widely used in patients affected by drug-resistant epilepsy and West syndrome. "( Scotopic threshold response changes after vigabatrin therapy in a child without visual field defects: a new electroretinographic marker of early damage?
Manfredi, M; Parisi, P; Piazza, G; Tommasini, P, 2004
)
2.03
"Vigabatrin has shown promise in treating IS patients, particularly those with tuberous sclerosis."( Pharmacologic treatment of the catastrophic epilepsies.
Conry, JA, 2004
)
1.04
"Vigabatrin has been recorded to have a beneficial effect in this disorder."( The United Kingdom Infantile Spasms Study comparing vigabatrin with prednisolone or tetracosactide at 14 days: a multicentre, randomised controlled trial.
Edwards, SW; Hancock, E; Johnson, AL; Kennedy, CR; Lux, AL; Newton, RW; O'Callaghan, FJ; Osborne, JP; Verity, CM,
)
1.1
"Vigabatrin has been shown to be particularly effective in treating infantile spasms in the setting of tuberous sclerosis complex."( Managing epilepsy in tuberous sclerosis complex.
Thiele, EA, 2004
)
1.04
"Vigabatrin has emerged as an accepted first-line medication for infantile spasms in Norway and many other countries, although it has not been shown that this therapy in general is as effective as ACTH/steroids. "( [Infantile spasms].
Nustad, A; Rasmussen, M; Sandvig, I; Skjeldal, OH, 2005
)
1.77
"Vigabatrin has been shown to be a generally well tolerated and effective antiepileptic drug (AED) in a wide variety of seizure types affecting both children and adults, particularly those with IS and CPS."( Vigabatrin.
Collins, SD; Ramsay, RE; Wheless, JW, 2007
)
2.5
"Vigabatrin has been demonstrated to elevate central GABA levels (Mattson et al."( Vigabatrin, a GABA transaminase inhibitor, reversibly eliminates tinnitus in an animal model.
Bauer, CA; Brozoski, TJ; Spires, TJ, 2007
)
2.5
"Vigabatrin has proved to be effective against infantile spasms due to TSC."( Management of epilepsy in tuberous sclerosis complex.
Bombardieri, R; Cerminara, C; Curatolo, P; D'Argenzio, L, 2008
)
1.07
"Vigabatrin has been used as both add-on, and monotherapy in the treatment of spasms."( Vigabatrin in the management of generalized seizures in children.
Appleton, RE, 1995
)
2.46
"Vigabatrin has a definite role to play in the management of persons with intractable complex partial seizures where standard anti-epileptic therapy has failed to achieve control."( Vigabatrin use in 72 patients with drug-resistant epilepsy.
Buchanan, N, 1994
)
3.17
"Vigabatrin has been shown to aggravate "nonprogressive myoclonic epilepsies." Vigabatrin has been well tolerated in children, with mild drowsiness and agitation being the most commonly reported side effects."( The role of vigabatrin in the management of infantile epileptic syndromes.
Appleton, RE, 1993
)
1.39
"Vigabatrin has been effective in patients with refractory epilepsy."( [Gamma-vinyl-GABA: the first trials in Italy].
de Romanis, F; Sopranzi, N, 1993
)
1.01
"Vigabatrin has been shown to protect against hippocampal neuronal cell death in experimental models of epilepsy."( Treatment with antiepileptic drugs: possible neuroprotective effects.
Pitkänen, A, 1996
)
1.02
"Vigabatrin has been shown to be efficient in infants with infantile spasms and tuberous sclerosis, in open studies. "( Randomized trial comparing vigabatrin and hydrocortisone in infantile spasms due to tuberous sclerosis.
Chiron, C; Dulac, O; Dumas, C; Jambaqué, I; Mumford, J, 1997
)
2.04
"Vigabatrin has been recommended as a treatment for some forms of childhood epilepsy; therefore, further studies are needed to assess the risks in children."( Low-dose vigabatrin (gamma-vinyl GABA)-induced damage in the immature rat brain.
Del Bigio, MR; Seshia, SS; Sidhu, RS; Tuor, UI, 1997
)
1.44
"Vigabatrin (VGB) has been shown through several studies to be safe and effective as add-on therapy, particularly for the treatment of partial seizures in patients with severe epilepsies followed for years in hospital-based clinics. "( Multicentre clinical evaluation of vigabatrin (Sabril) in mild to moderate partial epilepsies. French Neurologists Sabril Study Group.
Arzimanoglou, AA; Dumas, C; Ghirardi, L, 1997
)
2.02
"Vigabatrin (VGB) has been approved in Europe and is prescribed for either once or twice-daily administration. "( Once-daily versus twice-daily vigabatrin: is there a difference? The results of a double-blind pilot study.
Blankenhorn, V; Krämer, G; Mumford, JP; Richens, A; Stefan, H; Thümler, R; Zahner, B, 1999
)
2.03
"Vigabatrin (VGB) has been shown to be an effective drug in the treatment of infantile spasms (West syndrome) in predominantly retrospective and open but also in prospective studies. "( Randomised, placebo-controlled study of vigabatrin as first-line treatment of infantile spasms.
Appleton, RE; Mumford, JP; Peters, AC; Shaw, DE, 1999
)
2.01
"Vigabatrin (VGB) has demonstrated high efficacy in infantile spasms (IS) due to tuberous sclerosis. "( Mental and behavioural outcome of infantile epilepsy treated by vigabatrin in tuberous sclerosis patients.
Chiron, C; Dulac, O; Dumas, C; Jambaqué, I; Mumford, J, 2000
)
1.99
"Vigabatrin has been in clinical use for 18 years. "( [Vigabatrin in childhood epilepsy--personal experience].
Buljina, A; Catibusić, F; Gavranović, M; Uzicanin, S; Zubcević, S, 1999
)
2.66
"Vigabatrin has been associated with visual field loss and electrophysiological abnormalities."( Visual electrophysiological effect of a GABA transaminase blocker.
Barnes, P; Edson, AS; Harding, GF; Robertson, KA; Wild, J,
)
0.85
"Vigabatrin has been found most effective against complex partial and secondarily generalized tonic-clonic seizures in both adults and children."( Vigabatrin as add-on therapy for adult complex partial seizures: a double-blind, placebo-controlled multicentre study. The Canadian Vigabatrin Study Group.
Bruni, J; Desforges, C; Guberman, A; Vachon, L, 2000
)
2.47
"Vigabatrin (VGB) has been shown in a number of clinical trials with varying designs to be effective and well-tolerated as both add-on therapy and monotherapy in epilepsy with partial seizures with or without secondary generalization as well as in infantile spasms. "( Long-term open multicentre, add-on trial of vigabatrin in adult resistant partial epilepsy. The Canadian Vigabatrin Study Group.
Bruni, J; Guberman, A, 2000
)
2.01
"Vigabatrin has been an important anticonvulsant drug for over 10 years with a reputation for high efficacy and excellent tolerability. "( Visual field defects and other ophthalmological disturbances associated with vigabatrin.
Sankar, R; Spence, SJ, 2001
)
1.98
"Vigabatrin (VGB) has been shown to cause visual field constriction and other forms of mild visual dysfunction. "( Visual function is stable in patients who continue long-term vigabatrin therapy: implications for clinical decision making.
Johnson, MA; Krauss, GL; Medura, MT; Miller, NR; Miller, TA; Paul, SR, 2001
)
1.99
"Vigabatrin has been considered the drug of choice for infantile spasms secondary to tuberous sclerosis, and possibly, according to many neurologists, for all cases of infantile spasm."( Medical treatment of patients with infantile spasms.
Holmes, GL; Lepejian, GA; Mikati, MA,
)
0.85
"Vigabatrin has been studied in adult drug-resistant epilepsy since 1982 in single-blind and double-blind studies followed by long-term, open evaluations. "( Vigabatrin in refractory epilepsy in adults and its application in children.
Dam, M, 1991
)
3.17
"1. Vigabatrin has proved to be a very effective antiepileptic in clinical trials, with excellent long term tolerability. "( Effects of long term vigabatrin on somatosensory evoked potentials in epileptic patients.
Beaumont, D; Chauvel, P; Gisselbrecht, D; Liegeois-Chauvel, C; Marquis, P; Pantieri, R, 1989
)
1.22

Actions

Vigabatrin can cause electrophysiologic evidence of retinal dysfunction and clinically detectable disturbances of visual sensory function. It acts as an anticonvulsant on convulsive epileptic seizures and increases seizures in generalized non-convulsive epilepsy.

ExcerptReferenceRelevance
"Vigabatrin can cause retinopathy, resulting in bilateral visual field constriction. "( Vigabatrin-induced peripheral visual field defects in patients with refractory partial epilepsy.
Bittman, RM; Christen, EM; Sagar, SM; Sergott, RC, 2010
)
3.25
"Vigabatrin acts to increase GABA levels in the presynaptic nerve terminal by inhibiting the activity of GABA-transaminase."( Vigabatrin: effect on brain GABA levels measured by nuclear magnetic resonance spectroscopy.
Behar, K; Mattson, RH; Petroff, OA; Rothman, D, 1995
)
2.46
"Vigabatrin did not cause cognitive impairment either acutely or in the long term."( Effect of vigabatrin on sedation and cognitive function in patients with refractory epilepsy.
Blacklaw, J; Brodie, MJ; Gillham, RA; McKee, PJ, 1993
)
1.41
"Vigabatrin may also cause a decrease in excitation-related amino acids."( Vigabatrin.
Connelly, JF, 1993
)
2.45
"Vigabatrin can cause electrophysiologic evidence of retinal dysfunction and clinically detectable disturbances of visual sensory function."( Visual dysfunction in patients receiving vigabatrin: clinical and electrophysiologic findings.
Endres, M; Girkin, CA; Johnson, MA; Krauss, GL; Miller, NR; Paul, SR; Perry, JD, 1999
)
2.01
"Vigabatrin, because of its ability to increase brain GABA concentration, acts as an anticonvulsant on convulsive epileptic seizures and increases seizures in generalized non-convulsive epilepsy. "( Potentiation of gamma-vinyl GABA (vigabatrin) effects by glycine.
Depaulis, A; Liu, Z; Marescaux, C; Seiler, N; Vergnes, M, 1990
)
2

Treatment

Vigabatrin is the treatment of choice when the underlying cause is tuberous sclerosis complex (TSC) Treatment resulted in spasms cessation in 16 of 18 (88.9%) patients with infantile spasms.

ExcerptReferenceRelevance
"Vigabatrin may be the treatment of choice in tuberous sclerosis."( Treatment of infantile spasms.
Edwards, SW; Hancock, EC; Osborne, JP, 2013
)
1.11
"Vigabatrin (VGB), a treatment for the childhood epilepsy, infantile spasms (IS), is implicated in visual field constriction. "( Changes in the ERG d-wave with vigabatrin treatment in a pediatric cohort.
Dragas, R; Westall, C; Wright, T, 2014
)
2.13
"The vigabatrin treatment successfully prevented forward acoustic masking from enhancing the ABR."( Forward acoustic masking enhances the auditory brainstem response in a diotic, but not dichotic, paradigm in salicylate-induced tinnitus.
Chen, L; Liu, XP, 2015
)
0.9
"Vigabatrin is the treatment of choice when the underlying cause is tuberous sclerosis complex (TSC)."( Improving Outcomes in Infantile Spasms: Role of Pharmacotherapy.
Appleton, R; Iyer, A, 2016
)
1.16
"Vigabatrin treatment resulted in spasms cessation in 16 of 18 (88.9%) patients with infantile spasms, whereas 6 of 13 (46.2%) patients with focal seizures became seizure free."( Vigabatrin and mental retardation in tuberous sclerosis: infantile spasms versus focal seizures.
Ko, TS; Lee, EH; Yum, MS, 2013
)
2.55
"The vigabatrin treatment increased both number of GABA-immunoreactive neurons in FN-LHA projections and GABA content in the hypothalamus."( Cerebellar fastigial nuclear GABAergic projections to the hypothalamus modulate immune function.
Cao, BB; Huang, Y; Lu, JH; Peng, YP; Qiu, YH; Xu, FF, 2013
)
0.87
"Vigabatrin treatment is frequently associated with irreversible retinal injury and produces retinal electrophysiological changes in nearly all patients. "( A controlled study comparing visual function in patients treated with vigabatrin and tiagabine.
Johnson, MA; Krauss, GL; Miller, NR; Sheth, S, 2003
)
2
"Vigabatrin treated patients had marked visual field constrictions in kinetic perimetry (mean radius 39.6 degrees OD, 40.5 degrees OS), while tiagabine patients had normal findings (mean 61 degrees OD, 62 degrees OS) (differences OD and OS, p=0.001), which were similar to epilepsy control patients (mean 60 degrees OD, 61 degrees OS). "( A controlled study comparing visual function in patients treated with vigabatrin and tiagabine.
Johnson, MA; Krauss, GL; Miller, NR; Sheth, S, 2003
)
2
"In vigabatrin-treated animals, GABA synthesis was 28% lower compared to controls [p < 0.05; vigabatrin-treated, 0.043 +/- 0.011 micromol/(g min); non-treated, 0.060 +/- 0.014 micromol/(g min)] and GAD(67) was 60% lower."( Evidence that GAD65 mediates increased GABA synthesis during intense neuronal activity in vivo.
Battaglioli, G; Behar, KL; de Graaf, RA; Martin, DL; Patel, AB, 2006
)
0.85
"In vigabatrin treated patients a functional or structural retinal changes may occur, what can be measured by electrophysiological and visual field testing. "( [Retinal dysfunction in patients treated with vigabatrin].
Hampel-Osipowicz, E; Lubiński, W; Podboraczyńska-Jodkoi, K, 2007
)
1.22
"In vigabatrin-treated animals [13C]glutamine, a common intermediate for [13C]GABA synthesis from glucose or acetate, was accumulated to similar amounts during infusions with [1,2(-13)C2]glucose or [1,2(-13)C2]acetate."( Metabolic precursors and compartmentation of cerebral GABA in vigabatrin-treated rats.
Cerdán, S; Preece, NE, 1996
)
1.05
"Vigabatrin treatment significantly reduced GAD67 protein in all regions except olfactory bulb, whereas GAD65 protein decreased significantly only in cerebellum."( Elevation of brain GABA levels with vigabatrin (gamma-vinylGABA) differentially affects GAD65 and GAD67 expression in various regions of rat brain.
Martin, DL; Sheikh, SN, 1998
)
1.3
"Vigabatrin treatment was started either 1 h, or 2 or 7 days after the beginning of kainic acid-induced (9 mg/kg, i.p.) status epilepticus and continued via subcutaneous osmotic minipumps for 2 months (75 mg/kg per day)."( Effects of vigabatrin treatment on status epilepticus-induced neuronal damage and mossy fiber sprouting in the rat hippocampus.
Halonen, T; Jolkkonen, E; Nissinen, J; Pitkänen, A; Tuunanen, J, 1999
)
1.41
"Vigabatrin use in treatment-refractory partial epilepsy is associated with increased occurrence of depression and of psychosis, although the frequency of psychosis is apparently lower than previously reported. "( Psychiatric adverse events during vigabatrin therapy.
Devinsky, O; Levinson, DF, 1999
)
2.03
"Vigabatrin (VGB) treatment is neuroprotective in various models of status epilepticus (SE) and delays the development of kindling via mechanisms that are assumed to relate to the elevation of GABA levels in the brain. "( Chronic elevation of brain GABA levels beginning two days after status epilepticus does not prevent epileptogenesis in rats.
Halonen, T; Nissinen, J; Pitkänen, A, 2001
)
1.75
"When vigabatrin treatment was stopped, 1 case became worse, 1 case was slightly better, and 1 case remained stationary."( [Study of visual field and vigabatrin treatment in children].
Billette de Villemeur, T; Doummar, D; Laroche, L; Momtchilova, M; Pelosse, B; Roubergue, A, 2001
)
1.06
"Five vigabatrin-treated young adults with field defects were identified using this stimulus."( Field-specific visual-evoked potentials: identifying field defects in vigabatrin-treated children.
Bohn, RL; Conway, M; Harding, GF; Spencer, EL; Wild, JM, 2002
)
1
"Treatment of vigabatrin (60 mg/kg/day, 7-14 days), an anti-seizure drug that inhibits the catabolism of GABA, not only blocked AGS, but also significantly attenuated the loudness response."( Loudness perception affected by early age hearing loss.
Fu, Q; Kumaraguru, A; Li, J; Manohar, S; Sun, W; Zhang, C, 2014
)
0.76
"Pretreatment with vigabatrin, but not rapamycin, suppressed the spasms."( Validation of the rat model of cryptogenic infantile spasms.
Chachua, T; Velíšek, L; Velíšková, J; Yum, MS, 2011
)
0.69
"Pretreatment with vigabatrin increased the threshold of paroxysmal pentylenetetrazol-induced seizure."( Vigabatrin modulates benzodiazepine receptor activity in vivo: a positron emission tomography study in baboon.
Bottlaender, M; Brouillet, E; Fuseau, C; Mazière, M; Schmid, L, 1996
)
2.06
"Treatment with vigabatrin was associated with a high prevalence of peripheral visual field defects. "( Visual field defects associated with vigabatrin therapy.
Degg, C; Eke, T; Harding, GF; Lawden, MC; Wild, JM, 1999
)
0.93

Toxicity

Vigabatrin had a good safety profile with a low rate of discontinuation due to nonophthalmologic and ophthalmologic adverse effects. In clinical trials, it was generally well-tolerated with an adverse event profile similar to that of other AEDs.

ExcerptReferenceRelevance
" Drop-outs were caused by adverse events in 2 cases (ataxia and psychotic symptoms respectively), seizure breakthrough in 4 cases and reasons unrelated to treatment in 4 patients."( Six-year follow-up study on the efficacy and safety of vigabatrin in patients with epilepsy.
Galimberti, CA; Iudice, A; Manni, R; Morini, R; Mumford, JP; Perucca, E; Tartara, A, 1992
)
0.53
" Thirty-seven patients discontinued vigabatrin for the following reasons: benefit-to-risk evaluation, 8; seizure breakthrough, 6; adverse events, 6; seizure breakthrough and adverse events, 5; moved or lost, 4; no longer eligible for study, 2; non-drug-related death, 2; narcotic abuse, 1; and patient request, three."( Multicenter long-term safety and efficacy study of vigabatrin for refractory complex partial seizures: an update.
Ben-Menachem, E; Browne, TR; Mattson, RH; McBride, RG; Penry, JK; Sherry, KM; Smith, DB; Treiman, DM; Wilder, BJ, 1991
)
0.81
" Monkeys exhibited no adverse clinical effects except for occasional loose stools at 300 mg/kg/day."( Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor.
Gerbig, CG; Gibson, JP; Hurst, GH; Loudy, DE; Newberne, JW; Yarrington, JT, 1990
)
0.57
" There was a very low rate of drop out for adverse events (1."( Efficacy and safety of vigabatrin in the long-term treatment of refractory epilepsy.
Beaumont, D; Remy, C, 1989
)
0.59
" Finally, gabapentin is a very safe add-on medication."( The new anticonvulsant drugs. Implications for avoidance of adverse effects.
Krämer, G; Schmidt, D, 1994
)
0.29
" Adverse effects of antiepileptic treatment may affect the patient's quality of life to an even greater extent than the occurrence of seizures."( Adverse effects of established and new antiepileptic drugs: an attempted comparison.
Gram, L; Rogvi-Hansen, B, 1995
)
0.29
"Standard antiepileptic drugs (AEDs) are associated with a wide variety of acute and chronic adverse events and with many interactions with each other and with non-AEDs that complicate patient management."( Overview of the safety of newer antiepileptic drugs.
Shorvon, S; Stefan, H, 1997
)
0.3
" We investigated whether this drug was comparable to standard first-line monotherapy in efficacy and incidence of adverse events."( Safety and efficacy of vigabatrin and carbamazepine in newly diagnosed epilepsy: a multicentre randomised double-blind study. Vigabatrin European Monotherapy Study Group.
Chadwick, D, 1999
)
0.61
" After initial maintenance doses were reached, doses were adjusted downwards (in the case of adverse events) or upwards (in the case of seizures) by the clinician."( Safety and efficacy of vigabatrin and carbamazepine in newly diagnosed epilepsy: a multicentre randomised double-blind study. Vigabatrin European Monotherapy Study Group.
Chadwick, D, 1999
)
0.61
"Time to withdrawal for lack of efficacy or adverse events did not differ between groups (p=0."( Safety and efficacy of vigabatrin and carbamazepine in newly diagnosed epilepsy: a multicentre randomised double-blind study. Vigabatrin European Monotherapy Study Group.
Chadwick, D, 1999
)
0.61
"To determine the incidence of psychiatric adverse events associated with vigabatrin therapy, we reviewed data from US and non-US double-blind, placebo-controlled trials of vigabatrin as add-on therapy for treatment-refractory partial epilepsy."( Psychiatric adverse events during vigabatrin therapy.
Devinsky, O; Levinson, DF, 1999
)
0.81
""Verbatim" terms from investigators' reports had been translated into standard "preferred" terms using an adverse event dictionary."( Psychiatric adverse events during vigabatrin therapy.
Devinsky, O; Levinson, DF, 1999
)
0.58
" Clinical experience suggests that these adverse events respond to reduction of vigabatrin dose or to counteractive psychotropic treatment."( Psychiatric adverse events during vigabatrin therapy.
Devinsky, O; Levinson, DF, 1999
)
0.81
" The toxic effect of gamma-vinyl-GABA was mimicked by a 24-h treatment with GABA (100 microM) and the GABA(A) receptor agonist, muscimol (10 microM), but not the GABA(B) receptor agonist, baclofen (10 microM)."( GABA(A)-mediated toxicity of hippocampal neurons in vitro.
Lukasiuk, K; Pitkänen, A, 2000
)
0.31
" However, on rare occasions, they can progress to more severe cutaneous disorders, including Stevens-Johnson syndrome and toxic epidermal necrolysis."( Therapeutic safety monitoring: what to look for and when to look for it.
Harden, CL, 2000
)
0.31
" Serious adverse events were assessed individually."( Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom.
Mawer, GE; Sander, JW; Wong, IC, 2001
)
0.31
" The adverse events with LTG reported by this study were similar to those reported in the literature."( Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom.
Mawer, GE; Sander, JW; Wong, IC, 2001
)
0.31
" Life-threatening adverse reactions were rare."( Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom.
Mawer, GE; Sander, JW; Wong, IC, 2001
)
0.31
"Doctors should advise patients of recognised adverse events of proposed therapy."( Ethical dilemmas of potential adverse events.
Beran, RG, 2001
)
0.31
" So the search for more effective drugs with minimal adverse effect profiles will continue."( Adverse effects of new antiepileptic drugs.
Onat, F; Ozkara, C, 2004
)
0.32
" Five hundred micromolar GABA and 50 microM tiagabine were not toxic in the presence or absence of light."( Acute vigabatrin retinotoxicity in albino rats depends on light but not GABA.
Benz, AM; Ishikawa, M; Izumi, M; Izumi, Y; Thio, LL; Zorumski, CF, 2004
)
0.8
" The main outcome measures were change of visual field, visual acuity, and ocular adverse effects."( Short-term treatment of cocaine and/or methamphetamine abuse with vigabatrin: ocular safety pilot results.
Brodie, JD; Dewey, SL; Fechtner, RD; Federico, M; Figueroa, E; Khouri, AS; Ramirez, M, 2006
)
0.57
" No ocular adverse events were detected."( Short-term treatment of cocaine and/or methamphetamine abuse with vigabatrin: ocular safety pilot results.
Brodie, JD; Dewey, SL; Fechtner, RD; Federico, M; Figueroa, E; Khouri, AS; Ramirez, M, 2006
)
0.57
" There was no evidence of ocular or visual field adverse effects."( Short-term treatment of cocaine and/or methamphetamine abuse with vigabatrin: ocular safety pilot results.
Brodie, JD; Dewey, SL; Fechtner, RD; Federico, M; Figueroa, E; Khouri, AS; Ramirez, M, 2006
)
0.57
" Adverse events were seen in 13%."( Vigabatrin in the treatment of childhood epilepsy: a retrospective chart review of efficacy and safety profile.
Camposano, SE; Halpern, E; Major, P; Thiele, EA, 2008
)
1.79
" The aim of this study was to compare the adverse event (AE) profile of children and adults taking vigabatrin, using modified signal detection methods (SDMs)."( Paediatric post-marketing pharmacovigilance: comparison of the adverse event profile of vigabatrin prescribed to children and adults.
Aurich-Barrera, B; Brown, D; Shakir, S; Wilton, L, 2011
)
0.81
"Data from the vigabatrin prescription-event monitoring study an observational cohort study (cohort 10,177 patients), stratified into one paediatric (0-17 years) and one adult (≥ 18 years) age group were examined using summary statistics for adverse drug reactions (ADRs), reasons for stopping and deaths."( Paediatric post-marketing pharmacovigilance: comparison of the adverse event profile of vigabatrin prescribed to children and adults.
Aurich-Barrera, B; Brown, D; Shakir, S; Wilton, L, 2011
)
0.95
" Toxicologic observations were collected, including adverse clinical signs, body weight gains, food consumption, ophthalmoloscopy, electroretinograms, sexual maturation, motor activity, memory, and learning behaviors."( Oral toxicity of vigabatrin in immature rats: characterization of intramyelinic edema.
Bekersky, I; Collins, S; Garman, R; Jortner, B; Patterson, R; Sagar, S; Tolbert, D; Walzer, M; Wanaski, S, 2011
)
0.71
" In clinical trials, vigabatrin was generally well-tolerated with an adverse event profile similar to that of other AEDs."( Non-vision adverse events with vigabatrin therapy.
Kälviäinen, R; Walker, SD, 2011
)
0.97
" Physiopathologic mechanisms associated with these toxic effects are yet unclear and, besides discontinuation of the drug, when possible, there is no current validated treatment once visual loss is present."( [Ocular toxicity of drugs].
Audo, I, 2013
)
0.39
" Removal of this potential adverse effect with adjuvant intervention(s) would represent a significant advance in epilepsy therapeutics."( Aberrant mTOR signaling and disrupted autophagy: The missing link in potential vigabatrin-associated ocular toxicity?
Ainslie, GR; Gibson, KM; Pearl, PL; Vogel, KR, 2017
)
0.68
"Retinal toxicity is one of the most commonly discussed and concerning adverse effects of vigabatrin (VGB)."( The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study.
Huang, YF; Liu, C; Ma, J; Ma, Z; Tao, Y; Wang, Y; Yan, Z; Yang, J; Yang, Z, 2016
)
1.21
" We assessed the relationship between seizure frequency, etiology, vigabatrin dose, adverse events, medication discontinuation reasons, and electroencephalography (EEG) characteristics."( Effect of vigabatrin on seizure control and safety profile in different subgroups of children with epilepsy.
Coughlin, F; Jackson, MC; Jafarpour, S; Kapur, K; Klehm, J; Loddenkemper, T; Thome-Souza, S, 2017
)
1.09
"1 months, vigabatrin had a good safety profile with a low rate of discontinuation due to nonophthalmologic and ophthalmologic adverse effects."( Effect of vigabatrin on seizure control and safety profile in different subgroups of children with epilepsy.
Coughlin, F; Jackson, MC; Jafarpour, S; Kapur, K; Klehm, J; Loddenkemper, T; Thome-Souza, S, 2017
)
1.26
" The most common adverse events (AEs) were psychiatric disorders and nervous system disorders (n=8; 61."( Efficacy and safety of vigabatrin in Japanese patients with infantile spasms: Primary short-term study and extension study.
Ohtsuka, Y, 2018
)
0.79
" However, reports of adverse events of VGB, including VGB-associated visual field loss and brain abnormalities in neuroimaging, have raised concerns about the broader use of VGB and thus significantly limited its application."( Vigabatrin - new data on indications and safety in paediatric epilepsy.
Golec, W; Jóźwiak, S; Jurkiewicz, E; Sołowiej, E; Strzelecka, J, 2021
)
2.06
" The mainstay of treatment is with multiple anti-seizure medications (ASMs); however, the ASMs themselves can be associated with psychobehavioural adverse events, and effects (negative or positive) on cognition and sleep."( Psychobehavioural and Cognitive Adverse Events of Anti-Seizure Medications for the Treatment of Developmental and Epileptic Encephalopathies.
Schubert-Bast, S; Strzelczyk, A, 2022
)
0.72
"The aim of this study was to compare the safety profile of newer ASMs with older ASMs through an analysis of the US Food and Drug Administration Adverse Event Reporting System (FAERS) database, with a focus on suicidality."( Newer Antiseizure Medications and Suicidality: Analysis of the Food and Drug Administration Adverse Event Reporting System (FAERS) Database.
Doughty, BJ; Hurd, KL; Leppien, EE; McCall, KL; Piper, BJ; Strong, KN, 2023
)
0.91
" The results of this case control study of FDA adverse event reports spanning 10 years and 6309 cases of suicidality expand our understanding of the safety profile of newer ASMs."( Newer Antiseizure Medications and Suicidality: Analysis of the Food and Drug Administration Adverse Event Reporting System (FAERS) Database.
Doughty, BJ; Hurd, KL; Leppien, EE; McCall, KL; Piper, BJ; Strong, KN, 2023
)
0.91
" REMS can have elements to assure safe use (ETASU), such as patient registries, dispensing restrictions, and physician training and certification requirements."( Physician experiences with and perceptions of risk evaluation and mitigation strategy programs with elements to assure safe use.
Abdurrob, A; Brown, BL; Dejene, SZ; Kesselheim, AS; McGraw, SA; Sarpatwari, A, 2023
)
0.91

Pharmacokinetics

The pharmacokinetic profile of this compound in infants and young children is still poorly understood, as is the minimal effective dose. For drugs that are eliminated renally completely unchanged (gabapentin, pregabalin and vigabatrin) or mainly unchanged (levetiracetam and topiramate), the Pharmacokinetic variability is less pronounced and more predictable.

ExcerptReferenceRelevance
" In group I, the half-life of the R(-) isomer was significantly shorter than that of the S(+) isomer; in group II, the half-lives were comparable."( Pharmacokinetics of the individual enantiomers of vigabatrin (gamma-vinyl GABA) in epileptic children.
Beaumont, D; Chiron, C; D'Athis, P; Dulac, O; Olive, G; Pons, G; Rey, E; Richard, MO; Vauzelle, F, 1990
)
0.53
" Pharmacodynamic interactions take place at the level of receptor sites, where they may have additive or potentiating effects."( Pharmacokinetic and pharmacodynamic drug interactions during treatment with vigabatrin.
Richens, A, 1995
)
0.52
" The plasma VGB concentration-time data were analyzed by mixed-effects modeling to estimate population pharmacokinetic parameters and to identify any significant demographic covariates."( A comparison of population and standard two-stage pharmacokinetic analyses of vigabatrin data.
Bhargava, VO; Hutcheson, SJ; Wei, G; Weir, SJ; Yu, DK, 1994
)
0.52
" Slight changes in the terminal phase half-life and renal clearance were evident in the higher dosage groups."( Pharmacokinetics of vigabatrin following single and multiple oral doses in normal volunteers.
Antony, KK; Elberfeld, JM; Hoke, JF; Okerholm, RA; Sussman, NM; Yuh, L, 1993
)
0.61
" Three of the new drugs, gabapentin, topiramate and vigabatrin, are more promising on the basis of their pharmacokinetic features."( Comparative pharmacokinetics of the newer antiepileptic drugs.
Bialer, M, 1993
)
0.54
"To assess the possible occurrence of pharmacokinetic interactions between the antiepileptic agents felbamate and vigabatrin, two randomized, double-blind, placebo-controlled, crossover studies were conducted in healthy male volunteers."( Pharmacokinetic interaction studies between felbamate and vigabatrin.
Banfield, C; Colucci, R; Glue, P; Lim, J; Lin, C; Meehan, J; Nomeir, A; Radwanski, E; Reidenberg, P; Rey, E, 1995
)
0.75
" The terminal elimination half-life (t1/2z) is relatively long in neonates; it then decreases during the first postnatal month to lower values than in adults, and then progressively increases with age due to an age-dependent decrease in the metabolic rate."( Clinical pharmacokinetics of antiepileptic drugs in paediatric patients. Part II. Phenytoin, carbamazepine, sulthiame, lamotrigine, vigabatrin, oxcarbazepine and felbamate.
Avanzini, G; Battino, D; Estienne, M, 1995
)
0.5
"Antiepileptic drugs (AEDs) in broad use today have a number of pharmacokinetic liabilities, including a propensity for clinically meaningful drug interactions."( Pharmacokinetic profile of topiramate in comparison with other new antiepileptic drugs.
Perucca, E, 1996
)
0.29
" All the drugs can be conveniently given as a twice daily dosage apart from gabapentin, which has a short half-life and a midday dose is needed."( Clinical pharmacokinetics of newer antiepileptic drugs. Lamotrigine, vigabatrin, gabapentin and oxcarbazepine.
Binnie, CD; Elwes, RD, 1996
)
0.53
"This article surveys the pharmacokinetic parameters for the new antiepileptic drugs (AEDs): felbamate, gabapentin, lamotrigine, oxcarbazepine, tiagabine, topiramate, and vigabatrin."( Pharmacokinetics of new antiepileptic drugs.
Gram, L, 1996
)
0.49
" The pharmacokinetic parameters of the two enantiomers have been studied after administration of a single oral 125 mg dose of the racemate to six neonates."( Pharmacokinetics of the individual enantiomers of vigabatrin in neonates with uncontrolled seizures.
Chiron, C; d'Athis, P; Dulac, O; Dumas, C; Olive, G; Pons, G; Rey, E; Vauzelle-Kervroëdan, F, 1996
)
0.55
"Standard antiepileptic drugs (AEDs) have a number of pharmacokinetic shortcomings, and AEDs with more favorable profiles would be preferred."( Pharmacokinetics and interaction profile of topiramate: review and comparison with other newer antiepileptic drugs.
Johannessen, SI, 1997
)
0.3
" A pharmacokinetic study of the S(+) and R(-) enantiomers of vigabatrin was performed before and during dialysis."( Pharmacokinetics of the S(+) and R(-) enantiomers of vigabatrin during chronic dosing in a patient with renal failure.
Chiron, C; Guillonneau, M; Jacqz-Aigrain, E; Loirat, C; Macher, MA; Montes, C; Rey, E, 1997
)
0.79
" Orally administered GBP did not significantly alter the pharmacokinetic parameters of parenteral PT."( Effect of vigabatrin and gabapentin on phenytoin pharmacokinetics in the dog.
Al-Hassan, MI; Bawazir, SA; Matar, KM; Nicholls, PJ; Tekle, A, 2000
)
0.71
" Orally administered GBP did not significantly alter the pharmacokinetic parameters of parental PT."( Effect of vigabatrin and gabapentin on phynytoin pharmacokinetics in the dog.
al-Hassan, MI; Bawazir, SA; Matar, KM; Nicholls, PJ; Tekle, A,
)
0.53
"The pharmacokinetic properties of a drug are the primary deter-minant of the extent and duration of drug action, and influence susceptibility to clinically important drug interactions."( The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come?
Johannessen, SI; Perucca, E, 2003
)
0.32
"The aim of the study was to obtain pharmacokinetic data for carbamazepine (CBZ) and its fractions not bound with proteins in bitherapy with lamotrigine (LTG), topiramate (TPM), vigabatrin (VGB) or valproic acid (VPA) in children and adolescents treated for epilepsy."( Pharmacokinetic interactions of carbamazepine with some antiepileptic drugs during epilepsy treatment in children and adolescents.
Steinborn, B, 2005
)
0.52
" For pharmacokinetic calculations of total and free CBZ, one-compartment model was used according to standardized procedure."( Pharmacokinetic interactions of carbamazepine with some antiepileptic drugs during epilepsy treatment in children and adolescents.
Steinborn, B, 2005
)
0.33
"No significant differences in pharmacokinetic parameters of unbound CBZ in four groups of patients on bitherapy with CBZ and LTG, TPM, VGB or VPA were found."( Pharmacokinetic interactions of carbamazepine with some antiepileptic drugs during epilepsy treatment in children and adolescents.
Steinborn, B, 2005
)
0.33
" For drugs that are eliminated renally completely unchanged (gabapentin, pregabalin and vigabatrin) or mainly unchanged (levetiracetam and topiramate), the pharmacokinetic variability is less pronounced and more predictable."( Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed?
Johannessen, SI; Tomson, T, 2006
)
0.56
"To investigate the pharmacokinetic interrelationship of vigabatrin in blood and the brain (frontal cortex vs."( Vigabatrin extracellular pharmacokinetics and concurrent gamma-aminobutyric acid neurotransmitter effects in rat frontal cortex and hippocampus using microdialysis.
Patsalos, PN; Ratnaraj, N; Tong, X, 2009
)
2.04
" In contrast, levetiracetam was without affect on tiagabine or vigabatrin concentrations and co-administration with gabapentin, tiagabine or vigabatrin had no effect on levetiracetam brain concentrations, indicating the pharmacodynamic nature of interaction between these antiepileptic drugs in the mouse pentylenetetrazole model."( Pharmacodynamic and pharmacokinetic interaction profiles of levetiracetam in combination with gabapentin, tiagabine and vigabatrin in the mouse pentylenetetrazole-induced seizure model: an isobolographic analysis.
Andres-Mach, MM; Czuczwar, SJ; Dudra-Jastrzebska, M; Luszczki, JJ; Patsalos, PN; Ratnaraj, N; Sielski, M, 2009
)
0.8
"Vigabatrin pharmacokinetic data from six randomized controlled clinical trials and one open-label study were analyzed using nonlinear mixed-effects modeling."( Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms.
Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014
)
2.11
" Covariate analysis indicated that age, creatinine clearance (CLCR), and body weight were important predictors of vigabatrin pharmacokinetic parameters."( Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms.
Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014
)
0.88
"The model adequately described vigabatrin pharmacokinetic and enabled predictions of systemic exposures in pediatric patients 1-12 months of age."( Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms.
Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014
)
0.96
" Furthermore, the review gives an overview of the pharmacokinetic parameters of vigabatrin across different species and drug-food and drug-drug interactions involving vigabatrin."( Pharmacokinetic aspects of the anti-epileptic drug substance vigabatrin: focus on transporter interactions.
Frølund, S; Holm, R; Nielsen, CU; Nøhr, MK, 2014
)
0.87
" However, the pharmacokinetic profile of this compound in infants and young children is still poorly understood, as is the minimal effective dose, critical information given the risk of exposure-related retinal toxicity with vigabatrin."( Proposition of a Minimal Effective Dose of Vigabatrin for the Treatment of Infantile Spasms Using Pediatric and Adult Pharmacokinetic Data.
Bienayme, H; Chiron, C; Duhamel, P; Dulac, O; Jullien, V; Nabbout, R; Ounissi, M; Pons, G; Rodrigues, C, 2019
)
0.96
" This work was conducted with the purpose to determine the pediatric doses of vigabatrin that allow a similar exposure than effective doses in adults (2-3 g/day) through a pharmacokinetic (PK) study, using both pediatric and adult data."( Pharmacokinetic evaluation of vigabatrin dose for the treatment of refractory focal seizures in children using adult and pediatric data.
Chiron, C; Dulac, O; Gaillard, S; Jullien, V; Nabbout, R; Ounissi, M; Rodrigues, C, 2019
)
1.03

Compound-Compound Interactions

ExcerptReferenceRelevance
" The aim of the study was to investigate the influence of PP alone and in combination with various doses of vigabatrin (VGB) on brain GABA levels."( Influence of pyridoxal 5'-phosphate alone and in combination with vigabatrin on brain GABA measured by 1H-NMR-spectroscopy.
Boesiger, P; Mueller, SG; Weber, OM; Wieser, HG, 2001
)
0.76
" Measurement of total brain antiepileptic drug concentrations revealed that levetiracetam in combination with gabapentin at the fixed-ratio of 1:4 significantly elevated (21%) total brain gabapentin concentrations."( Pharmacodynamic and pharmacokinetic interaction profiles of levetiracetam in combination with gabapentin, tiagabine and vigabatrin in the mouse pentylenetetrazole-induced seizure model: an isobolographic analysis.
Andres-Mach, MM; Czuczwar, SJ; Dudra-Jastrzebska, M; Luszczki, JJ; Patsalos, PN; Ratnaraj, N; Sielski, M, 2009
)
0.56

Bioavailability

Vigabatrin (VGB) decreases serum phenytoin (PHT) concentration by lowering the oral bioavailability of PHT. Increasing the dose of VGB 10-fold decreased the absolute bioavailability to 4.

ExcerptReferenceRelevance
" Data suggest a lower bioavailability in children."( Vigabatrin. Clinical pharmacokinetics.
Olive, G; Pons, G; Rey, E, 1992
)
1.73
" Vigabatrin was shown to be well absorbed in rat, dog and man, whereas dose-limited absorption occurred in the monkey."( Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor.
Gerbig, CG; Gibson, JP; Hurst, GH; Loudy, DE; Newberne, JW; Yarrington, JT, 1990
)
1.48
"8 h and a relative bioavailability of 92% +/- 11%."( Effect of food on the absorption of vigabatrin.
Frisk-Holmberg, M; Kerth, P; Meyer, P, 1989
)
0.55
" Both pulsed emission with a specific absorption rate (SAR) of 4 W/kg and continuous emission with high SAR (32 W/kg) were tested."( Effects of radiofrequency exposure on the GABAergic system in the rat cerebellum: clues from semi-quantitative immunohistochemistry.
de Seze, R; Mausset, AL; Montpeyroux, F; Privat, A, 2001
)
0.31
"The possibility that vigabatrin (VGB) decreases serum phenytoin (PHT) concentration by lowering the oral bioavailability of PHT was investigated in 21 patients with epilepsy."( Vigabatrin-induced decrease in serum phenytoin concentration does not involve a change in phenytoin bioavailability.
Bartoli, A; Gatti, G; Marchiselli, R; Michelucci, R; Perucca, E; Pisani, F; Richens, A; Tassinari, CA; Timmings, P; Zaccara, G, 1993
)
2.05
" The oral bioavailability of vigabatrin is high (60-70%), however, little is known about the mechanism(s) mediating the intestinal absorption."( The absorptive flux of the anti-epileptic drug substance vigabatrin is carrier-mediated across Caco-2 cell monolayers.
Brodin, B; Hansen, SH; Holm, R; Nielsen, CU; Nøhr, MK, 2014
)
0.94
"1 %) and relative bioavailability (F) (26."( Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms.
Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014
)
0.67
"8mM, the model estimated a maximal oral absorption rate (Vmax) of 64."( Is oral absorption of vigabatrin carrier-mediated?
Holm, R; Juul, RV; Kreilgaard, M; Nielsen, CU; Nøhr, MK; Thale, ZI, 2015
)
0.73
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

At acute dosing of 500 mg/kg, vigabatrin slightly decreased behavioral activity of rats through decreasing the number of trials completed and percent of correct responses. Results present a novel interpretation of synergistic inhibition of certain epileptic discharges.

ExcerptRelevanceReference
" At acute dosing of 500 mg/kg, vigabatrin slightly decreased behavioral activity of rats through decreasing the number of trials completed and percent of correct responses."( Effects of single and repeated administration of vigabatrin on the performance of rats in a 5-choice serial reaction time task.
Mazurkiewicz, M; Riekkinen, P; Sirviö, J, 1992
)
0.82
" The usual dosage of vigabatrin as add-on treatment in adults is 2 to 4g daily."( Vigabatrin. Clinical pharmacokinetics.
Olive, G; Pons, G; Rey, E, 1992
)
2.05
"The relationship between vigabatrin gamma-vinyl GABA (GVG, vigabatrin) daily dosage or steady-state plasma concentrations (CSS), platelet GABA-transaminase (GABA-T) inhibition, and seizure reduction were studied in 16 children with refractory epilepsy."( Gamma-vinyl GABA (vigabatrin): relationship between dosage, plasma concentrations, platelet GABA-transaminase inhibition, and seizure reduction in epileptic children.
Armijo, JA; Arteaga, R; Herranz, JL; Valdizán, EM,
)
0.77
" On the basis of these and other studies, we conclude that (a) GVG is a promising drug for the treatment of childhood epilepsy, (b) GVG is effective both in partial and generalized epilepsies, (c) GVG seems to be effective in the treatment of symptomatic infantile spasms, (d) no clear dose-response relationship has been demonstrated, (e) a dose of 40-80 mg/kg/day is recommended, and (f) although tolerance is excellent, hyperactivity seems to occur more frequently in children than in adults."( Treatment of pediatric epilepsies with gamma-vinyl GABA (vigabatrin).
Dulac, O; Gram, L; Sabers, A, 1992
)
0.53
" In the present study, we determined, in rat pups, the effect of nigral infusions of gamma-vinyl-GABA (GVG) on clonic-tonic seizures induced by flurothyl, generated a dose-response curve of the GVG effect and investigated the possible role of the nigral GABAA receptor in mediating the GVG effect."( Is the anticonvulsant effect of substantia nigra infusion of gamma-vinyl-GABA (GVG) mediated by the GABAA receptor in rat pups?
Moshé, SL; Sperber, EF; Xu, SG, 1991
)
0.28
" The relationship held over an extensive range of experimental conditions including different drugs, different dosage levels of the same drug, different time intervals after administration of the same drug, and both single and multiple injections of drugs."( Regulation of the GABAA receptor/ion channel complex by intracellular GABA levels.
Davies, M; Wood, JD, 1991
)
0.28
" Its anticonvulsant effects against 3-mercaptopropionic acid (MPA)-induced seizures in mice is related to the elevation of whole brain GABA concentrations: The mentioned doses of MDL 72483 which cause a decrease of GABA-T activity by 50%, produce within 5 h after dosing an increase of GABA concentration by about 3 mumol."( (4S)-4-amino-5,6-heptadienoic acid (MDL 72483): a potent anticonvulsant GABA-T inhibitor.
Casara, P; Knödgen, B; Sarhan, S; Seiler, N, 1991
)
0.28
" An increase in the low frequency bands of the EEG and a decrease in the faster activity were correlated with the vigabatrin dosage injected."( The effect of vigabatrin on central nervous system oxygen toxicity in rats.
Bitterman, N; Harel, D; Tzuk-Shina, T, 1991
)
0.85
"Twenty children aged 2 months to 18 years were included in a dose-response study of vigabatrin as add-on therapy to preexisting antiepileptic drugs (up to two per patient)."( Dose-response study of vigabatrin in children with refractory epilepsy.
Armijo, JA; Arteaga, R; Beaumont, D; Farr, IN; Herranz, JL; Valdizan, E, 1991
)
0.82
" The once daily dosing schedule was well tolerated and side effects were usually mild and always reversible."( Long-term evaluation of once daily vigabatrin in drug-resistant partial epilepsy.
Ben-Menachem, E; Mumford, J; Persson, L, 1990
)
0.56
" Higher doses caused chronic diarrhea, thus limiting the dosage in this species."( Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor.
Gerbig, CG; Gibson, JP; Hurst, GH; Loudy, DE; Newberne, JW; Yarrington, JT, 1990
)
0.57
" Lumbar punctures were carried out prior to treatment and at the end of each dosage regimen and cerebrospinal fluid (CSF) evaluated for concentrations of free and total GABA, homocarnosine (GABA-histidine dipeptide), homovanillic acid (HVA), 5-hydroxyindole acetic acid (5-HIAA) and vigabatrin."( The effect of different vigabatrin treatment regimens on CSF biochemistry and seizure control in epileptic patients.
Ben-Menachem, E; Dahlgren, L; Haegele, KD; Hardenberg, J; Huebert, N; Mumford, JP; Persson, LI; Schechter, PJ, 1989
)
0.76
" The inhibition produced by the drug is dose-dependent and, in the dose range used in man, the dose-response curves are comparable."( The effect of vigabatrin on brain and platelet GABA-transaminase activities.
Bolton, JB; Richens, A; Rimmer, E; Williams, J, 1989
)
0.64
"A study was conducted to assess the impact of single dosing and different dosing intervals of vigabatrin [gamma vinyl GABA (GVG)] in 11 patients with drug-resistant complex partial seizures."( Pharmacokinetic effects of vigabatrin on cerebrospinal fluid amino acids in humans.
Ben-Menachem, E, 1989
)
0.79
" Significant inhibition of the platelet GABA-T was produced by treatment with all three doses and a dose-response relationship was demonstrated."( Inhibition of the enzyme, GABA-aminotransferase in human platelets by vigabatrin, a potential antiepileptic drug.
Kongola, G; Richens, A; Rimmer, E, 1988
)
0.51
"gamma-Vinyl GABA (GVG), an irreversible inhibitor of GABA degradation, was administered to seizure-susceptible gerbils at different dosage regimens."( One to three day dose intervals during subchronic treatment of epileptic gerbils with gamma-vinyl GABA: anticonvulsant efficacy and alterations in regional brain GABA levels.
Frey, HH; Löscher, W, 1987
)
0.27
" Renal clearance values for the S(+)-enantiomer are not affected by concomitant dosing with the pharmacologically inactive R(-)-enantiomer."( Kinetics of the enantiomers of vigabatrin after an oral dose of the racemate or the active S-enantiomer.
Haegele, KD; Schechter, PJ, 1986
)
0.56
" Although there appears to be a clear dose-response relationship up to 3 g/day, it is not well documented if higher doses result in proportionately higher brain GABA levels."( Vigabatrin: effect on brain GABA levels measured by nuclear magnetic resonance spectroscopy.
Behar, K; Mattson, RH; Petroff, OA; Rothman, D, 1995
)
1.73
" The current dosage regime of anticonvulsants were maintained during the trial period."( Open label trial with vigabatrin in children with intractable epilepsy.
Wong, V,
)
0.45
" After 1-month observation, the patients entered a 7-month treatment period that involved administration of placebo for 1 month followed by VGB at the initial dosage of 40 mg/kg/day, to be increased to 60 and 80 mg/kg/day at 2-month intervals if seizures persisted."( Efficacy and tolerability of vigabatrin in children with refractory partial seizures: a single-blind dose-increasing study.
Buti, D; Cianchetti, C; Dalla Bernardina, B; Fontana, E; Fusco, L; Galeone, D; Gnanasakthy, A; Iudice, A; Torelli, D; Vigevano, F, 1995
)
0.58
" The plasma concentration ratio of the [R] to [S] enantiomers appears to remain constant across the vigabatrin dosage interval in adult volunteers, and in the present study this has also proved to be the case in 12 chronically treated adult epileptic patients."( Plasma vigabatrin enantiomer ratios in adults and children.
Appleton, DB; Burke, CJ; Eadie, MJ; Nagarajan, L; Schramm, T, 1993
)
0.96
" Oral dosing [3 mg/ml of drinking water, giving doses of GVG of 194 +/- 38 mg/kg/day and of EOS of 303 +/- 42 mg/kg/day (mean +/- SD)] was followed by microdialysis at 2, 8, and 21 days."( The effect of chronic treatment with the GABA transaminase inhibitors gamma-vinyl-GABA and ethanolamine-O-sulphate on the in vivo release of GABA from rat hippocampus.
Fowler, LJ; Qume, M; Whitton, PS, 1995
)
0.29
" We evaluated the cognitive and quality-of-life (QOL) effects of VGB in a double-blinded, add-on, placebo-controlled, parallel group dose-response study of patients with focal epilepsy whose complex partial seizures (CPS) were difficult to control."( Effects of differing dosages of vigabatrin (Sabril) on cognitive abilities and quality of life in epilepsy.
Arnett, JL; Dodrill, CB; Sommerville, KW; Sussman, NM, 1995
)
0.57
"Data from published research were extracted and evaluated according to study design, sample size, dosing regimen, outcome measures, and treatment efficacy and safety."( Treatment of infantile spasms.
Casto, DT; Haines, ST, 1994
)
0.29
" In an attempt to image these changes in vivo, we performed high-field MRI on seven treated and four control dogs at baseline and after 15 weeks of dosing with vigabatrin (300 mg/kg/d)."( MRI monitoring of vigabatrin-induced intramyelinic edema in dogs.
Arezzo, JC; Gibson, JP; Heydorn, WE; Kastin, SJ; McBride, RG; Schroeder, CE; Sussman, NM; Weiss, KL; Yarrington, JT, 1994
)
0.82
" ZNS daily dosage is 400-600 mg."( Antiepileptic drugs in development: prospects for the near future.
Leppik, IE, 1994
)
0.29
" Slight changes in the terminal phase half-life and renal clearance were evident in the higher dosage groups."( Pharmacokinetics of vigabatrin following single and multiple oral doses in normal volunteers.
Antony, KK; Elberfeld, JM; Hoke, JF; Okerholm, RA; Sussman, NM; Yuh, L, 1993
)
0.61
"5), but not with higher dosage (placebo 28, VGB 22, NS, 95% CI -18 to +11)."( Adjuvant vigabatrin in refractory epilepsy: a ceiling to effective dosage in individual patients?
Blacklaw, J; Brodie, MJ; Friel, E; Gillham, RA; McKee, PJ; Thompson, GG,
)
0.55
" Clinical trials and pharmacokinetic data are reviewed, as well as neuropathology, adverse effects, drug interactions, and dosage guidelines."( Vigabatrin.
Connelly, JF, 1993
)
1.73
" In addition to their current antiepileptic therapy, 10 patients with complex partial seizures (CP) (4 male, 6 female), aged between 22 and 57 years received placebo for 1 month, subsequently 2 g vigabatrin for 2 months and thereafter a titrated optimal dosage vigabatrin for another 2 months."( [Clinical and EEG/ERP brain mapping studies with vigabatrin in therapy refractory epileptic patients].
Anderer, P; Dieterich, HA; Pfersmann, D; Saletu, B; Semlitsch, HV, 1993
)
0.73
"A 7-year-old boy with intractable epilepsy developed acute psychosis 3 days after initiating a rapid vigabatrin dosage escalation."( Vigabatrin-associated reversible acute psychosis in a child.
Beltrán Marqués, M; Cánovas Martínez, A; Delgado Cordón, F; Escrivá Aparisi, A; Ordovás Baines, JP, 1995
)
1.95
" In a similarly designed United States trial, LTG was significantly superior to placebo at a 500-mg/day dosage but not at a 300-mg/day dosage."( Expanding antiepileptic drug options: clinical efficacy of new therapeutic agents.
Ben-Menachem, E, 1996
)
0.29
" All the drugs can be conveniently given as a twice daily dosage apart from gabapentin, which has a short half-life and a midday dose is needed."( Clinical pharmacokinetics of newer antiepileptic drugs. Lamotrigine, vigabatrin, gabapentin and oxcarbazepine.
Binnie, CD; Elwes, RD, 1996
)
0.53
" We conclude that vigabatrin in SSADH deficiency should be administered in a gradually increasing dosage combined with frequent evaluation of the clinical condition and the EEG."( Seizures in a boy with succinic semialdehyde dehydrogenase deficiency treated with vigabatrin (gamma-vinyl-GABA).
Gibson, KM; Korinthenberg, R; Lehnert, W; Matern, D, 1996
)
0.85
" This may be related to dosage and speed of introduction."( Psychotic and severe behavioural reactions with vigabatrin: a review.
Ferrie, CD; Panayiotopoulos, CP; Robinson, RO, 1996
)
0.55
" Once-a-day dosing should be as effective as divided doses."( Human brain GABA levels rise rapidly after initiation of vigabatrin therapy.
Behar, KL; Collins, TL; Mattson, RH; Petroff, OA; Rothman, DL, 1996
)
0.54
" Specific indications and dosage schedules have been provided."( New antiepileptic drugs.
Brodie, MJ; Wilson, EA, 1996
)
0.29
" With a view to better defining the drug's dose-response relationships in the presence of concomitant alternative antiepileptic drugs."( Plasma concentrations of vigabatrin in epileptic patients.
López, E; Quintana, B; Rodriguez, I; Sánchez-Alcaraz, A, 1996
)
0.6
"The relationship between the ratio of vigabatrin concentration to dosage (VGB C/D) and both patient age and the presence of other antiepileptic drugs (AEDs) was analyzed retrospectively by bivariate and multivariate methods in 179 patients with epilepsy (114 children and 65 adults)."( Vigabatrin serum concentration to dosage ratio: influence of age and associated antiepileptic drugs.
Armijo, JA; Arteaga, R; Bravo, J; Cuadrado, A, 1997
)
2.01
" In the test of physical dependence-producing potential with the drug-admixed food method in rats, vigabatrin and diazepam were given to rats mixed with food for 28 days in an increasing dosage schedule, followed by feeding a drug-free diet to observe withdrawal signs for 7 days."( Drug dependence study on vigabatrin in rhesus monkeys and rats.
Takada, K; Yanagita, T, 1997
)
0.82
" Vigabatrin mean dosage during phase 3 was 63."( Vigabatrin in refractory childhood epilepsy. The Brazilian Multicenter Study.
Chisté, MA; da Costa, JC; Diament, A; Gherpelli, JL; Guerreiro, CA; Guerreiro, MM; Manreza, ML; Nunes, ML; Palmini, A; Pedroso, F; Reed, UC; Rotta, NT; Silva, EA; Vega-Gutiérrez, L; Vizioli, J, 1997
)
2.65
" A 6-month multicentre, open-label study, involved addition of gabapentin to pre-existing treatment at the initial dosage of 1200 mg and subsequent adjustment between 900 and 2400 mg/day according to efficacy and tolerability."( Gabapentin add-on therapy with adaptable dosages in 610 patients with partial epilepsy: an open, observational study. The French Gabapentin Collaborative Group.
Arzimanoglou, A; Baulac, M; Cavalcanti, D; Portal, JJ; Semah, F, 1998
)
0.3
" Awake mice were dosed with [1-(13)C]glucose, and brain extracts were analyzed by 13C NMR spectroscopy."( Quantification of the GABA shunt and the importance of the GABA shunt versus the 2-oxoglutarate dehydrogenase pathway in GABAergic neurons.
Fonnum, F; Hassel, B; Johannessen, CU; Sonnewald, U, 1998
)
0.3
"This clinical study provides support for the pharmacological evidence that this preparation may be administered on a once or twice daily basis, depending on the individual patient's preference, total dosage and co-medication."( Once-daily versus twice-daily vigabatrin: is there a difference? The results of a double-blind pilot study.
Blankenhorn, V; Krämer, G; Mumford, JP; Richens, A; Stefan, H; Thümler, R; Zahner, B, 1999
)
0.59
" Four of the six partial clinical responders had deterioration of spasms with additional VGB dosage increases."( Vigabatrin in the treatment of infantile spasms.
Koo, B, 1999
)
1.75
" The results show that whether or not the introduction of vigabatrin results in an increase or a reduction in costs to the healthcare system depends largely on 3 factors: (i) the administered dosage of vigabatrin; (ii) the effect that vigabatrin has on hospital admissions; and (iii) the proportion of epileptic patients who take the drug."( The economic effects of introducing vigabatrin, a new antiepileptic medication.
Champagne, F; Contandriopoulos, AP; Kennedy, W; Reinharz, D; Tessier, G, 1995
)
0.81
"No significant relationship was seen between dosage and serum levels, nor between serum levels and efficacy or side-effect."( [In children with refractory epilepsy: vigabatrin or lamotrigine?].
Armijo, JA; Arteaga, R; Caviedes, BE; Herranz, JL,
)
0.4
" Once-a-day dosing is sufficient to increase GABA."( Acute effects of vigabatrin on brain GABA and homocarnosine in patients with complex partial seizures.
Collins, T; Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 1999
)
0.64
" Because dosing is often modest, cost should rarely be the overriding factor in choosing a drug for a patient with newly diagnosed epilepsy in the developed world."( Monostars: an aid to choosing an antiepileptic drug as monotherapy.
Brodie, MJ, 1999
)
0.3
" The dosage was escalated by 25 mg/kg weekly until spasms ceased or the maximum dose of 130 mg/kg was reached."( Vigabatrin in infantile spasms: preliminary result.
Chiemchanya, S; Phusirimongkol, S; Visudhiphan, P; Visudtibhan, A, 1999
)
1.75
" There is a lack of data on the dose-response characteristics of vigabatrin and the development of visual field defects."( Visual field defects and other ophthalmological disturbances associated with vigabatrin.
Sankar, R; Spence, SJ, 2001
)
0.78
" There was no statistically significant relationship between the frequency of electrodiagnostic abnormalities and the duration of use or the total cumulative dosage of Vigabatrin in any of the three groups."( Vigabatrin effect on inner retinal function.
Coupland, SG; Leonard, BC; Ross, TM; Zackon, DH, 2001
)
1.95
"A highly sensitive and specific method is proposed for the determination of vigabatrin (I) and gabapentin (II) in their dosage forms and spiked human plasma."( Spectrofluorimetric determination of vigabatrin and gabapentin in dosage forms and spiked plasma samples through derivatization with 4-chloro-7-nitrobenzo-2-oxa-1,3-diazole.
Al-Deeb, OA; Belal, F; Hassan, EM; Khalil, NY,
)
0.63
" The combination PP and low-medium dosed VGB (1000-2000 mg/d) did not increase the GABA+/Cr signals."( Influence of pyridoxal 5'-phosphate alone and in combination with vigabatrin on brain GABA measured by 1H-NMR-spectroscopy.
Boesiger, P; Mueller, SG; Weber, OM; Wieser, HG, 2001
)
0.55
" Corticotropin (adrenocorticotropic hormone) or corticosteroids have been the gold standard treatment for the last 40 years, but there is little agreement on the best agent to use, or the dosage and duration of the treatment."( A risk-benefit assessment of treatments for infantile spasms.
Nabbout, R, 2001
)
0.31
"There was no statistically significant difference in visual field size comparing baseline values with first year and second year follow-up examinations either in patients who stopped VGB treatment (n = 11) or in patients who continued VGB treatment on a reduced dosage (n = 4)."( Is visual field constriction in epilepsy patients treated with vigabatrin reversible?
Jokiel, B; Pfeiffer, S; Rüther, K; Schmidt, T; Schmitz, B; Tiel-Wilck, K, 2002
)
0.55
" No significant correlations were found between drug dosage and POBF and PA for the vigabatrin treated epilepsy group."( Epilepsy patients treated with vigabatrin exhibit reduced ocular blood flow.
Embleton, SJ; Gupta, AK; Hosking, SL; Roff Hilton, EJ, 2003
)
0.83
" The high dosage of GABA needed to affect the light responses of HCs could be due to strong GABA uptake systems in the intact rabbit retina."( The effects of GABA and vigabatrin on horizontal cell responses to light and the effect of vigabatrin on the electroretinogram.
Hanitzsch, R; Küppers, L, 2002
)
0.62
" If the cumulative dosage is more than 3 kg of vigabatrin, the visual field controls should be performed more frequently because of the dosage-toxicity relationship."( [Vigabatrin-associated bilateral simple optic nerve atrophy with visual field constriction. A case report and a survey of the literature].
Mardin, CY; Viestenz, A, 2003
)
1.49
" Patients randomized to GBP started on 1800 mg/d and could have their dosage increased stepwise to 2400 and 3600 mg/d if seizures persisted."( Serum concentrations and effects of gabapentin and vigabatrin: observations from a dose titration study.
Johannessen, SI; Larsson, S; Lindberger, M; Luhr, O; Tomson, T, 2003
)
0.57
" Although its half-life is relatively short (6 to 8 hours), its duration of action is longer than anticipated from its pharmacokinetics in plasma, and a twice-daily dosing regimen is adequate to produce the desired response."( The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come?
Johannessen, SI; Perucca, E, 2003
)
0.32
" At baseline (before VGB), serum PHT remained unaffected (85 +/- 30 micromol l(-1)) after switching PHT dosage to the intravenous route, indicating that the oral availability of the drug was virtually complete."( Vigabatrin-induced decrease in serum phenytoin concentration does not involve a change in phenytoin bioavailability.
Bartoli, A; Gatti, G; Marchiselli, R; Michelucci, R; Perucca, E; Pisani, F; Richens, A; Tassinari, CA; Timmings, P; Zaccara, G, 1993
)
1.73
" The relationship between dosage and damage is obscure."( Vigabatrin-associated loss of vision: rarebit perimetry illuminates the dose-damage relationship.
Frisén, L, 2004
)
1.77
"Adrenocorticotropic hormone (ACTH) is probably effective for the short-term treatment of infantile spasms, but there is insufficient evidence to recommend the optimum dosage and duration of treatment."( Practice parameter: medical treatment of infantile spasms: report of the American Academy of Neurology and the Child Neurology Society.
Adams-Webber, T; Ashwal, S; Ballaban-Gill, K; Baram, TZ; Duchowny, M; Hirtz, D; Mackay, MT; Pellock, JM; Shields, WD; Shinnar, S; Snead, OC; Stephens, D; Weiss, SK; Wyllie, E, 2004
)
0.32
" Furthermore, we show that on different variables, there might be different optimal dosage combinations, which might complicate the clinical application of polytherapy."( The interaction between vigabatrin and diazepam on the electroencephalogram during active behaviour in rats: an isobolic analysis.
Bouwman, BM; Heesen, E; van Rijn, CM, 2004
)
0.63
" In all participants TMS procedures were carried out before and after administering GVG for three consecutive days at a daily dosage of 50 mg/kg."( Effect of Vigabatrin on motor responses to transcranial magnetic stimulation: an effective tool to investigate in vivo GABAergic cortical inhibition in humans.
Bernardi, G; Brusa, L; Caramia, MD; Galati, S; Marciani, MG; Palmieri, MG; Pierantozzi, M; Stanzione, P, 2004
)
0.73
" The effects of the following factors on contrast sensitivity and visual acuity were examined: type of seizure (infantile spasms versus other), ERG result, duration of vigabatrin therapy, cumulative dosage of vigabatrin, and other seizure medications (other versus no other medication)."( Reduced visual function associated with infantile spasms in children on vigabatrin therapy.
Buncic, JR; Hammoudi, DS; Lee, SS; Logan, WJ; Madison, A; Mirabella, G; Snead, OC; Westall, CA, 2005
)
0.76
" These results present a novel interpretation of synergistic inhibition of certain epileptic discharges using vigabatrin and another drug, and that for successful synergistic treatment of epilepsies carefully designed timed dosage regimens are essential."( Antiepileptic action induced by a combination of vigabatrin and tiagabine.
Fueta, Y; Kunugita, N; Schwarz, W, 2005
)
0.79
"The method was demonstrated for quantification of vigabatrin in both tablet and sachet dosage forms and proved to be a very specific and fast (8 min) means of routine analysis of the drug in dosage forms, in assay or dissolution testing."( Application of capillary zone electrophoresis with indirect UV detection to the determination of a model drug, vigabatrin, in dosage forms.
Lucy, C; Shafaati, A, 2005
)
0.79
" The medication dosage varied from 1 to 20 mg/kg daily."( [The efficacy of topiramate (topamax) in the treatment of resistant epilepsy in children].
Belousova, ED; Dorofeeva, MIu; Ermakov, AIu, 2005
)
0.33
" For these older drugs it has been common practice to adjust the dosage to achieve a serum drug concentration within a predefined 'therapeutic range', representing an interval where most patients are expected to show an optimal response."( Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed?
Johannessen, SI; Tomson, T, 2006
)
0.33
" Application of the method to the analysis of vigabatrin in serum of dosed patients proved feasible."( Fluorescent high-performance liquid chromatographic analysis of vigabatrin enantiomers after derivatizing with naproxen acyl chloride.
Hsieh, CY; Kwan, AL; Wang, SY; Wu, HL, 2008
)
0.84
" Length of treatment with this drug ranged from 13 months to 5 years and the mean daily dosage was 1581 mg."( Vigabatrin-induced visual dysfunction in Chinese patients with refractory epilepsy.
Hui, AC; Lam, DS; Lam, PT; Leung, T; Liu, DT; Man, BL; Wong, KK,
)
1.57
" Linear regression analysis was used to evaluate a dose-response relationship between logarithms of VGB doses and their resultant maximum possible antinociceptive effects (MPAE) in the hot-plate test in mice."( Dose-response relationship analysis of vigabatrin doses and their antinociceptive effects in the hot-plate test in mice.
Czuczwar, SJ; Luszczki, JJ,
)
0.4
" Affected versus unaffected patients, respectively, had a median age of 11 months versus 5 years, therapy duration 3 months versus 12 months, and dosage 170 mg/kg/day versus 87 mg/kg/day."( Cerebral MRI abnormalities associated with vigabatrin therapy.
Conry, JA; de Menezes, MS; Elling, NJ; Ferri, R; Gaillard, WD; Gilles, E; Goodkin, HP; Heffron, A; Kadom, N; McCarter, R; McClintock, WM; Molloy-Wells, E; Pearl, PL; Saneto, RP; Trzcinski, S; Vezina, LG, 2009
)
0.62
" There is no validated therapeutic range, but to the recommended dosage of 1 to 3 g a day correspond plasma concentrations ranging from 0,8 to 36 mg/L (6 - 279 micromol/L)."( [Therapeutic drug monitoring of vigabatrin].
Bentué-Ferrer, D; Tribut, O; Verdier, MC,
)
0.41
" The mean initial dosage of VGB was 36."( [Effectiveness of vigabatrin in west syndrome associated with tuberous sclerosis].
Ando, N; Fujimoto, S; Hattori, A; Ishikawa, T; Ito, T; Kobayashi, S; Togari, H, 2010
)
0.69
" Parameters of drug dosage were compared."( Electrophysiological evaluation of retinal function in children receiving vigabatrin medication.
Andréasson, S; Kjellström, U; Ponjavic, V,
)
0.36
" Increased degrees of vacuolation were observed on PND 67 only after a dosage of 50mg/kg/day, and were attenuated during recovery."( Oral toxicity of vigabatrin in immature rats: characterization of intramyelinic edema.
Bekersky, I; Collins, S; Garman, R; Jortner, B; Patterson, R; Sagar, S; Tolbert, D; Walzer, M; Wanaski, S, 2011
)
0.71
" Results of the US trials have demonstrated vigabatrin to be an effective and generally well-tolerated therapy for rCPS in adults, with an optimal dosage of 3 g/day for most patients, and an onset of response generally within 2 weeks."( Vigabatrin therapy for refractory complex partial seizures: review of clinical trial experience in the United States.
Faught, E, 2011
)
2.07
" Its efficacy in achieving improved seizure control should be apparent within 12 weeks in patients with rCPS and within 2-4 weeks after attaining appropriate dosage for patients with IS."( Balancing clinical benefits of vigabatrin with its associated risk of vision loss.
Pellock, JM, 2011
)
0.66
"Male Sprague-Dawley rats were dosed rectally with five different gels, varying in buffer capacity, the amount of vigabatrin, and co-administration of proline or tryptophan."( Rectal absorption of vigabatrin, a substrate of the proton coupled amino acid transporter (PAT1, Slc36a1), in rats.
Broberg, ML; Frølund, S; Holm, R; Jensen, A; Kall, MA; Nielsen, AL; Nielsen, CU, 2012
)
0.91
" In addition to demographics and vigabatrin dosing information, data included seizure type/frequency at presentation and subsequent follow-up."( Vigabatrin for childhood partial-onset epilepsies.
Agricola, K; Fordyce, S; Franz, DN; Greiner, HM; Krueger, DA; Lynch, ER; Tudor, C, 2012
)
2.1
" The efficacy and adverse events of ACTH with different dosage regimens were reviewed and analyzed."( Adrenocorticotropic hormone for the treatment of West Syndrome in children.
Lam, WM; Manasco, KB; Shumiloff, NA, 2013
)
0.39
" If prednisolone or vigabatrin is used, high dosage is recommended."( Treatment of infantile spasms.
Edwards, SW; Hancock, EC; Osborne, JP, 2013
)
0.71
" Several derivatization methods have been developed and used for their determination in bulk or pharmaceutical dosage forms."( A simple high-throughput method for determination of antiepileptic analogues of γ-aminobutyric acid in pharmaceutical dosage forms using microplate fluorescence reader.
Martinc, B; Vovk, T, 2013
)
0.39
"The aim of the study was to evaluate the relationship between the area of isopters obtained using semi-automated kinetic perimetry (SKP) and Vigabatrin dosage in epilepsy patients with pretreatment baseline examination during 2-years of the follow-up."( Relationship between the area of isopters and Vigabatrin dosage during two years of observation.
Brzozowska, A; Jedrych, M; Juenemann, AG; Koss, MJ; Ksiazek, K; Ksiazek, P; Maciejewski, R; Nowomiejska, K; Rejdak, K; Rejdak, R; Schiefer, U; Zarnowski, T, 2014
)
0.86
" The purpose of this investigation was to describe the relationship between vigabatrin dosage and daily seizure rate for adults and children with rCPS and identify relevant covariates that might impact seizure frequency."( Population dose-response analysis of daily seizure count following vigabatrin therapy in adult and pediatric patients with refractory complex partial seizures.
Hutmacher, MM; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2015
)
0.88
" A dose-response model related seizure-count data to vigabatrin dosage to identify dosages for pediatric rCPS patients."( Vigabatrin pediatric dosing information for refractory complex partial seizures: results from a population dose-response analysis.
Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014
)
2.09
" There was neither effect of age of initiation of VGB treatment nor sex of the child on survival statistics and no significant effect of cumulative dosage on the occurrence of VGB-RD."( Vigabatrin retinal toxicity in children with infantile spasms: An observational cohort study.
Buncic, JR; Cortese, F; Kumarappah, A; Snead, OC; Westall, CA; Wright, T, 2014
)
1.85
" In animals dosed during PNDs 7-14 or during PNDs 14-30, the first changes were found in the thalamus."( Vigabatrin-induced CNS changes in juvenile rats: Induction, progression and recovery of myelin-related changes.
Downes, N; Mullins, P; Rasmussen, AD; Richmond, E; Wegener, KM, 2015
)
1.86
"2) months, the median peak dosage was 141."( A lack of clinically apparent vision loss among patients treated with vigabatrin with infantile spasms: The UCLA experience.
Hussain, SA; Li, M; Sankar, R; Schwarz, MD; Tsao, J; Wu, JY; Wu, YW; Zhou, R, 2016
)
0.67
" For vigabatrin, demonstration of similar dose-response between pediatrics and adults allowed for selection of a pediatric dose."( Role of Quantitative Clinical Pharmacology in Pediatric Approval and Labeling.
Bhattaram, A; Earp, JC; Florian, J; Krudys, K; Lee, JE; Lee, JY; Liu, J; Mehrotra, N; Mulugeta, Y; Sinha, V; Yu, J; Zhao, P, 2016
)
0.95
"OCT and complete dosing data was available for 19 patients."( Optical coherence tomography to monitor vigabatrin toxicity in children.
Alexander, J; Bazemore, M; Berl, MM; de Beaufort, H; Elling, N; Geddie, B; Hutcheson, K; Jaafar, MS; Karwoski, B; Madigan, W; McClintock, W; Miller, M; Origlieri, C; Taylormoore, J, 2016
)
0.7
" Both were treated with several antiepileptic drugs, including VGB up to a maximum dosage of 200 mg/kg/day."( [Reversible alterations in the neuroimages associated with vigabatrine treatment in infants with epileptic spasms].
Fernandez-Garcia, MA; Garcia-Esparza, E; Garcia-Penas, JJ; Gomez-Martin, H; Perez-Sebastian, I; Sirvent-Cerda, S, 2017
)
0.7
" Caution should be exercised in the use of high VGB dosage (i."( Risk of vigabatrin-associated brain abnormalities on MRI in the treatment of infantile spasms is dose-dependent.
Hussain, SA; Li, M; Salamon, N; Sankar, R; Schwarz, MD; Tsao, J; Wu, JY; Zhou, R, 2017
)
0.89
" Of 15 patients (aged ≥4weeks and <2years) enrolled, with the exception of two patients who did not receive vigabatrin, 13 were treated with a titrated dosage of vigabatrin (50-150mg/kg/day; limited to 3000mg/day)."( Efficacy and safety of vigabatrin in Japanese patients with infantile spasms: Primary short-term study and extension study.
Ohtsuka, Y, 2018
)
1
" All symptoms were recovered by reducing the dosage of VGB."( Efficacy of vigabatrin therapy for tuberous sclerosis with infantile spasms.
Hino-Fukuyo, N; Kiluchi, A; Kobayashi, T; Kure, S; Nakayama, T; Numata-Uematsu, Y; Sato, H; Suzuki-Muromoto,, S; Uematsu, M, 2016
)
0.81
" The review presents the current published data on the incidence of seizures in pregnant women, specificity of therapy with antiepileptic drugs (AEDs), frequency of fetal malformations in pregnant women taking AEDs regularly and their dependence on the frequency, dosage and nature of therapy."( [Modern aspects of antiepileptic therapy during pregnancy].
Kispayeva, TT; Nurakhmetova, AS,
)
0.13
" For each patient we recorded dates of infantile spasms onset, response to vigabatrin, relapse (if any), and quantified duration and dosage of vigabatrin after response."( High vigabatrin dosage is associated with lower risk of infantile spasms relapse among children with tuberous sclerosis complex.
Bebin, EM; Goyal, M; Hussain, SA; Krueger, DA; Northrup, H; Peters, JM; Sahin, M; Schmid, E; Wu, JY, 2018
)
1.23
" Furthermore, most preclinical antiepileptogenic studies lack information needed for translation, such as dose-blood level relationship, brain target engagement, and dose-response, and many use treatment parameters that cannot be applied clinically, for example, treatment initiation before or at the time of injury and dosing higher than tolerated human equivalent dosing."( Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy?
Bar-Klein, G; Friedman, A; Hameed, MQ; Jozwiak, S; Kaminski, RM; Klein, P; Klitgaard, H; Koepp, M; Löscher, W; Prince, DA; Rotenberg, A; Twyman, R; Vezzani, A; Wong, M, 2020
)
0.56
" We evaluated: 50% or greater reduction in seizure frequency, treatment withdrawal, adverse effects, dose-response analysis, cognitive outcomes and quality of life."( Vigabatrin add-on therapy for drug-resistant focal epilepsy.
Bresnahan, R; Gianatsi, M; Maguire, MJ; Marson, AG; Tudur Smith, C, 2020
)
2
" Twenty-three of the 25 VABAM cases have a peak dosage of VGB between 50 and 150 mg/kg/day."( Risk of vigabatrin-associated brain abnormalities on MRI: A retrospective and controlled study.
Gao, J; Han, F; He, W; Liu, K; Luo, XM; Shi, XY; Wan, L; Wang, J; Wang, QH; Wang, YY; Xu, Y; Yang, G; Yang, XY; Zou, LP, 2022
)
1.16
" In addition, we once again verified that the peak dosage of VGB was the risk factor of VABAM."( Risk of vigabatrin-associated brain abnormalities on MRI: A retrospective and controlled study.
Gao, J; Han, F; He, W; Liu, K; Luo, XM; Shi, XY; Wan, L; Wang, J; Wang, QH; Wang, YY; Xu, Y; Yang, G; Yang, XY; Zou, LP, 2022
)
1.16
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
anticonvulsantA drug used to prevent seizures or reduce their severity.
EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitorAn EC 2.6.1.* (transaminase) inhibitor that interferes with the action of 4-aminobutyrate--2-oxoglutarate transaminase (EC 2.6.1.19).
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (1)

ClassDescription
gamma-amino acidA non-proteinogenic amino-acid in which the amino group is located on the carbon atom at the position gamma to the carboxy group.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (18)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
endonuclease IVEscherichia coliPotency0.22390.707912.432431.6228AID1708
thioredoxin reductaseRattus norvegicus (Norway rat)Potency0.63100.100020.879379.4328AID588453
USP1 protein, partialHomo sapiens (human)Potency33.58750.031637.5844354.8130AID504865
arylsulfatase AHomo sapiens (human)Potency0.84921.069113.955137.9330AID720538
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency5.01190.035520.977089.1251AID504332
Bloom syndrome protein isoform 1Homo sapiens (human)Potency56.23410.540617.639296.1227AID2364; AID2528
D(1A) dopamine receptorHomo sapiens (human)Potency0.00370.02245.944922.3872AID488982
chromobox protein homolog 1Homo sapiens (human)Potency0.00530.006026.168889.1251AID488953
ATP-dependent phosphofructokinaseTrypanosoma brucei brucei TREU927Potency0.16940.060110.745337.9330AID485368
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Gamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)Ki3,200.00006.00006.00006.0000AID71251
Bile salt export pumpHomo sapiens (human)IC50 (µMol)133.00000.11007.190310.0000AID1473738
4-aminobutyrate aminotransferase, mitochondrialSus scrofa (pig)Ki1,745.00000.30001.25002.2000AID1725381; AID71251
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
Gamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)Ki3,200.00006.00006.00006.0000AID71251
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (78)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
G protein-coupled receptor signaling pathwayGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathwayGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
negative regulation of adenylate cyclase activityGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
gamma-aminobutyric acid signaling pathwayGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
chemical synaptic transmissionGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
synaptic transmission, GABAergicGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
neuron-glial cell signalingGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
response to hypoxia4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
copulation4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
locomotory behavior4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
response to xenobiotic stimulus4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
gamma-aminobutyric acid metabolic process4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
gamma-aminobutyric acid biosynthetic process4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
response to iron ion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
negative regulation of gamma-aminobutyric acid secretion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
cerebellum development4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of heat generation4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of insulin secretion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
negative regulation of dopamine secretion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
response to nicotine4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
exploration behavior4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
response to ethanol4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
negative regulation of blood pressure4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of dopamine metabolic process4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
behavioral response to cocaine4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of uterine smooth muscle contraction4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of inhibitory postsynaptic potential4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of prolactin secretion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
positive regulation of aspartate secretion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
gamma-aminobutyric acid catabolic process4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
osteoblast differentiationGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathwayGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
gamma-aminobutyric acid signaling pathwayGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
negative regulation of cell population proliferationGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
positive regulation of glutamate secretionGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
negative regulation of gamma-aminobutyric acid secretionGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
negative regulation of epinephrine secretionGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
negative regulation of dopamine secretionGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
response to nicotineGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
response to ethanolGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
negative regulation of synaptic transmissionGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
synaptic transmission, GABAergicGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
regulation of postsynaptic membrane potentialGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
positive regulation of growth hormone secretionGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
regulation of presynaptic membrane potentialGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
neuron-glial cell signalingGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (38)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
G protein-coupled GABA receptor activityGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
protein bindingGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
protein heterodimerization activityGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
transmembrane signaling receptor activityGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
4-aminobutyrate transaminase activity4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
pyridoxal phosphate binding4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
succinate-semialdehyde dehydrogenase binding4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
4-aminobutyrate:2-oxoglutarate transaminase activity4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
identical protein binding4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
metal ion binding4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
(S)-3-amino-2-methylpropionate transaminase activity4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
iron-sulfur cluster binding4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
G protein-coupled GABA receptor activityGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
G protein-coupled GABA receptor activityGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
protein bindingGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
protein heterodimerization activityGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
G protein-coupled neurotransmitter receptor activity involved in regulation of postsynaptic membrane potentialGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
G protein-coupled neurotransmitter receptor activity involved in regulation of presynaptic membrane potentialGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
extracellular matrix protein bindingGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (38)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
cytoplasmGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
plasma membraneGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
neuron projectionGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
postsynaptic membraneGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
G protein-coupled GABA receptor complexGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
G protein-coupled receptor heterodimeric complexGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
GABA receptor complexGamma-aminobutyric acid type B receptor subunit 2Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
mitochondrion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
mitochondrial matrix4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
4-aminobutyrate transaminase complex4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
mitochondrion4-aminobutyrate aminotransferase, mitochondrialHomo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
extracellular spaceGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
endoplasmic reticulum membraneGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
plasma membraneGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
synaptic vesicleGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
axolemmaGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
mitochondrial membraneGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
presynaptic membraneGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
neuronal cell bodyGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
dendritic spineGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
dendritic shaftGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
postsynaptic membraneGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
Schaffer collateral - CA1 synapseGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
glutamatergic synapseGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
GABA-ergic synapseGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
G protein-coupled GABA receptor complexGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
G protein-coupled receptor heterodimeric complexGamma-aminobutyric acid type B receptor subunit 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (131)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID716867Retinotoxicity in Wistar albino rat assessed as increase mesopic implicit time at 200 mg/kg, ip administered QD for 45 to 90 days relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID716868Retinotoxicity in Wistar albino rat assessed as increase cone implicit time at 200 mg/kg, ip administered QD for 45 to 90 days relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID716661Toxicity in ip dosed Wistar albino rat2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID716652Retinotoxicity in male Wistar albino rat assessed as photopic ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 66 +/- 5.6 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID716656Retinotoxicity in female Wistar albino rat assessed as 15Hz flicker ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 33.4 +/- 3.2 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID476929Human intestinal absorption in po dosed human2010European journal of medicinal chemistry, Mar, Volume: 45, Issue:3
Neural computational prediction of oral drug absorption based on CODES 2D descriptors.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID716626Inhibition of cocaine-induced conditioned place preference in rat assessed as time spent in the chamber at 300 mg/kg, ip administered 2.5 hrs prior to cocaine-challenge measured after 12 days for 15 mins (Rvb = 7.1 +/- 0.6 mins)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1544803Inhibition of GABA aminotransferase in mouse brain homogenates using GABA and alpha-ketoglutarate as substrates preincubated for 30 mins followed by beta-NADP addition and measured for 20 mins by spectrophotometric method2019Bioorganic & medicinal chemistry letters, 07-15, Volume: 29, Issue:14
Novel benzothiazole hydrazine carboxamide hybrid scaffolds as potential in vitro GABA AT enzyme inhibitors: Synthesis, molecular docking and antiepileptic evaluation.
AID71253Ratio of KI to that of Kinact was determined against gamma-aminobutyric acid aminotransferase2003Journal of medicinal chemistry, Dec-04, Volume: 46, Issue:25
Design, synthesis, and biological activity of a difluoro-substituted, conformationally rigid vigabatrin analogue as a potent gamma-aminobutyric acid aminotransferase inhibitor.
AID716644Retinotoxicity in male Wistar albino rat assessed as standard combined ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 362.4 +/- 62.2 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1725383Covalent inhibition of GABA-AT (unknown origin) assessed as kinact/Ki ratio2020ACS medicinal chemistry letters, Oct-08, Volume: 11, Issue:10
Mechanism-Based Design of 3-Amino-4-Halocyclopentenecarboxylic Acids as Inactivators of GABA Aminotransferase.
AID225513Effective dose required for anticonvulsive activity in maximal electroshock seizure (MES) test; Not effective2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID25607Dissociation constant pKa was reported.1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Synthesis and evaluation of mono-, di-, and trifluoroethenyl-GABA derivatives as GABA-T inhibitors.
AID110847In vivo brain GABA-T activity was measured in mice 6 hour after intraperitoneal administration at a dose of 1.9 mM / kg.1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Synthesis and evaluation of mono-, di-, and trifluoroethenyl-GABA derivatives as GABA-T inhibitors.
AID689061Inhibition of rat GABA aminotransferase by modified Scott and Jacoby method2012Bioorganic & medicinal chemistry, Oct-01, Volume: 20, Issue:19
Synthesis and evaluation of novel heteroaromatic substrates of GABA aminotransferase.
AID716877Inactivation of GABA-AT2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID225508Effective dose required for anticonvulsive activity in bicuculline (BIC) test2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID716636Retinotoxicity in male Wistar albino rat assessed as scotopic ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 302.1 +/- 46 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID71251Tested for inhibitory activity against gamma-aminobutyric acid aminotransferase from pig brain2003Journal of medicinal chemistry, Dec-04, Volume: 46, Issue:25
Design, synthesis, and biological activity of a difluoro-substituted, conformationally rigid vigabatrin analogue as a potent gamma-aminobutyric acid aminotransferase inhibitor.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID71252Tested for time dependent inactivation of gamma-aminobutyric acid aminotransferase from pig brain by the compound2003Journal of medicinal chemistry, Dec-04, Volume: 46, Issue:25
Design, synthesis, and biological activity of a difluoro-substituted, conformationally rigid vigabatrin analogue as a potent gamma-aminobutyric acid aminotransferase inhibitor.
AID716632Retinotoxicity in female Wistar albino rat assessed as scotopic ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 294.4 +/- 31.5 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID716643Retinotoxicity in male Wistar albino rat assessed as standard combined ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 397.1 +/- 58.9 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID224087Protection from picrotoxin-induced (0.27 mmol/kg) convulsion over 16 hr at 100 mg/kg in 4 mice2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID725314Time dependent inhibition of pig brain GABA-AT using GABA as substrate at 5 mM up to 150 mins2013Bioorganic & medicinal chemistry, Feb-15, Volume: 21, Issue:4
Probing the steric requirements of the γ-aminobutyric acid aminotransferase active site with fluorinated analogues of vigabatrin.
AID1725380Mechanism based inactivation of pig brain GABA-AT assessed as inactivation rate constant using GABA as substrate in presence of NADP+ and alpha-ketoglutarate by SSDH coupled enzyme based UV-Vis spectrophotometry2020ACS medicinal chemistry letters, Oct-08, Volume: 11, Issue:10
Mechanism-Based Design of 3-Amino-4-Halocyclopentenecarboxylic Acids as Inactivators of GABA Aminotransferase.
AID716872Retinotoxicity in female Wistar albino rat assessed as reduction in 10 Hz flicker ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1725382Mechanism based inactivation of pig brain GABA-AT assessed as ratio of Kinact to Ki using GABA as substrate in presence of NADP+ and alpha-ketoglutarate by SSDH coupled enzyme based UV-Vis spectrophotometry2020ACS medicinal chemistry letters, Oct-08, Volume: 11, Issue:10
Mechanism-Based Design of 3-Amino-4-Halocyclopentenecarboxylic Acids as Inactivators of GABA Aminotransferase.
AID716660Retinotoxicity in male Wistar albino rat assessed as 15Hz flicker ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 36.2 +/- 3.6 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID716875Retinotoxicity in male Wistar albino rat assessed as reduction in 10 Hz flicker ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID107134Brain GABA level was measured in mice 6 hour after intraperitoneal administration at a dose of 1.9 mM/ kg.1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Synthesis and evaluation of mono-, di-, and trifluoroethenyl-GABA derivatives as GABA-T inhibitors.
AID224089Protection from picrotoxin-induced (0.27 mmol/kg) convulsion over 6 hr at 100 mg/kg in 4 mice2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID716647Retinotoxicity in female Wistar albino rat assessed as photopic ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 62.6 +/- 8.2 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID716639Retinotoxicity in female Wistar albino rat assessed as standard combined ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 393.1 +/- 56.4 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID716655Retinotoxicity in female Wistar albino rat assessed as 15Hz flicker ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 33.7 +/- 3.5 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID716871Retinotoxicity in female Wistar albino rat assessed as reduction in 10 Hz flicker ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID716878Inactivation of GABA-AT in rat brain homogenate2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID716648Retinotoxicity in female Wistar albino rat assessed as photopic ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 62.2 +/- 5.1 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID73475Concentration dependent inactivation of Gamma-amino-N-butyrate transaminase2002Journal of medicinal chemistry, Sep-26, Volume: 45, Issue:20
Inactivation and inhibition of gamma-aminobutyric acid aminotransferase by conformationally restricted vigabatrin analogues.
AID1725381Binding affinity pig brain GABA-AT assessed as inactivation constant using GABA as substrate in presence of NADP+ and alpha-ketoglutarate by SSDH coupled enzyme based UV-Vis spectrophotometry2020ACS medicinal chemistry letters, Oct-08, Volume: 11, Issue:10
Mechanism-Based Design of 3-Amino-4-Halocyclopentenecarboxylic Acids as Inactivators of GABA Aminotransferase.
AID716876Retinotoxicity in male Wistar albino rat assessed as reduction in 10 Hz flicker ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID716667Retinotoxicity in Wistar albino rat assessed as increase rod implicit time at 200 mg/kg, ip administered QD for 45 to 90 days relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID716659Retinotoxicity in male Wistar albino rat assessed as 15Hz flicker ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 44.4 +/- 6.3 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID224088Protection from picrotoxin-induced (0.27 mmol/kg) convulsion over 3 hr at 100 mg/kg in 4 mice2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID716640Retinotoxicity in female Wistar albino rat assessed as standard combined ERG at 200 mg/kg, ip administered QD for 90 days by electroretinogram analysis (Rvb = 379.2 +/- 32.6 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID716651Retinotoxicity in male Wistar albino rat assessed as photopic ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 73.7 +/- 14.3 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID229378Ratio of kinact to that of KI.2002Journal of medicinal chemistry, Sep-26, Volume: 45, Issue:20
Inactivation and inhibition of gamma-aminobutyric acid aminotransferase by conformationally restricted vigabatrin analogues.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID227699Virtual screen for compounds with anticonvulsant activity2003Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16
Topological virtual screening: a way to find new anticonvulsant drugs from chemical diversity.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID25416Half life at a concentration 1 mM.1998Bioorganic & medicinal chemistry letters, Sep-22, Volume: 8, Issue:18
General synthesis of 3-substituted alkenyl GABA as potential anticonvulsants.
AID521220Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay2007Nature chemical biology, May, Volume: 3, Issue:5
Chemical genetics reveals a complex functional ground state of neural stem cells.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID716631Retinotoxicity in female Wistar albino rat assessed as scotopic ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 290.3 +/- 39 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID539464Solubility of the compound in 0.1 M phosphate buffer at 600 uM at pH 7.4 after 24 hrs by LC/MS/MS analysis2010Bioorganic & medicinal chemistry letters, Dec-15, Volume: 20, Issue:24
Experimental solubility profiling of marketed CNS drugs, exploring solubility limit of CNS discovery candidate.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID716663Toxicity in Wistar albino rat assessed as mortality at 200 mg/kg, ip measured up to 3 weeks2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID225517Anticonvulsive activity in picrotoxin (PCR) induced seizure test2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID224091Protection from picrotoxin-induced (0.27 mmol/kg) convulsion over 9 hr at 100 mg/kg in 4 mice2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID130085Dose required to produce a 50% reduction in general motor activity after injection in mice1990Journal of medicinal chemistry, Feb, Volume: 33, Issue:2
Synthesis, brain uptake, and pharmacological properties of a glyceryl lipid containing GABA and the GABA-T inhibitor gamma-vinyl-GABA.
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID225516Effective dose required for anticonvulsive activity in pentylenetetrazole (PTZ) test; Not effective2000Bioorganic & medicinal chemistry letters, Apr-03, Volume: 10, Issue:7
Design and synthesis of anticonvulsive agents as gamma-vinyl GABA-based potential dual acting prodrugs and their biological activities.
AID716624Reduction in nucleus accumbens dopamine in freely moving rat assessed as reduction in cocaine-induced increase in dopamine level at 300 mg/kg, ip administered 60 mins prior to cocaine-challenge by microdialysis method relative to control2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID73478Time dependent inactivation of Gamma-amino-N-butyrate transaminase2002Journal of medicinal chemistry, Sep-26, Volume: 45, Issue:20
Inactivation and inhibition of gamma-aminobutyric acid aminotransferase by conformationally restricted vigabatrin analogues.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID716635Retinotoxicity in male Wistar albino rat assessed as scotopic ERG at 200 mg/kg, ip administered QD for 45 days by electroretinogram analysis (Rvb = 274.6 +/- 41.7 uV)2012Journal of medicinal chemistry, Jan-12, Volume: 55, Issue:1
(1S, 3S)-3-amino-4-difluoromethylenyl-1-cyclopentanoic acid (CPP-115), a potent γ-aminobutyric acid aminotransferase inactivator for the treatment of cocaine addiction.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347050Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347151Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID588349qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID504836Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation2002The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16
Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID1347045Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347405qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347058CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347059CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347049Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588378qHTS for Inhibitors of ATXN expression: Validation
AID1347410qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library2019Cellular signalling, 08, Volume: 60A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID1347057CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,629)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990196 (12.03)18.7374
1990's546 (33.52)18.2507
2000's468 (28.73)29.6817
2010's307 (18.85)24.3611
2020's112 (6.88)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 75.68

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index75.68 (24.57)
Research Supply Index7.57 (2.92)
Research Growth Index4.78 (4.65)
Search Engine Demand Index135.46 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (75.68)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials200 (11.57%)5.53%
Reviews254 (14.69%)6.00%
Case Studies175 (10.12%)4.05%
Observational11 (0.64%)0.25%
Other1,089 (62.98%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (27)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Sabril Patient Registry [NCT01073579]9,423 participants (Actual)Observational2009-08-31Completed
Inhibiting GABA Transaminase to Relieve Obesity Induced Hyperinsulinemia and Insulin Resistance [NCT04062890]Phase 240 participants (Anticipated)Interventional2019-12-15Not yet recruiting
Acceptability Study of a New Paediatric Form of Vigabatrin in Infants and Children With Infantile Spasms or Pharmacoresistant Partial Epilepsy. Observational, Descriptive, Open-label, Multi-centric, Non-randomized Study [NCT02220114]38 participants (Actual)Interventional2014-05-31Completed
Bioequivalence Study of Vigabatrin ORPHELIA Pharma 500mg Soluble Tablets and SabrilTM 500mg Granules for Oral Administration [NCT04468282]Phase 120 participants (Actual)Interventional2017-04-04Completed
Sabril for Treatment of Adult Refractory Partial Seizures Symptomatic of Tuberous Sclerosis: An Open Label, Phase IV Prospective Safety and Tolerability Study [NCT01266291]Phase 41 participants (Actual)Interventional2010-08-31Terminated(stopped due to Was not possible to enroll sufficient number of subjects to draw any worthwhile conclusions from the study.)
A Randomised Controlled Trial of the Ketogenic Diet in the Treatment of Epilepsy in Children Under the Age of Two Years [NCT02205931]Phase 4160 participants (Anticipated)Interventional2015-01-31Recruiting
Preventing Epilepsy Using Vigabatrin In Infants With Tuberous Sclerosis Complex (PREVeNT Trial) A Randomized, Double-blind, Placebo-controlled Seizure Prevention Clinical Trial for Infants With TSC [NCT02849457]Phase 284 participants (Actual)Interventional2016-12-31Completed
The Effect of Vigabatrin on Insulin Sensitivity [NCT04321395]Phase 26 participants (Anticipated)Interventional2021-08-23Recruiting
Efficacy of Vigabatrin With High Dose Prednisolone Combination Therapy Versus Vigabatrin Alone for Infantile Spasm: a Randomized Trial [NCT04302116]250 participants (Anticipated)Interventional2020-05-18Recruiting
Double-Blind, Randomized, Placebo- Controlled Trial of Vigabatrin for Short Term Abstinence From Cocaine in Cocaine Dependent Parolees [NCT00527683]Phase 2100 participants (Actual)Interventional2007-04-30Completed
Vigabatrin for Treatment of Cocaine Dependence: A Phase II Study [NCT00611130]Phase 2186 participants (Actual)Interventional2008-01-31Completed
An Open-Label, Single and Multiple Oral Dose Pharmacokinetic Study of Vigabatrin in Infants With Infantile Spasms [NCT01413711]Phase 40 participants (Actual)Interventional2012-06-30Withdrawn
A Phase 1 Randomized, Double-Blind, Placebo-Controlled, Parallel Group, Intravenous Cocaine and Oral Gamma Vinyl-Gamma-Amino Butyric Acid (VIGABATRIN) Interaction Study [NCT00626834]Phase 124 participants (Actual)Interventional2008-02-29Completed
Vigabatrin for Treatment of Cocaine Dependence: A Phase II Study [NCT01281202]Phase 2/Phase 3207 participants (Actual)Interventional2011-01-31Completed
Phase 1 Study of Vigabatrin (GVG) for Methamphetamine Dependence [NCT00506935]Phase 117 participants (Actual)Interventional2006-07-31Completed
A Prospective, Open-label Study of the Structure and Function of the Retina in Adult Patients With Refractory Complex Partial Seizures Treated With Vigabatrin (Sabril®) [NCT01278173]Phase 465 participants (Actual)Interventional2010-12-31Completed
Effects of Vigabatrin on Cocaine Self-Administration [NCT00373581]Phase 21 participants (Actual)Interventional2006-04-30Terminated(stopped due to Funding ran out)
VIGABatrin in Post-anoxic STATus Epilepticus - Phase IIa [NCT04772547]Phase 222 participants (Anticipated)Interventional2021-09-22Recruiting
A Phase 3, Randomized, Open-Label Study to Evaluate the Efficacy and Safety of AMZ002, Compared to Vigabatrin, in the Treatment of Infantile Spasms [NCT05128344]Phase 30 participants (Actual)Interventional2023-04-30Withdrawn(stopped due to Strategic decision)
A Phase II, Double-Blind, Placebo-Controlled, Pilot Trial of Vigabatrin for the Treatment of Cocaine and Alcohol Dependence [NCT01335867]Phase 232 participants (Actual)Interventional2011-04-30Terminated(stopped due to interim analysis of efficacy completed and termination recommended)
Open Label Safety and Tolerability Trial of CPP-109 (Vigabatrin) in Adults With Treatment Refractory Tourette's Disorder [NCT01585207]Phase 1/Phase 24 participants (Actual)Interventional2012-07-31Completed
Effect of Vigabatrin in Refractory Autoimmune Encephalitis Patients - A Pilot Study [NCT03003143]0 participants (Actual)Interventional2016-11-30Withdrawn
A Phase 3 Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study to Assess the Efficacy, Safety, and Tolerability of Cannabidiol Oral Solution as Adjunctive Therapy With Vigabatrin as Initial Therapy in Patients With Infantile Spasms [NCT03421496]Phase 32 participants (Actual)Interventional2018-09-05Terminated(stopped due to The study was terminated due to slow enrollment and failure to identify adequate patients that met entry criteria.)
Vigabatrin for Treatment of Methamphetamine Dependence: A Phase II Study [NCT00730522]Phase 255 participants (Actual)Interventional2008-07-31Terminated(stopped due to To conserve remaining capital, Sponsor decided to terminate the study early.)
A Novel Approach to Infantile Spasms: Combined Cosyntropin Injectable Suspension, 1 mg/mL and Vigabatrin Induction Therapy [NCT03347526]Phase 3394 participants (Anticipated)Interventional2018-04-19Suspended(stopped due to Study on enrollment hold as a precaution per the pharmaceutical company.)
Prednisolone vs. Vigabatrin in the First-line Treatment of Infantile Spasms [NCT02299115]Phase 30 participants (Actual)Interventional2017-09-05Withdrawn(stopped due to Most centres are now using oral steroids as 1st line treatment so question of efficacy is no longer of high interest.)
Randomized, Placebo-controlled, Double-blind and Double-dummy Clinical Trial Comparing the Safety, Tolerability, and Efficacy of Vigabatrin and Rapamycin in a Preventive Treatment of Infants With Tuberous Sclerosis Complex [NCT04987463]Phase 2/Phase 360 participants (Anticipated)Interventional2021-05-07Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00611130 (2) [back to overview]Proportion of Subjects in Each Treatment Group Abstinent During the Last 2 Weeks of Treatment.
NCT00611130 (2) [back to overview]Medication Compliance
NCT00730522 (1) [back to overview]The Proportion of Subjects in Each Treatment Group Who Are Amphetamine Abstinent During the Last 2 Weeks of the Treatment Phase (Weeks 11 and 12).
NCT01266291 (2) [back to overview]Number of Participants Safely Tolerating Sabril
NCT01266291 (2) [back to overview]Number of Patients Who Become Seizure Free While Taking Sabril
NCT01278173 (2) [back to overview]Change From Reference Value in Average RNFL (Retinal Nerve Fiber Layer) Thickness (µm) as Measured by SD-OCT (Spectral Domain-Optical Coherence Tomography)
NCT01278173 (2) [back to overview]Mean Change From Reference Value in Field Width as Measured by 30-2 SITA Fast in Field Sensitivity (Mean Deviation - MD in dB)
NCT01281202 (2) [back to overview]Abstinence
NCT01281202 (2) [back to overview]Number of Participants With Cocaine Use
NCT01335867 (5) [back to overview]Cocaine Withdrawal Severity
NCT01335867 (5) [back to overview]Disease Severity and Improvement
NCT01335867 (5) [back to overview]Measures of Cocaine Craving
NCT01335867 (5) [back to overview]Number of Participants With a Reduction in Cocaine Use
NCT01335867 (5) [back to overview]Proportion of Heavy Drinking Days
NCT01585207 (1) [back to overview]Global Severity Score on the Y-GTSS

Proportion of Subjects in Each Treatment Group Abstinent During the Last 2 Weeks of Treatment.

Number of subjects in the CPP-109 Vigabatrin Group vs. Number in Placebo Group abstinent from using cocaine during Weeks 11 and 12 of the Treatment Phase. (NCT00611130)
Timeframe: Week 13

Interventionparticipants (Number)
CPP-109 Vigabatrin Tablets, 500 mg7
Matching Placebo Tablets5

[back to top]

Medication Compliance

Using retained urine samples and prior to unblinding, up to 12 specimens/ subject were analyzed for vigabatrin levels. Compliance assessment based on > or = 70% of urines in subjects assigned to vigabatrin having quantitative levels of vigabatrin indicaticative of taking drug within the last 24 hours of clinic visit. (NCT00611130)
Timeframe: Week 2, 4, 6 & 9-11

Interventionparticipants (Number)
Number of Vigabatrin Completers AnalyzedNumber Medication Compliant
Treatment Phase Completers6124

[back to top]

The Proportion of Subjects in Each Treatment Group Who Are Amphetamine Abstinent During the Last 2 Weeks of the Treatment Phase (Weeks 11 and 12).

(NCT00730522)
Timeframe: Weeks 11-12

InterventionParticipants (Count of Participants)
Vigabatrin4
Placebo2

[back to top]

Number of Participants Safely Tolerating Sabril

"Antiepileptic Drug (AED) levels in blood~Comprehensive panel (blood test)~Complete Blood Count with differential (blood test)~Visual field tests testing~Ophthalmology exam assessment~Frequency and severity of adverse events reported by subjects throughout their involvement with the study" (NCT01266291)
Timeframe: Outcome measures will be assessed at the initiation of Sabril (titration), and at three and five months after starting Sabril. After this time, the subjects will have completed the study.

InterventionParticipants (Count of Participants)
Treatment With Sabril (Vigabatrin)0

[back to top]

Number of Patients Who Become Seizure Free While Taking Sabril

"Seizure freedom~Responder rate (complex partial seizures only)" (NCT01266291)
Timeframe: Seizure freedom will be assessed for the two month treatment phase of the study (months 4 and 5)

InterventionParticipants (Count of Participants)
Treatment With Sabril (Vigabatrin)0

[back to top]

Change From Reference Value in Average RNFL (Retinal Nerve Fiber Layer) Thickness (µm) as Measured by SD-OCT (Spectral Domain-Optical Coherence Tomography)

Mean change from the reference value in average RNFL thickness (µm) as measured by SD-OCT. The reference value was defined as the average of the assessments performed at Visits 1 (baseline), 2 and 3 (first month of dosing). Thinning of the RNFL, that is, a negative change from the reference value, has been associated with ophthalmological disease. (NCT01278173)
Timeframe: Baseline (Month 0), Month 3, Month 6, Month 9, Month 12

Interventionµm (Mean)
Left eye, 3 months (N=54)Left eye, 6 months (N=48)Left eye, 9 months (N=44)Left eye, 12 months (N=39)Right eye, 3 months (N=52)Right eye, 6 months (N=47)Right eye, 9 months (N=43)Right eye, 12 months (N=39)
Sabril0.704.155.636.450.734.216.507.19

[back to top]

Mean Change From Reference Value in Field Width as Measured by 30-2 SITA Fast in Field Sensitivity (Mean Deviation - MD in dB)

Mean change from the reference value in 30-2 SITA mean deviation, which was generated using the University of Iowa Visual Field Reading Center (VFRC) normative database and the Humphrey Field Analyzer (HFA) normative database. The reference value was defined as the average of the assessments performed at Visits 1 (baseline), 2 and 3 (first month of dosing). The mean change from the reference value are presented for Months 3, 6, 9 and 12. A negative change from the reference value indicates a decrease in the central visual field. (NCT01278173)
Timeframe: Baseline (Month 0), Month 3, Month 6, Month 9, Month 12

InterventiondB (Mean)
VFRC database: Left eye, 3 months (N=50)VFRC database: Left eye, 6 months (N=45)VFRC database: Left eye, 9 months (N=39)VFRC database: Left eye, 12 months (N=36)VFRC database: Right eye, 3 months (N=50)VFRC database: Right eye, 6 months (N=45)VFRC database: Right eye, 9 months (N=39)VFRC database: Right eye, 12 months (N=36)HFA database: Left eye, 3 months (N=51)HFA database: Left eye, 6 months (N=45)HFA database: Left eye, 9 months (N=40)HFA database: Left eye, 12 months (N=37)HFA database: Right eye, 3 months (N=51)HFA database: Right eye, 6 months (N=45)HFA database: Right eye, 9 months (N=40)HFA database: Right eye, 12 months (N=37)
Sabril-0.28-0.24-0.14-0.130.08-0.110.02-0.27-0.32-0.37-0.33-0.150.00-0.23-0.07-0.47

[back to top]

Abstinence

The number of subjects in each treatment group who are cocaine abstinent during the last 2 weeks of the Treatment Phase (Weeks 8 and 9). (NCT01281202)
Timeframe: Weeks 8-9

Interventionparticipants (Number)
CPP-109 Vigabatrin Tablets5
Matching Placebo9

[back to top]

Number of Participants With Cocaine Use

(NCT01281202)
Timeframe: Week 3 - 9

,
Interventionparticipants (Number)
Week 3Week 4Week 5Week 6Week 7Week 8Week 9
CPP-109 Vigabatrin Tablets95918886848381
Placebo96959390858281

[back to top]

Cocaine Withdrawal Severity

Measure of cocaine withdrawal severity will include Cocaine Selective Severity Assessment scores. Minimum score is 0 Maximum score is 119 Higher score is indicative of worse cocaine withdrawal symptoms. (NCT01335867)
Timeframe: 8 weeks

Interventionscore on a scale (Mean)
Vigabatrin8.0
Placebo6.5

[back to top]

Disease Severity and Improvement

Number of subjects in each group rated as improved or very much improved at the end of the trial (NCT01335867)
Timeframe: 8 weeks

InterventionParticipants (Count of Participants)
Vigabatrin5
Placebo2

[back to top]

Measures of Cocaine Craving

Measures of cocaine craving at the end of the trial will be measured using the Brief Substance Craving Ccale. Craving intensity + Craving frequency + Craving Duration each measured on a 4 point scale. Sum of the three scales was overall craving composite. Higher numbers meaning greater craving. Maximum score 12 minimum 0. (NCT01335867)
Timeframe: 8 weeks

Interventionscore on a scale (Mean)
Vigabatrin1.44
Placebo0.38

[back to top]

Number of Participants With a Reduction in Cocaine Use

The primary outcome measure for reduction in cocaine use will be the number of benzoylecgonine (BE) negative urine samples. The main outcome is the number of participants in each group who reported all BE negative urine samples in the last three weeks of the trial. (NCT01335867)
Timeframe: last 3 weeks of the trial

Interventionparticipants (Number)
Vigabatrin0
Placebo2

[back to top]

Proportion of Heavy Drinking Days

The primary outcome measure for reduction in alcohol use will be recorded using the Timeline Followback method. (NCT01335867)
Timeframe: 8 weeks

Interventionproportion of heavy drinking days (Mean)
Vigabatrin.26
Placebo.20

[back to top]

Global Severity Score on the Y-GTSS

The Global Severity score is the sum of the Total Tic score and the TD Impairment score. It is rated by the Investigator on the Yale Global Tic Severity Score ( Y-GTSS, a widely accepted measure of drug efficacy in TD. Scale from 0- 100. Higher score indicates more impairment. (NCT01585207)
Timeframe: weekly from baseline to end of study (10weeks)

Interventionunits on a scale (Mean)
BaselineWeek 0Week 1Week 2Week 3Week 4Week 6Week 8Week 10
Vigabatrin80.2578.756169.75615958.7560.8870.33

[back to top]