Vigabatrin
(Synonyms: 氨己烯酸; γ-Vinyl-GABA) 目录号 : GC37905
Inhibitor of GABA transaminase
Cas No.:68506-86-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Vigabatrin is an irreversible GABA transaminase (GABA-T) inhibitor.1 It inhibits rat brain GABA-T when used at a concentration of 0.1 mM. Vigabatrin is selective for rat brain GABA-T over P. fluorescens GABA-T at 10 mM and is 100-fold selective over rat brain glutamic acid decarboxylase (GAD). Vigabatrin (1,500 mg/kg) decreases brain GABA-T activity without affecting GAD activity in mice.2 It reduces the incidence of myoclonus in a mouse model of audiogenic seizures.3 Vigabatrin also increases the electroconvulsive threshold in mouse model of maximal electroshock-induced seizures and reduces the number of clonic convulsions induced by pentylenetetrazol in mice.4 Formulations containing vigabatrin have been used in the treatment of seizures and infantile spasms.
1.Lippert, B., Metcalf, B.W., Jung, M.J., et al.4-Amino-hex-5-enoic acid, a selective catalytic inhibitor of 4-aminobutyric-acid aminotransferase in mammalian brainEur. J. Biochem.74(3)441-445(1977) 2.Jung, M.J., Lippert, B., Metcalf, B.W., et al.g-Vinyl GABA (4-amino-hex-5-enoic acid), A new selective irreversible inhibitor of GABA-T: Effects on brain GABA metabolism in miceJ. Neurochem.29(5)797-802(1977) 3.Meldrum, B.S., and Murugaiah, K.Anticonvulsant action in mice with sound-induced seizures of the optical isomers of g-vinyl GABAEur. J. Pharm.89(1-2)149-152(1983) 4.Luszczki, J.J., and Czuczwar, S.J.Isobolographic characterization of interactions between vigabatrin and tiagabine in two experimental models of epilepsyProg. Neuropsychopharmacol. Biol. Psychiatry31(2)529-538(2007)
| Cas No. | 68506-86-5 | SDF | |
| 别名 | 氨己烯酸; γ-Vinyl-GABA | ||
| 化学名 | 4-amino-5-hexenoic acid | ||
| Canonical SMILES | C=CC(N)CCC(O)=O | ||
| 分子式 | C6H11NO2 | 分子量 | 129.16 |
| 溶解度 | 10mg/mL in PBS, pH 7.2 | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 7.7423 mL | 38.7117 mL | 77.4234 mL |
| 5 mM | 1.5485 mL | 7.7423 mL | 15.4847 mL |
| 10 mM | 0.7742 mL | 3.8712 mL | 7.7423 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Vigabatrin - new data on indications and safety in paediatric epilepsy
Neurol Neurochir Pol 2021;55(5):429-439.PMID:34541635DOI:10.5603/PJNNS.a2021.0063.
Introduction: Vigabatrin (VGB), a second-generation antiepileptic drug, is effective for the treatment of infantile spasms and focal seizures, primarily in tuberous sclerosis complex (TSC) patients. 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. Aim of the study: The goal of this review was to summarise the recent therapeutic guidelines, the use of VGB in focal seizures and new VGB applications as a disease-modifying treatment in TSC patients. Moreover, we discuss the current opinions on potential VGB-associated toxicity and the safety of VGB.
Vigabatrin
Neurotherapeutics 2007 Jan;4(1):163-72.PMID:17199033DOI:10.1016/j.nurt.2006.11.008.
Refractory epilepsies such as infantile spasms (IS) and complex partial seizures (CPS) can have a severe negative impact on the neurological integrity and quality of life of affected patients, in addition to drastically increasing their risk of premature mortality. Early identification of potentially effective pharmacotherapy agents is important. 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. A bilateral, concentric constriction of the peripheral visual field characterizes the visual field defect (VFD) associated with Vigabatrin, well characterized by numerous studies. This peripheral VFD presents in 30-50% of patients with exposure of several years; however, most of these patients are asymptomatic. In well-controlled studies, the earliest onset in patients with CPS is 11 months and at 5 months in infants, with average onsets being more than 5 years and 1 year, respectively. Patients with a peripheral VFD retain an average 65 degrees of lateral vision (normal, 90 degrees). The fact that many patients never develop the vigabatrin-related peripheral VFD, despite long-term exposure at high doses, may support the hypothesis that the injury is an idiosyncratic adverse drug reaction (as opposed to a strict dose- or duration-dependent toxicity). Effective testing methods are available to aid in the early detection and management of the peripheral VFD. This article discusses issues of importance to clinical decision-making in the use of Vigabatrin to assist the physician and patient in assessing the benefits of Vigabatrin therapy and understanding the potential risks of the VFD and uncontrolled seizures.
Vigabatrin
Epilepsia 1999;40 Suppl 5:S11-6.PMID:10530689DOI:10.1111/j.1528-1157.1999.tb00914.x.
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. This produces an increase in central nervous system (CNS) GABA levels. VGB is among the few antiepileptic drugs (AEDs) that was synthesized with a specific targeted mechanism in mind and was subsequently demonstrated to function by that mechanism. Tiagabine, a GABA reuptake blocker, is the only other "designer drug" among the currently available AEDs. Therefore, VGB is among the few AEDs for which the mechanism of action is well understood. Recently, safety issues have been raised with regard to the use of Vigabatrin. This article reviews the mechanism of action, pharmacokinetics, safety, and efficacy of VGB.
Vigabatrin: Lessons Learned From the United States Experience
J Neuroophthalmol 2018 Dec;38(4):442-450.PMID:29280765DOI:10.1097/WNO.0000000000000609.
Vigabatrin was introduced as an antiseizure medication in the United Kingdom in 1989 and was extensively used until 1997 when concerns arose regarding peripheral visual field loss. When the drug was approved in the United States in 2009, it carried a black box warning for the risk of permanent visual loss, and the pharmaceutical company was mandated to create a drug registry to assess for visual deficits. 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. The Vigabatrin vision study, a prospective, longitudinal, single-arm, open-label study, confirmed that adult patients with refractory complex partial seizures had a large number of visual deficits at baseline. An unexpected finding during the first year of therapy with Vigabatrin was an increase in retinal thickness on optical coherence tomography. The experience from Vigabatrin in the United States emphasizes the importance of baseline eye findings when considering the potential of drug toxicity involving the visual pathways.
Vigabatrin for infantile spasms
Pharmacotherapy 2011 Mar;31(3):298-311.PMID:21361740DOI:10.1592/phco.31.3.298.
Infantile spasms describe a pediatric epilepsy syndrome characterized by frequent clusters of brief symmetric muscle contractions; the condition is often associated with developmental delay. When infantile spasms are accompanied by hypsarrhythmia on electroencephalogram, the condition is labeled West syndrome. The mainstay of treatment for infantile spasms is adrenocorticotropic hormone; however, Vigabatrin, a vinyl derivative of γ-aminobutyric acid, has been used for the treatment of infantile spasms in Europe since 1989. In 2009, Vigabatrin was approved by the United States Food and Drug Adminstration (FDA) for use as monotherapy in the treatment of infantile spasms in patients aged 1 month-2 years when the benefits of treatment outweigh the risks. Results from numerous trials examining the role of Vigabatrin in infantile spasms have been published; many of these trials were small, open-label, or noncontrolled. Although clinical trials have provided some insight into the utility of Vigabatrin for the treatment of infantile spasms, these studies have notable limitations. In addition, Vigabatrin is associated with a black-box warning that describes the potential for permanent bilateral concentric visual field defects. Currently, Vigabatrin is available through a manufacturer-sponsored program in accordance with its FDA-approved Risk Evaluation and Mitigation Strategy. Although several guidelines recommend Vigabatrin as a first-line therapy for infantile spasms, specifically infantile spasms related to tuberous sclerosis, it is still unclear whether Vigabatrin should supersede hormone therapy as first-line therapy. Further research comparing the two therapies is needed.