Product Data?SheetEthosuximideCat. No.:CAS No.:分?式:分?量:作?靶点:作?通路:储存?式:HY-B137877-67-8C?H??NO?141.17Calcium ChannelMembrane Transporter/Ion Channel; Neuronal SignalingPowderIn solvent-20°C4°C-80°C-20°C3 years2 years6 months1 monthInhibitors?Agonists?Screening Libraries溶解性数据体外实验DMSO : ≥ 125 mg/mL (885.46 mM)* \Mass1 mg5 mg10 mgSolventConcentration制备储备液1 mM5 mM10 mM7.0837 mL1.4167 mL0.7084 mL35.4183 mL7.0837 mL3.5418 mL70.8366 mL14.1673 mL7.0837 mL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；?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?式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个?内使?，-20°C 储存时，请在 1 个?内使?。体内实验请根据您的实验动物和给药?式选择适当的溶解?案。以下溶解?案都请先按照 In Vitro ?式配制澄清的储备液，再依次添加助溶剂： 为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的?作液，建议您现?现配，当天使?； 以下溶剂前显?的百分?是指该溶剂在您配制终溶液中的体积占?；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的?式助溶1. 请依序添加每种溶剂：?10% DMSO ?? 40% PEG300 ?? 5% Tween-80 ?? 45% salineSolubility: ≥ 2.08 mg/mL (14.73 mM); Clear solution此?案可获得 ≥ 2.08 mg/mL (14.73 mM，饱和度未知) 的澄清溶液。 以 1 mL ?作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加? 50 μL Tween-80，混合均匀；然后继续加? 450 μL ?理盐?定容? 1 mL。2. 请依序添加每种溶剂：?10% DMSO ?? 90% (20% SBE-β-CD in saline)Solubility: ≥ 2.08 mg/mL (14.73 mM); Clear solutionPage 1 of 2 www.MedChemExpress.cn
此?案可获得 ≥ 2.08 mg/mL (14.73 mM，饱和度未知) 的澄清溶液。
以 1 mL ?作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD ?理盐??溶液中，混合均匀。
3. 请依序添加每种溶剂：?10% DMSO ?? 90% corn oilSolubility: ≥ 2.08 mg/mL (14.73 mM); Clear solution
此?案可获得 ≥ 2.08 mg/mL (14.73 mM，饱和度未知) 的澄清溶液，此?案不适?于实验周期在半个?以上的实验。 以 1 mL ?作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL ??油中，混合均匀。
BIOLOGICAL ACTIVITY
?物活性
Ethosuximide 是?种?泛使?的抗癫痫药物，可改善多种神经退?性疾病模型的表型，且可阻断低电压激活的 T 型钙通道。
IC?? & Target体外研究
calcium channel[1]
The efficacy of Ethosuximide in generalized absence epilepsy is thought to be due to blockade of the low voltage activated T-type calcium channel. There is no reduction in total Tau levels in Ethosuximide treated Tau transgenic worms as compare to vehicle controls. The rescuing effect of Ethosuximide is therefore not due to transgene
suppression or reduced expression of toxic mutant Tau protein. Quantification of the amount of soluble and insoluble (RIPA-extractable) Tau relative to total Tau levels reveals a significant reduction in aberrantly-folded, insoluble Tau and a corresponding increase in soluble Tau in Ethosuximide-treated compare with untreated worms[1].
Concentrations of 2 μM or more of Ethosuximide not only are found to be less effective than 1 μM concentration of Ethosuximide, but also induce cell toxicity. GABA staining immuno?uorescence images show that after treatment with Ethosuximide, GABA positive neuron increases by 3 and 6.5 fold for concentrations of 0.1 and 1 μM, respectively. BrdU staining shows nuclei proliferation after 2 to 3 days of Ethosuximide exposure. The mean of nuclei is 15.98±0.41 for the low concentration of Ethosuximide while it is 25.27±0.48 for the high concentration after Brdu staining. This number is 11.05±0.2 for lithium chloride[2].
PROTOCOL
Kinase Assay [1]
Vehicle- and Ethosuximide-treated Tau V337M worms are lysed and separated into soluble and insoluble fractions. Fractions are separated by SDS-PAGE and western blotted using anti-human Tau T46 and anti-actin antibodies. The abundance of Tau protein in each fraction is quantified by densitometry and normalized against beta-actin. Total Tau levels in lysates are expressed as the percentage of actin-normalized Tau relative to vehicle control lysates; Tau levels in sequentially extracted fractions are expressed as the percentage of actin-normalized Tau relative to the sum of both fractions (soluble+RIPA) combined[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay
Neuronal stem cells from the forebrain Cortex of a 3-day-old rat are used in this study. The cells are differentiated by withdrawal of basic ?broblastic growth factor (bFGF) and exposed to Ethosuximide at two concentrations of 0.1 μM and 1 μM. Before drug treatment, the cells are rinsed once with PBS, and the medium is replaced with fresh, bFGF-free DMEM/F12 medium containing different concentration of Ethosuximide. Medium exchange is done every day for 6 days with medium containing Ethosuximide. Then, cells are ?xed for immunocytochemistry[2].MCE has not independently confirmed the accuracy of these methods. They are for reference only.
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REFERENCES
[1].?Chen X, et al. Ethosuximide ameliorates neurodegenerative disease phenotypes by modulating DAF-16/FOXO target gene expression. Mol Neurodegener. 2015 Sep 29;10:51.
[2].?Sondossi K, et al. Analysis of the antiepileptic, ethosuximide impacts on neurogenesis of rat forebrain stem cells. Fundam Clin Pharmacol. 2014 Oct;28(5):512-8.
McePdfHeightCaution: Product has not been fully validated for medical applications. For research use only.
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