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NXY-059
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
NXY-059图片
CAS NO:168021-79-2
包装与价格：
包装价格(元)
10mg电议
50mg电议
200mg电议

产品介绍
NXY-059 (NXY-059) 是神经保护自旋陷阱苯基丁硝酮 (PBN) 的二磺酰基衍生物，NXY-059、其母体 PBN 及其水解/氧化产物 MNT 都是非常强大的自由基清除剂。
Cas No.168021-79-2
别名4-[[(1,1-二甲基乙基)氧化亚氨基]甲基]-1,3-苯二磺酸二钠,NXY-059
化学名disodium;4-[(Z)-[tert-butyl(oxido)azaniumylidene]methyl]benzene-1,3-disulfonate
Canonical SMILESCC(C)(C)[N+](=CC1=C(C=C(C=C1)S(=O)(=O)[O-])S(=O)(=O)[O-])[O-].[Na+].[Na+]
分子式C11H13NNa2O7S2
分子量381.33
溶解度DMF: 20 mg/ml,DMSO: 20 mg/ml,Ethanol: 2 mg/ml,PBS (pH 7.2): 10 mg/ml
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

Disufenton sodium (NXY-059) is the disulfonyl derivative of the neuroprotective spin trap phenylbutynitrone(PBN), both NXY-059, its parent PBN and their hydrolysis/oxidation product MNT are very powerful scavengers of free radicals. IC50 value:Target: Neuroprotectantin vitro: Disufenton sodium is more soluble than the spin trapping agent α-phenyl-N-tert-butyl nitrone (PBN) [1]. In an in vitro blood-brain barrier (BBB) model, 250 mM of Disufenton sodium administered at the onset or up to 4 h after oxygen glucose deprivation (OGD) produces a significant reduction in the increased BBB permeability caused by OGD. Furthermore, OGD produces a huge influx of tissue plasminogen activator across the BBB, which is substantially reduced by Disufenton sodium [2]. in vivo: Disufenton sodium reduces infarct volume in rats subjected to 2 hours of middle cerebral artery occlusion in a dose-dependent manner. At equimolar doses (3.0 mg/kg for Disufenton sodium and 1.4 mg/kg for PBN), Disufenton sodium is more efficacious than PBN. Similar results are obtained when a recovery period of 7 days is allowed. The window of therapeutic opportunity for Disufenton sodium is 3 to 6 hours after the start of recirculation [1]. Disufenton sodium, a free radical-trapping agent, has a substantial protective effect, lessening the disability caused by an experimentally induced stroke in a primate species. Disufenton sodium treatment reduces the overall amount of brain damage by >50% of saline-treatment values, with similar levels of protection afforded to both white and gray matter [3].

References:
[1]. Kuroda S, et al. Neuroprotective effects of a novel nitrone, NXY-059, after transient focal cerebral ischemia in the rat. J Cereb Blood Flow Metab, 1999, 19(7), 778-787.
[2]. Marshall JW, et al. NXY-059, a free radical--trapping agent, substantially lessens the functional disability resulting from cerebral ischemia in a primate species. Stroke, 2001, 32(1), 190-198.
[3]. Culot M, et al. Cerebrovascular protection as a possible mechanism for the protective effects of NXY-059 in preclinical models: an in vitro study. Brain Res, 2009, 19(1294), 144-152.