CAS NO: | 168021-79-2 |
包装 | 价格(元) |
10mg | 电议 |
50mg | 电议 |
200mg | 电议 |
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 SMILES | CC(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 tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation 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: |