NXY-059

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].

Signaling Pathways >> Others >> Others

Research Areas >> Neurological Disease

[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.

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