Neuroprotective agent improves outcome after ischemic stroke
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The first neuroprotective agent to show positive results in a phase 3 trial significantly reduces disability after ischemic stroke, according to results of the Stroke-Acute Ischemic NXY Treatment (SAINT I) trial published in the February 9, 2006 issue of The New England Journal of Medicine.
The trial involved 1,699 patients with acute ischemic stroke randomly assigned to receive either a 72-hour infusion of NXY-059 (AstraZeneca, Wilmington, DE) or placebo within six hours of the onset of ischemic stroke. The primary endpoint was disability at 90 days as measured by the Rankin scale, with 0 meaning no residual disability and 5 indicating bedbound and requiring constant care.
Dr. James Grotta, of the University of Texas at Houston, and his fellow SAINT I investigators report that disability was significantly reduced in the treatment arm at 90 days. The odds ratio for improvement was 1.20 across all categories of the Rankin scale.
However, mortality and rates of serious and non-serious adverse events were similar in both arms of the study. Active treatment did not result in improvements in neurological function compared with placebo. The subset of patients who also received alteplase had a lower incidence of intracranial hemorrhage.
“Neuroprotective drugs don’t do anything to the artery with regards to recanalization or increased flow,” Dr. Grotta told Reuters Health. “The mechanism of action is to correct imbalances at the cellular level that result from the blockage.” The drug soaks up free radicals.
Dr. Grotta said that SAINT II, involving 3,200 patients, is ongoing to confirm the SAINT I results. Results of SAINT II are expected in 2007. “If the results are positive, then we can expect FDA approval,” Dr. Grotta remarked.
Editorialist Dr. Gregory del Zoppa cautions that while promising, the results with NXY-059 might not yield a significant benefit in the bigger picture of ischemic stroke. He writes “effective strategies for ischemic stroke may need to provide protection to the entire neurovascular unit,” rather than reducing neuronal cell damage alone.
N Engl J Med 2006;354:588-600.
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