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Figure 1. Ischemic pathways that result in the formation of free radicals.
(Figure omitted. See article PDF.)
Figure 2. NXY-059 & formation of nonreactive spin adduct upon reaction with a free radical. R** : Free radical.
(Figure omitted. See article PDF.)
Figure 3. Neuroprotective effect of NXY-059 in rats, following either transient or permanent middle cerebral artery occlusion. (A) Control and NXY-treated rats were subjected to 2 h of middle cerebral artery occlusion (MCAO), treated 90 min following reperfusion and 48 h after recirculation. Histological damage was assessed in terms of infarct volume. The plasma free concentration was calculated using the derived data from the NXY-059 10-mg/kg/h dose.
(B) The percentage reduction of infarct volume by NXY-059 treatment is plotted versus the corresponding unbound plasma concentration in rats, 24 h following permanent MCAO and infusion of NXY-059. Reproduced from [22].
(Figure omitted. See article PDF.)
Figure 4. Therapeutic time-window of NXY-059 following either transient or permanent middle cerebral artery occlusion in rats. Temporary middle cerebral artery occlusion (MCAO) in rats was carried out for 2 h, infusion of NXY-059 30 mg/kg/h was initiated at different time points (triangle points), following reperfusion, and histological damage was determined 48 h after recirculation. Rats subjected to permanent MCAO were administered with 50 mg/kg/h of NXY-059 at various time points (square points) and infarct volume was measured 24 h, following occlusion (*p < 0.05). Data were recalculated from [20,22].
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Figure 5. Modified Rankin scale scores at 90 days, after stroke onset. (A) Results from the SAINT-I study with p = 0.038 calculated in favor of NXY-059 treatment versus placebo for the primary outcome. (B) Results from the SAINT-II study, indicating no significant differences in the distribution of the modified Rankin Scale for the NXY-059 compared with the placebo group. (A) was reproduced from [3] and (B) from [4].
(Figure omitted. See article PDF.)
Stroke is the second biggest cause of death in the industrialized world and the primary cause of disability. Current pharmacological treatment is limited to thrombolysis using recombinant tissue plasminogen activator (t-PA) [1]. The main drawbacks of thrombolysis are its limited availability to stroke patients, the short therapeutic time-window of 3 h following stroke onset and, critically, the associated risk...