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Treatment with XPro1595, a selective inhibitor of solTNF that crosses the intact blood-brain barrier (BBB), in cuprizone-fed mice did not prevent toxin-induced oligodendrocyte loss and demyelination, but it permitted profound early remyelination due to improved phagocytosis of myelin debris by CNS macrophages and prevented disease-associated decline in motor performance

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The absence of serious adverse events across varied doses, administration routes, and treatment durations represents a key safety finding that distinguishes AOD-9604s clinical profile

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Exogenous antioxidantsDouble-edged swords in cellular redox state: Health beneficial effects at physiologic doses versus deleterious effects at high doses