Superoxide dismutase mimetics

Increased oxidative burden contributes to the pathophysiology of ALS with advanced glycation end-products, markers of lipid peroxidation (4-hydroxy-2-nonenal-histidine, crotonaldehyde-lysine), and markers of protein glycooxidation localized to motor neurons of ALS patients. A number of free radicals, including superoxide and nitric oxide, likely cause damage to motor neurons via the formation of peroxynitrite and subsequent nitration of tyrosine residues on proteins (e.g., neurofilaments), which are central to neuronal function. Spinal cord tissue from ALS patients has increased levels of 3-nitrotyrosine and 3-nitro-4-hydroxyphenylacetic acid, both products formed through the action of peroxynitrite.

EUK-8 94 and EUK-134 95 demonstrated a benefit in the ALS mouse model. Given prophylactically, they delayed disease onset.107 AEOL-10150 96 is a manganese porphryrin catalytic antioxidant that decomposes biological oxidants such as peroxinitrite via its ability to cycle between Mn(III) and Mn(Iv) states, and may reduce the oxidative burden. In a transgenic mouse model of ALS (SOD-1 (G93A)), AEOL-10150 improved motor activity of mice and resulted in an approximately 30-day increase in the mean survival age.108

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