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Positive Data on AEOL 11207 in Pre-Clinical Epilepsy Model

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Aeolus Pharmaceuticals, Inc. announced the publication of data on AEOL 11207 in epilepsy in Neurobiology of Disease. The article, titled "Mitochondrial oxidative stress and epilepsy in SOD2 deficient mice: Attenuation by a 2 lipophilic metalloporphyrin," was authored by Li-Ping Liang, Simon Waldbaum, Shane Rowley, Ting-Ting Huang, Brian J. Day and Manisha Patel, of the University of Colorado, National Jewish Health, Stanford University and the VA Palo Alto Health Care System, and was sponsored by a grant from the National Institutes for Health (NIH) and the CURE Foundation.

Epileptic seizures are a common feature associated with inherited mitochondrial diseases. The study investigated the role of mitochondrial oxidative stress in epilepsy resulting from mitochondrial dysfunction using cross-bred mutant mice lacking mitochondrial manganese superoxide dismutase (MnSOD or SOD2) and a lipophilic metalloporphyrin catalytic antioxidant.

AEOL11207 treated Sod2 -/- mice showed a decrease in the average number and duration of spontaneous behavioral seizures based on daily observation from 17 to 20 days old compare to vehicle treated Sod2 -/- mice. Only 60% of AEOL 11207-treated Sod2 -/- mice exhibited spontaneous seizure activity compared to 100% of vehicle-treated Sod2 -/- mice. Seizures from AEOL11207- treated Sod2 -/- mice occurred less frequently and had shorter duration as compared to vehicle-treated Sod2 -/- mice. Furthermore, the continuous seizure event those last longer than 60 s was not observed in AEOL 11207 treated Sod2 -/- mice. The AEOL 11207 group showed no detectable adverse events up to 20 days of treatment and no mortality resulting from treatment. No differences were observed in seizure severity between vehicle and AEOL 11207-treated Sod2 -/- mice.

The occurrence of epileptic seizures in Sod2 42 -/- mice and the ability of catalytic antioxidant therapy to attenuate seizure activity, mitochondrial dysfunction, and ATP levels suggest that ongoing mitochondrial oxidative stress can contribute to epilepsy associated with mitochondrial dysfunction and disease. Removal of reactive oxygen species (ROS) with catalytic antioxidants, such as AEOL 11207, may provide new therapeutic strategies for epilepsy and other pathological manifestations of mitochondrial diseases. The data from these studies suggests potential implications for inherited mitochondrial disorders resulting in epilepsy such as mitochondrial encephalopathy with ragged red fibers (MERRF), mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) and other metabolic disorders associated with seizures. Aeolus' compounds, including AEOL 11207, contain a manganese center that is capable of detoxifying a wide range of ROS and lipid peroxide radicals. AEOL11207 has potent H2O2 scavenging activity and is a potent inhibitor of mitochondrial ROS production.

"This study is an important step in confirming the role of oxidative stress in epilepsy and the potential role of AEOL 11207 as an effective treatment," stated Brian Day, PhD, Chief Science Officer of Aeolus Pharmaceuticals, Inc. "We look forward to continuing research in this important area of medicine."