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Axerion, AstraZeneca collaborate on biologic treatment approach for Alzheimer’s

Wednesday, May 2, 2012

Axerion Therapeutics, a private Connecticut-based biotech, and MedImmune, the global biologics arm of AstraZeneca, have entered into a research collaboration and sublicense arrangement to develop and commercialize a biologic approach for the treatment of Alzheimer’s disease.

The agreement with Axerion is the first collaboration signed within the new neuroscience innovative medicines unit that AstraZeneca announced in February 2012. Under this model, AstraZeneca and MedImmune will conduct neuroscience discovery research and early development for small and large molecules by tapping into the best available external science and sharing cost, risk and reward with other research partners active in psychiatry, neurology and pain research.

Axerion has granted the AstraZeneca neuroscience innovative medicines unit an exclusive sublicense to research, develop and commercialize a pre-clinical biologic that targets the binding of A-beta oligimers to prion proteins. In exchange, the AstraZeneca’s unit will provide Axerion with certain upfront and milestone payments, plus R&D funding during the time both companies are working together on the program. Additionally, Axerion will earn royalties on product sales. The financial terms of the deal have not been disclosed.

“We are confident that this collaboration will accelerate the development of an urgently needed therapy for Alzheimer’s disease,” said Sylvia McBrinn, CEO of Axerion. “It is our hope that this collaboration will advance a novel therapy that works quite differently from the Alzheimer’s drug candidates currently in development.”

The two companies will collaborate to develop a biologic approach that blocks the toxic effects of amyloid-beta (A-beta) mediated through binding of A-beta oligomers to cellular prion protein in the brain. This drug development effort will build on published preclinical results which demonstrate that cellular prion protein mediates A-beta oligomer induced memory dysfunction and synaptic toxicity, and that inhibition of this interaction can have favorable therapeutic effects in models of Alzheimer’s disease. Directly targeting toxic A-beta oligomer binding has the potential to provide superior safety and efficacy versus agents that affect amyloid processing or clearance.

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