Eisai Co., Ltd. (Headquarters: Tokyo, CEO: Haruo Naito, “Eisai”) announced today further details of the options that it has as part of the agreement to jointly develop and commercialize its investigational next generation Alzheimer's disease (AD) treatment candidates E2609, a BACE inhibitor, and BAN2401, an anti-amyloid beta (Aβ ) protofibril antibody, with Biogen Idec (Headquarters: Massachusetts, the United States, CEO: George A. Scangos), which was initially announced on March 5, 2014 (“Collaboration Agreement”). This notice is made to coincide with the annual report (10-K) publicly disclosed by Biogen Idec on February 4 (EST).
Based on the Collaboration Agreement, Eisai will serve as the operational and regulatory lead in the co-development of E2609 and BAN2401 and will pursue marketing authorizations for both compounds worldwide. The companies will also co-promote the products following marketing approval in major markets such as the United States, the European Union and Japan (“Co-promotion Territory”). Both companies will cover an equal share of the overall costs, including research and development expenses, with Eisai booking all sales for E2609 and BAN2401 and the profits to be split equally between the companies. As financial consideration of this Collaboration Agreement, Eisai has received payments upfront and will receive development, approval and commercial milestone payments as well. For any regions outside the Co-promotion Territory, Eisai will exclusively commercialize the products and pay royalties to Biogen Idec.
Meanwhile, regarding the anti-amyloid beta antibody BIIB037 and an anti-tau monoclonal antibody being developed by Biogen Idec as anti-AD treatments, Eisai also holds options to jointly develop and commercialize these products. If Eisai exercises either or both of the options, separate collaboration agreements will be made with Biogen Idec on terms and conditions that mirror the above-mentioned Collaboration Agreement. The options held by Eisai regarding BIIB037 and the anti-tau antibody are as follows:
How this therapy could help:
The memory loss and functional decline of AD have been linked to abnormal protein deposits that build up in the brain. Among those proteins are amyloid and tau. Deposits of abnormal tau, so-called neurofibrillary tangles, form in the neurons and are linked to increasing impairment and loss of brain cells associated both with AD and with other neurodegenerative diseases, known as tauopathies, such as progressive supranuclear palsy and frontotemporal dementia. BIIB092 is an antibody targeting extracellular tau and may reduce the spreading of tau from one cell to the next, potentially slowing the progress of the disease.