Six years after Eisai and University College London teamed up to discover new treatments for neurological diseases, they are moving their first candidate into the clinic: a tau-targeting monoclonal antibody for Alzheimer’s disease. The duo are also reupping their alliance for another five years.
Under the initial agreement, inked in 2012, Eisai and UCL researchers worked together to discover and develop new targets and drugs for diseases such as Alzheimer’s, Parkinson’s and other related disorders. The partnership survived a 2013 R&D cull, even as the Japanese pharma laid off 130 employees around the world and eliminated medicinal chemistry at its U.K. R&D site.
Their anti-tau candidate, dubbed E2814, is designed to delay progression of Alzheimer’s and other tauopathies, or conditions in which tau proteins aggregate in the brain, including progressive supranuclear palsy, corticobasal degeneration and Pick disease. The partners plan to start phase 1 trials within Eisai’s fiscal 2018, which ends March 31, 2019.
E2814 is designed to stop tau tangles from spreading to different areas of the brain by targeting tau “seeds,” or “specially shaped tau aggregates that have the ability to transfer between cells and spread,” Eisai said in a statement. The hope is that preventing further buildup of the protein may slow disease progression.
“By combining the knowledge of UCL, which conducts world-class research into neurodegenerative disorders and is the operational hub of the UK Dementia Research Institute, together with the knowledge of Eisai, who possesses a rich pipeline for dementia treatments, we are doing our utmost to link the results of joint research starting with E2814 to new medicines in order to contribute to patients who are awaiting curative therapies as soon as possible,” said Teiji Kimura, chief discovery officer of Eisai’s neurology unit, in the statement.
Eisai and UCL, along with numerous other players, are working in an area that has not seen a new treatment approved in more than 15 years. Much of Alzheimer’s research has focused on amyloid plaques forming in the brain and triggering cognitive decline and the destruction of brain cells. But a series of failures of amyloid-targeting drugs—including Eisai and Biogen’s BACE inhibitor, which reduced plaques but failed to improve symptoms—suggest that Alzheimer’s research sorely needs new approaches.
Researchers are working on alternative hypotheses, including one linking the amount of herpes virus in a person's brain to the presence of Alzheimer's markers. But, as a Stat News article pointed out in October, the amyloid hypothesis remains entrenched, and academics pursuing new approaches often struggle to obtain funding and get their work published.