Lilly and AZ begin new Alzheimer’s tie-up
Eli Lilly and AstraZeneca (AZ) have said they are to co-develop a potentially disease-modifying treatment for Alzheimer’s disease (AD), in the aftermath of the high-profile failure of a Lilly dementia drug last month.
The companies will develop MEDI1814, an antibody selective for amyloid-beta 42 (Aβ42), which is in phase 1 trials, building on an existing collaboration related to AZD3293, a BACE inhibitor in two pivotal phase 3 trials.
The build-up of plaques in the brain containing the peptide amyloid-beta is one of the characteristics of AD. MEDI1814 binds selectively to Aβ42, a form of amyloid-beta which is particularly associated with the disease. Binding dose-dependently reduces levels of this peptide, potentially slowing disease progression.
Jan Lundberg, executive vice president of science and technology and president of Lilly Research Laboratories, said: “We are pleased to be expanding our alliance with AstraZeneca to further build our pipeline of potential medicines and diagnostic agents. AstraZeneca brings capabilities and expertise and most importantly shares our passion to bring new medicines to patients suffering from this debilitating illness.”
Mene Pangalos, executive vice president, IMED Biotech Unit and Business Development, AZ, added: “MEDI1814 has a unique mechanism among antibodies in clinical development and could provide a distinct approach to treating Alzheimer’s disease.”
Lilly will make a $30 million upfront payment to AZ, which it will charge to earnings in Q4 2016.
Details emerge about solanezumab failure in Alzheimer’s
The companies made the announcement as Lilly revealed further details about the failure of its solanezumab in the phase 3 EXPEDITION3 trial at the Clinical Trials on Alzheimer’s Disease meeting.
Lilly has abandoned plans to file solanezumab, and is winding up long-term trials.
The drug had already failed in two phase 3 trials in 2012 – but Lilly pressed on with a third trial in mild Alzheimer’s after spotting a trend in the data suggesting an effect in a small group of patients in the early stages of the disease.
But, as announced last month, solanezumab did not produce a statistically significant effect in EXPEDITION3, which had a much larger group of patients with mild disease.
Changes in amyloid plaques measured by positron emission tomography imaging did not reach statistical significance between treatment and placebo groups, showing the drug had failed to slow the build-up of the plaques as much as was hoped.
Patients did not experience a statistically significant slowing in cognitive decline compared with patients treated with placebo – the trial’s primary endpoint.
The 11% reduction in decline, as measured by a test measuring cognitive functions, including memory, attention and language abilities, did not produce a p-value showing statistical significance.
Solanezumab did produce a statistically significant effect compared with placebo in secondary endpoints – although these figures were not adjusted for multiple comparisons as the trial failed to meet its main goal.
The secondary endpoints were measured by a mini mental state examination, semi-structured interviews and a scale measuring performance in everyday activities, such as conversation, preparing a meal, or shopping.
A different functional ability questionnaire did not show a statistically significant difference in the arm receiving solanezumab compared with placebo.
The solanezumab failure means Biogen is now a leader in the hunt for a new treatment with its aducanumab, which is in phase 3 development.
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