AstraZeneca, Eli Lilly reach deal to co-develop amyloid-beta antibody MEDI1814 for Alzheimer's disease

AstraZeneca and Eli Lilly on Friday unveiled a global agreement to jointly develop the investigational selective amyloid-beta 42 antibody MEDI1814, which is currently in Phase I trials for the treatment of Alzheimer's disease. The deal builds on the companies' existing collaboration to develop the oral BACE inhibitor AZD3293, which is in late-stage testing for patients with early Alzheimer's disease. Mene Pangalos, executive vice president of AstraZeneca's IMED Biotech Unit, remarked that "MEDI1814 has a unique mechanism among antibodies in clinical development and could provide a distinct approach to treating Alzheimer's disease." 

According to the companies, amyloid-beta 42 is "a form of amyloid-beta that is particularly associated" with Alzheimer's disease, and that "binding dose-dependently reduces levels of this peptide, potentially slowing the progression." Under the terms of the agreement, Eli Lilly will make an upfront payment of $30 million to AstraZeneca, which the US drugmaker plans to record as a charge in the current quarter. Other financial terms of the agreement were not divulged. 

The agreement follows the recent failure of Eli Lilly's experimental anti-amyloid therapy solanezumab, which did not significantly slow the progression of cognitive decline versus placebo in the late-stage EXPEDITION3 study of patients with mild dementia due to Alzheimer's disease. Eric Siemers, distinguished medical fellow at Eli Lilly, said the EXPEDTION3 data are "without question disappointing," but the company "will continue to analyse study results and work with the external scientific community in the hopes of uncovering findings that will help shape and advance future Alzheimer's disease research."

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Meanwhile, other drugmakers have expressed confidence in their own Alzheimer's disease therapy programmes in the wake of Eli Lilly's setback with solanezumab. Last month, Merck & Co. revealed early-stage results showing that its investigational BACE1 inhibitor verubecestat lowered amyloid-beta plaque levels in patients with Alzheimer's disease, while recent leaked data from a Phase I study of Biogen's aducanumab suggested the experimental Alzheimer's disease drug was associated with significant reductions in amyloid beta plaque versus placebo in certain patients with prodromal or mild Alzheimer's disease.

For related analysis, read ViewPoints: Heads I win, tails you lose – solanezumab's near-miss seen as ideal result for others. See also Spotlight On: Solanezumab's near-miss could turn out to be worst-case-scenario for sector.

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