AbbVie and Mission Therapeutics inked an R&D pact focused on deubiquitylating enzymes (DUBs) in Alzheimer’s and Parkinson’s disease. By targeting these enzymes, the pair hopes to create drugs that attack the buildup of toxic proteins in these neurodegenerative diseases and stop them from getting worse.
Alzheimer’s and Parkinson’s are associated with malfunctioning proteins that fold incorrectly and accumulate in the brain. This buildup is thought to hobble and eventually kill nerve cells in the brain. AbbVie and Cambridge, U.K.-based Mission want to create drugs that modulate DUBs, which are involved in regulating the degradation of these proteins. Boosting degradation will cut protein accumulation and—the hope is—stop or delay disease progression.
While Mission specializes in DUBs and has a handful of programs in preclinical development, none of these will be part of the partnership. AbbBie and Mission will work on new DUB inhibitors through preclinical development, the duo said in a statement. They did not disclose financial details.
Both partners will work to identify DUB targets and discover “suitable compounds.” After that, AbbVie can choose to license up to four assets for development and commercialization. The Big Pharma will be on the hook for an upfront license fee, as well as the usual milestone and royalty payments down the line.
“There is an urgent need for new treatments that will make a positive impact on the lives of patients with Alzheimer’s and Parkinson’s disease. Mission’s scientists have developed impressive early research toward the understanding of these diseases. Together, we will work to advance this early science and develop meaningful therapies,” said James Summers, Ph.D., vice president of neuroscience discovery research at AbbVie.
The deal comes soon after Eli Lilly walked away from a second BACE inhibitor program for Alzheimer’s, joining Janssen, Merck and Roche. This class of drugs, as well as the vast majority of Alzheimer’s work, hinges on the amyloid hypothesis, which asserts that the buildup of amyloid beta proteins in the brain triggers processes that eventually lead to cognitive decline and the destruction of brain cells. However, numerous failures—including the ability of some drugs to reduce amyloid plaques, but not alleviate symptoms—suggest that Alzheimer’s is in grave need of new hypotheses.
Researchers are pursuing 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, the amyloid hypothesis remains entrenched and academics pursuing new approaches often struggle to obtain funding and get their work published.