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AbbVie/Alector: Another Alzheimer's Treatment Dumped

 |  By Robin Robinson  
   July 20, 2022

AbbVie quits one of two potential Alzheimer's treatments connected to Alector partnership.

In 2017, AbbVie and Alector joined together to develop and commercialize two therapeutics for Alzheimer’s. After a recent review of AL003, AbbVie has decided to abandon efforts for that drug, but will continue to pursue AL002, which is focused on targeting triggering receptors expressed on myeloid cells 2 (TREM2).

AL002 is an investigational, humanized monoclonal antibody whose role in potentially treating Alzheimer's was first identified in large-scale genome-wide association studies. Researchers found that reducing TREM2's functionality may contribute to AD progression and other types of dementia. By increasing TREM2 in the brain, there may be a way to target multiple pathologies linked to the disorder instead of just focusing on one pathology type.

The role of TREM2 in Alzheimer's treatment has been studied for many years.  In 2021, AL002 became the first product candidate to reach Phase 2 clinical development that targets TREM2. Results from the INVOKE-2 Phase II clinical trial, which looked into the safety and efficacy of the drug in slowing disease progression in people living with Alzheimer's were positive.

Alector's novel approach -- immuno-neurology— to treating neurodegenerative diseases focuses on the immune system. In 2018, the company doubled down on this theory by tripling its workforce and expanding its facility, all with the expectation of taking five drugs into clinical trials.

The abandoned drug, AL-003, was designed to treat Alzheimer's using the body's immune system to fight the neurodegeneration. AL003 is a molecule designed to modulate checkpoint receptors on the brain’s immune cells, targeting sialic acid-binding Ig-like lectin 3 (SIGLEC 3, also called CD33).

The monoclonal antibody counteracts the function of Siglec-3, a microglial transmembrane receptor that reportedly interacts with TREM2. The gene encoding Siglec-3, CD33, has been associated with AD risk via a protective variant, expression levels, and alternative splicing.

Robin Robinson is a contributing writer for HealthLeaders. 


KEY TAKEAWAYS

AbbVie backs out of partnering to develop AL003, a monoclonal antibody that counteracts the function of Siglec.

The companies will continue to work together on the AL002 program, focused on targeting Triggering Receptor Expressed on Myeloid cells 2 (TREM2).


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