Who We Are
Alectos Therapeutics discovers novel treatments to block the underlying progression of neurodegenerative diseases. Alectos identifies and develops innovative strategies to address complex neurological conditions, including Alzheimer’s disease and Parkinson’s disease.
The Alectos pipeline is focused on creating new therapeutics to treat patients living with these disorders. Our GBA2 program is a disease-modifying approach to correct lysosomal dysfunction in neurodegenerative diseases, including Parkinson’s disease. This program has recently been partnered with Biogen. Our OGA program is a strategy to prevent the accumulation and spread of toxic protein aggregates in the brain. Alectos partnered with Merck to pioneer the development of the first clinical OGA inhibitor. Alectos has repatriated this program and we are applying our deep knowledge and IP to advance novel OGA inhibitors as treatments for Alzheimer’s disease, frontotemporal dementia, and ischemic stroke. We welcome partnership inquiries regarding our OGA program and our advanced preclinical development candidates.
Development of novel agents as disease-modifying therapies for
neurodegenerative disease
News
Biogen and Alectos Therapeutics Announce License and Collaboration Agreement for AL01811, a Novel GBA2 Inhibitor for the Potential Treatment of Parkinson’s Disease
AL01811 is a preclinical selective GBA2 inhibitor with first-in-class potential as an oral disease modifying treatment for Parkinson’s Disease Alectos to receive a $15 million upfront payment and is eligible to receive potential future development and commercial milestone payments Cambridge, Mass. and Burnaby, British Columbia – June 6, 2022 – Biogen Inc. (Nasdaq: BIIB) – Biogen and Alectos Therapeutics have entered into a license and collaboration agreement to develop and [...]
O-GlcNAcylation of TDP-43 Suppresses Proteinopathies and Promotes TDP-43’s mRNA Splicing Activity
Pathological TDP-43 aggregation is characteristic of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD-TDP); however, how TDP-43 aggregation and function are regulated remain poorly understood. Here, we show that O-GlcNAc transferase OGT-mediated O-GlcNAcylation of TDP-43 suppresses ALS-associated proteinopathies and promotes TDP-43's splicing function. Biochemical and cell-based assays indicate that OGT's catalytic activity suppresses TDP-43 aggregation and hyperphosphorylation, whereas abolishment of TDP-43 O-GlcNAcylation impairs its RNA [...]
O-GlcNAcylation Regulates Dopamine Neuron Function, Survival and Degeneration in Parkinson Disease
The dopamine system in the midbrain is essential for volitional movement, action selection, and reward-related learning. Despite its versatile roles, it contains only a small set of neurons in the brainstem. These dopamine neurons are especially susceptible to Parkinson's disease and prematurely degenerate in the course of disease progression, while the discovery of new therapeutic interventions has been disappointingly unsuccessful. Here, we show that O-GlcNAcylation, an essential post-translational modification in [...]