Our Science
TB006, a humanized monoclonal antibody targeting Galectin-3, is a potentially revolutionary drug for Alzheimer’s Disease treatment
TB006 could reverse AD progress by blocking Gal-3, the root cause of Abeta oligomerization and plaque formation
Alzheimer's Disease is a brain disorder that starts slowly, then gradually worsens and robs people of their memory as well as other cognitive abilities that are required for daily living. It leads to the most common form of dementia and is characterized by abnormal clumping of amyloid beta (Abeta) proteins into toxic plaques. These plaques deposit in the brain, clogging communication between neurons, which results in symptoms of cognition defects.
In addition to these plaques, there is another protein involved called Galectin-3 (Gal3), which is found at abnormally high levels in the brains of Alzheimer’s Disease patients. Gal3 binds to Abeta, and acts as a glue, causing Abeta to bind to itself and form toxic plaques. The Abeta plaques then deposit onto neurons, blocking communication signals between neurons and leading to cognition defect symptoms in Alzheimer’s Disease patients.
TB006 is a revolutionary new drug developed to treat Alzheimer’s Disease. By binding to Gal3, the TB006 drug prevents Gal3 from acting as a glue. This reduces and dissolves the toxic Abeta plaques in the brain, which allows neurons to communicate again, thus resulting in the cognition improvement.
Therapeutic Efficacy of TB006
The potential therapeutical efficacy of TB006 was supported by strong pre-clinical AD animal model studies. Significant reduction in total Abeta plaques and other neurodegeneration biomarkers were achieved after just two -week treatment with mTB001, a surrogate of TB006, in two transgenic (APPSwe, 5xFAD) and Abeta injection induced AD mouse models
