Our Science
TB006, a humanized monoclonal antibody targeting Galectin-3, is a potentially revolutionary drug for Alzheimer’s Disease treatment
TB006 has potential to reverse AD progress by blocking Gal-3, which could promote 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 amyloid plaques, another key protein, Galectin-3 (Gal3), has been implicated in the pathogenesis of Alzheimer’s disease (AD). Gal3 is found at abnormally high levels in the brains of AD patients, where it binds to amyloid-beta (Aβ) and facilitates its aggregation. Acting as a molecular scaffold, Gal3 promotes the self-assembly of Aβ into toxic oligomers and plaques. These Aβ deposits accumulate on neuronal surfaces, disrupting synaptic signaling and contributing to cognitive decline in AD.
TB006 is an investigational monoclonal antibody designed to target Gal3. By selectively binding to Gal3, TB006 inhibits its adhesive function, thereby preventing the aggregation of Aβ and facilitating the dissolution of existing plaques. This mechanism restores synaptic integrity, potentially mitigating neurotoxicity and improving cognitive function in AD patients.
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
