Anti-Human Amyloid-β (Lecanemab) (A490-GRP)

Amyloid-β (Aβ) is a peptide that accumulates in the brains of individuals with Alzheimer’s disease, forming plaques that are a hallmark of the condition. These plaques are believed to contribute to the neurodegenerative processes seen in Alzheimer’s by disrupting cell function and triggering inflammatory responses. Amyloid-β is derived from the amyloid precursor protein (APP) through enzymatic cleavage. The aggregation of Aβ into oligomers and fibrils is a key pathological feature of Alzheimer’s disease, making it a significant target for therapeutic interventions aimed at reducing or preventing plaque formation1,2. Known as clone BAN-2401, Lecanemab is the humanized IgG1 version of the mouse monoclonal antibody mAb158, specifically engineered to selectively bind to large, soluble Aβ protofibrils. BAN-2401 has shown efficacy in reducing Aβ protofibrils in the brain and cerebrospinal fluid (CSF) of animal models. In clinical trials, it has exhibited potential as a disease-modifying treatment for Alzheimer's disease. Additionally, BAN-2401 has been utilized in preclinical research to study its binding to Aβ deposits in postmortem brain sections from individuals with Down's syndrome3,4.