Eisai and Biogen presented data at the 18th CTAD Conference confirming the pharmacological effect of lecanemab on Aβ protofibrils in cerebrospinal fluid. A large-scale study demonstrated that lecanemab slows Alzheimer’s disease progression by binding to protofibrils and amyloid plaques. In a Phase III study, the lecanemab group showed a significant increase in protofibrils in CSF compared to the placebo group. The findings suggest that lecanemab mobilizes protofibrils from the brain parenchyma, reducing neurotoxicity. Lecanemab is the only treatment targeting neurotoxic protofibrils and plaques, showing promising results in AD progression. Safety information, contraindications, and monitoring guidelines were also provided.

Read more at GlobeNewswire: New Data Presented at the Clinical Trials on Alzheimer’s