Alzheimer’s disease (AD), like other chronic progressive diseases, requires a long-term therapeutic strategy. Lecanemab dual mechanism of action removes protofibrils that continue to form and drive AD pathophysiology even after amyloid is cleared. Discontinuation of treatment is associated with reaccumulation of biomarkers and reversion to placebo rate of clinical decline.

To present support from the latest clinical, pharmacology, and modeling data for continued long-term maintenance lecanemab dosing further clinical benefit.

Data from the lecanemab phase 2 study (Study 201) and Clarity AD were pooled, and biomarker, amyloid PET, and CDR-SB scores were used to develop models describing the change in amyloid PET and plasma biomarkers with lecanemab treatment. A model was also developed to show how change in amyloid PET predicts slowing of disease progression. These models were used to explore the change in biomarkers/outcomes over 4 years, and to evaluate the effect of transitioning to less frequent lecane ab dosing following 18 to 24 months of initial treatment. 

Models included data for up to 110 months in Study 201 and up to 54 months of continuous lecanemab biweekly dosing in Clarity AD. Simulations projected that CDR-SB difference between lecanemab and placebo subjects continued increasing over the 4-year simulation period. Low amyloid and less severe disease at baseline were associated with slower disease progression. Continued treatment with lecanemab at less frequent dosing intervals following an initial treatment period was demonstrated to effectively maintain the benefit associated with lecanemab treatment on plasma biomarkers, amyloid PET, and clinical outcomes as compared to the initial dosing regimen.