Current therapeutic agents for Alzheimer’s disease temporarily improve symptoms but do not alter the underlying disease course. Some evidence suggests that amyloid removal slows the progression of the disease. While anti-amyloid antibodies have shown limited effects, a new humanized IgG1 monoclonal antibody binding to Aβ soluble protofibrils with high affinity, Lecanemab, has been shown to have the potential for disease modification.
A total of 1795 participants were enrolled, with 898 assigned to receive Lecanemab and 897 to receive placebo. The mean CDR-SB (Clinical Dementia Rating Sum of boxes) score at baseline was approximately 3.2 in both groups, consistent with early Alzheimer’s disease. One of the main results was the adjusted mean change in the CDR-SB score from baseline to 18 months, which was 1.21 in the Lecanemab and 1.66 in the placebo group. In a sub-study involving 698 participants, there were greater reductions in brain amyloid burden with Lecanemab than with placebo. Other mean differences between the two groups favoring Lecanemab were found in the ADAS-cog14 score and the ADCS-MCI-ADL score. Lecanemab resulted in infusion-related reactions in 26.4% of the participants and amyloid-related imaging abnormalities with edema or effusions in 12.6%.
Lecanemab reduced amyloid markers in early Alzheimer’s disease and resulted in a 27% reduction in cognitive decline on the CDR-SB scale at 18 months but was associated with adverse events. Longer trials are warranted to determine the efficacy and safety. Lecanemab has been approved by the FDA and EMA for patients with mild cognitive impairment or mild dementia due to Alzheimer’s disease. The US launch pricing is $26,500 per year, which is an unexpectedly reasonable price for a novel therapy. Approval by Swissmedic is pending.
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