Eisai presents new clinical data for four years of continuous treatment with lecanemab at Alzheimer’s Association International Conference 2025

Posted on 5 August, 2025 - ACNR News, Alzheimer's Disease, Industry News, Uncategorized

Eisai has presented new clinical data demonstrating that early Alzheimer’s disease (AD) patients continue to benefit from four years of Leqembi®▼(lecanemab) treatment, at the Alzheimer’s Association International Conference (AAIC) 2025, held in Toronto, Canada, and virtually on 30 July 2025 [1]. Key takeaways included:

  • Clarity AD Open Label Extension (OLE) data from the overall trial population (all apolipoprotein E ε4 [ApoE ε4*] genotypes) show that four years of lecanemab treatment slowed clinical decline by 1.75 points vs expected decline based on the Alzheimer’s Disease Neuroimaging Initiative (ADNI†) group on the global cognitive and functional scale Clinical Dementia Rating-Sum of Boxes (CDR-SB) [1]. ‡
  • No new safety findings were observed in the Clarity OLE data with continued lecanemab treatment over four years [1].

Lecanemab is an amyloid-beta (Aβ) monoclonal antibody that preferentially binds and clears toxic protofibrils§ (soluble Aβ aggregates), in addition to targeting and reducing Aβ plaques (insoluble Aβ aggregates) [1-5]. Aβ protofibrils are a key toxic form of Aβ that accumulate in the brain and cause neuronal injury [4,6,7].

In the European Union and the United Kingdom, lecanemab is indicated for the treatment of adult patients with a clinical diagnosis of mild cognitive impairment (MCI) and mild dementia due to AD (early AD) who are ApoE ε4 non-carriers or heterozygotes with confirmed amyloid pathology [8,9].

Clarity AD OLE data from the overall trial population show that four years of continuous lecanemab treatment slowed clinical decline by 1.75 vs expected decline based on the ADNI group, on the global and functional scale CDR-SB [1].

Over three years of treatment, including both the Clarity AD core study and the OLE, data showed that lecanemab demonstrated a reduction in cognitive decline—measured by CDR-SB—with a difference of 1.01 points compared to the expected decline observed in the ADNI cohort [1]. This benefit grew more pronounced after four years, with a reduction of 1.75 points [1]. Similarly, when benchmarked against the expected decline in the BioFINDER cohort, lecanemab showed a reduction of 1.40 points at three years and a greater reduction of 2.17 points at four years [1].

478 patients who completed the core Clarity AD study (18 months) continued to receive treatment for four years in the OLE [1].

Consistent safety profile observed over four years of lecanemab treatment [1].

No new safety findings were observed in the OLE with continued lecanemab treatment over four years [1]. Rates of amyloid-related imaging abnormalities (ARIA) decreased after the initial 12 months and remained consistent throughout four years of continuous treatment [1].

In the global Phase 3 Clarity AD core trial, the most common adverse events (>10%) for the overall population, including all ApoE ε4 genotypes, in the treatment group were infusion reactions, ARIA-H (combined cerebral microhaemorrhages, cerebral macrohaemorrhages, and superficial siderosis), ARIA-E (oedema/effusion), headache, and fall [2].

Eisai serves as the lead for lecanemab’s development and regulatory submissions globally, with both Eisai and Biogen co-commercialising and co-promoting the product, and Eisai having final decision-making authority. In the European Union and United Kingdom (excluding the Nordic countries), Eisai and Biogen will co-promote the medicine, with Eisai distributing the product as the Marketing Authorisation (MA) Holder. In the Nordic countries, Eisai and BioArctic will co-promote the medicine, with Eisai distributing the product as the MA Holder.

References

  1. van Dyck, C.H., et al. The Lecanemab Clarity AD Open-Label Extension in Early Alzheimer’s Disease: Initial Findings From the 48-Month Analysis. Presented at Alzheimer’s Association International Conference (AAIC), 2025.
  2. van Dyck, C.H., et al. Lecanemab in Early Alzheimer’s Disease. New England Journal of Medicine. 2023;388:9-21. https://www.nejm.org/doi/full/10.1056/NEJMoa2212948.
  3. Johannesson, M., et al. Lecanemab demonstrates highly selective binding to Aβ protofibrils isolated from Alzheimer’s disease brains. Molecular and Cellular Neuroscience. 2024;130:103949. https://doi.org/10.1016/j.mcn.2024.103949.
  4. Sehlin, D., et al. Large aggregates are the major soluble Aβ species in AD brain fractionated with density gradient ultracentrifugation. PLoS One. 2012;7(2):e32014. https://doi.org/10.1371/journal.pone.0032014.
  5. Söderberg, L., et al. Lecanemab, Aducanumab, and Gantenerumab — Binding Profiles to Different Forms of Amyloid‑Beta Might Explain Efficacy and Side Effects in Clinical Trials for Alzheimer’s Disease. Neurotherapeutics. 2022;20(1):195-206. https://doi.org/10.1007/s13311-022-01308-6.
    Amin, L., Harris, D.A. Aβ receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers. Nature Communications. 2021;12:3451. https://doi.org/10.1038/s41467-021-23507-z.
  6. Ono, K., Tsuji, M. Protofibrils of Amyloid-β are Important Targets of a Disease-Modifying Approach for Alzheimer’s Disease. International Journal of Molecular Sciences. 2020;21(3):952. https://doi.org/10.3390/ijms21030952.
  7. Lecanemab European Union Summary of Product Characteristics. Available at: https://www.ema.europa.eu/en/documents/product-information/leqembi-epar-product-information_en.pdf. Last accessed: July 2025.
  8. Lecanemab United Kingdom Summary of Product Characteristics. Available at: https://www.medicines.org.uk/emc/product/15908. Last accessed: July 2025.