TOKYO and CAMBRIDGE, Mass., Dec 4, 2025 - (JCN Newswire) - Eisai Co., Ltd. (Headquarters: Tokyo, CEO: Haruo Naito, "Eisai") and Biogen Inc. (Nasdaq: BIIB, Corporate headquarters: Cambridge, Massachusetts, CEO: Christopher A. Viehbacher, "Biogen") announced today that the latest findings on time savings with continued treatment with humanized anti-soluble aggregated amyloid-beta (Aβ) monoclonal antibody lecanemab (generic name, U.S. brand name LEQEMBI®) were presented at the 18th Clinical Trials on Alzheimer's Disease (CTAD) Conference. Additionally, a scientific symposium was held on the subcutaneous formulation (SC-AI), which was approved for maintenance treatment in the United States in August 2025, and the rolling supplemental Biologics License Application (sBLA) for initiation treatment was completed in November 2025. The application for a subcutaneous injectable formulation in Japan was submitted in November 2025.
Alzheimer's disease (AD) is a progressive, relentless disease with Aβ and tau as hallmarks, that is caused by a continuous underlying neurotoxic process driven by protofibrils* (PF) that begins before amyloid plaque removal and continues afterward.1,2,3 Only LEQEMBI fights AD in two ways - targeting both PF and amyloid plaque, which can impact tau downstream.
Estimating the 10-Year Time-Savings Benefits of Lecanemab Treatment (Presentation: December 3, 2:40 PM PT)
This analysis used data from the Clarity AD open-label extension (OLE) and 16 clinical studies of monoclonal antibodies for AD to estimate long-term AD progression over 10 years and the slowing effect of continued lecanemab treatment. The analysis evaluated estimated "time savings" (slowing of disease progression) compared to natural decline based on ADNI** (Alzheimer's Disease Neuroimaging Initiative) data (untreated group), using Clinical Dementia Rating - Sum of Boxes (CDR-SB). These results suggest that early initiation and long-term lecanemab treatment may continue to slow AD progression and help maintain cognitive function over a longer period.
Findings from each group:
- Time Savings from Mild Cognitive Impairment (MCI) Due to AD to Mild AD
- The time to progression from MCI due to AD to mild AD was 7.2 years in the untreated group, whereas with continued LEQEMBI treatment to the onset of moderate AD, progression to mild AD took 9.7 years, indicating a time savings of 2.5 years.
- In the low-amyloid group (patients who started treatment at an early stage: amyloid PET <60 centiloids), the time to progression from MCI to mild AD was 13.2 years with continued LEQEMBI treatment to the onset of moderate AD, suggesting a time savings of 6.0 years.
- Time Savings from MCI due to AD to Moderate AD
- The time to progression from MCI due to AD to moderate AD was 10.1 years in the untreated group, whereas with continued LEQEMBI treatment to the onset of moderate AD, progression to moderate AD took 13.6 years, indicating a time savings of 3.5 years.
- In the low-amyloid group, the time to progression with continued LEQEMBI treatment to the onset of moderate AD, progression to moderate AD took 18.4 years, suggesting a time savings of 8.3 years.
These findings indicate that earlier initiation of lecanemab treatment may provide a greater delay in disease progression. Furthermore, each additional year on LEQEMBI could further delay disease progression compared to stopping treatment, even long after plaque is expected to have been cleared.
Lecanemab Subcutaneous Formulation for Treatment Initiation in Early Alzheimer’s Disease: Optimizing Patient Care with a Potential New Option (Symposium Presentation: December 3, 3:10 PM)
In this symposium, the latest data from the lecanemab subcutaneous clinical development program were presented focusing on treatment initiation, including results from the subcutaneous (SC) formulation subcohort (n=273) in the Clarity AD trial open-label extension (OLE).. It was shown that weekly administration of lecanemab SC-AI at 500 mg (two 250 mg injections) demonstrated bioequivalence in drug exposure compared to intravenous dosing of 10 mg/kg every two weeks (exposure ratio: 104%, 90% CI: 99.1%–109%).
Based on clinical data and modeling analysis, the effect on amyloid removal in the brain and safety (ARIA-E incidence) was shown to be independent of the route of administration and explained by exposure, suggesting that weekly 500 mg SC dosing provides similar efficacy and safety to biweekly 10 mg/kg IV dosing. Additionally, ARIA-E incidence was also predicted to be comparable between SC and IV administration (12.4% overall, 30.9% in ApoE4 homozygotes).
In this sub-cohort which had prior exposure to lecanemab, safety evaluation showed systemic infusion reactions occurred in 0% of patients receiving 500 mg SC, all of whom had previously received IV lecanemab, and 1.4% of patients who initiated on 720 mg SC by vial, which is favorable compared to systemic infusion reactions in the IV group (26.4%). Immunogenicity assessment indicated a low incidence of anti-drug antibodies (ADA) at 1.4%.
These results indicate that the subcutaneous formulations of lecanemab, designed with consideration for the convenience of patients and their care partners, maintains efficacy with a low incidence of systemic infusion reactions, and is otherwise equivalent to conventional IV administration.
Eisai serves as the lead for lecanemab’s development and regulatory submissions globally with Eisai and Biogen co-commercializing and co-promoting the product and Eisai having final decision-making authority.
* Protofibrils are thought to be the most toxic Aβ species that contribute to brain damage in AD and play a major role in the cognitive decline of this progressive and devastating disease. Protofibrils can cause neuronal and synaptic damage in the brain, which can subsequently adversely affect cognitive function through multiple mechanisms.3 The mechanism by which this occurs has been reported not only by increasing the formation of insoluble Aβ plaques, but also by directly damaging signaling between neurons and other cells. It is believed that reducing protofibrils may reduce neuronal damage and cognitive impairment, potentially preventing the progression of AD. 4
** ADNI is a clinical research project launched in 2005 to develop methods to predict the onset and progression of AD and to confirm the effectiveness of treatments. The project involves a multi-year longitudinal observation targeting healthy elderly individuals as well as patients with mild cognitive impairment (MCI) and early stages of AD.
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