TOKYO and CAMBRIDGE, Mass., Dec 3, 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 data confirming the pharmacological effect of lecanemab (generic name, U.S. brand name LEQEMBI®), an anti-Aβ protofibril* antibody, on Aβ protofibrils (PF) in cerebrospinal fluid (CSF) was presented at the 18th Clinical Trials on Alzheimer’s Disease (CTAD) Conference. The findings represent the results from a large-scale clinical study demonstrating, for the first time, that binding of lecanemab to PF can be measured in CSF, enabling further understanding of how lecanemab slows Alzheimer’s disease (AD) progression.

AD is a progressive, relentless disease with Aβ and tau as hallmarks. It is caused by a continuous underlying neurotoxic process driven by PF that begins before amyloid plaque accumulation and continues after plaque removal.1,2,3 Only LEQEMBI fights AD in two ways: targeting both protofibrils and amyloid plaque, which can impact tau downstream.

In a CSF sub-cohort (n=410) of the Phase III Clarity AD study, total PF concentration in CSF was quantified using an ultrasensitive assay. Changes from baseline (pre-treatment) for the placebo group (natural course) and the lecanemab group were compared, and associations between PF changes and neurodegeneration biomarkers were analyzed.

Total CSF PF concentration in the placebo group increased by 19% at 12 months and 29% at 18 months. In contrast, the lecanemab group showed a 59% increase at 12 months and a 45% increase at 18 months. At 12 months, the difference compared with placebo was statistically significant (p=0.0126).

The increase in total CSF PF with lecanemab treatment suggests that lecanemab binds to PF (target engagement) and facilitates its mobilization from the vicinity of Aβ plaques within the brain parenchyma into the CSF (pharmacodynamic effect). This suggests that lecanemab is having the desired effect of mitigating the toxic effects of PF by mobilizing it outside of the brain parenchyma.

In the placebo group, a statistically significant correlation was observed between changes in CSF PF and changes in neurodegeneration biomarkers (total tau, neurogranin) as well as tau pathology biomarkers (p-tau181, MTBR-tau243**) at baseline. This correlation disappeared with lecanemab treatment, suggesting that lecanemab reduces neurotoxicity by binding to PF.

These findings reinforce lecanemab as the only AD treatment that targets neurotoxic PF and Aβ plaques, resulting in slower tau tangle accumulation on PET imaging.

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

** MTBR-tau243 is a novel biomarker composed of tau fragments that include residue 243 and the microtubule binding region, and is thought to arise during the formation of neurofibrillary tangles, a key pathological feature of AD. It has also been shown to have a strong correlation with tau PET.5

MEDIA CONTACTS

Eisai

Eisai Co., Ltd.
Public Relations Department
TEL: +81 (0)3-3817-5120

Eisai Europe, Ltd.
EMEA Communications Department
+44 (0) 7974-879-419
Emea-comms@eisai.net

Eisai Inc. (U.S.)
Libby Holman
+1-201-753-1945
Libby_Holman@eisai.com

Biogen Inc.
Madeleine Shin
+ 1-781-464-3260
public.affairs@biogen.com

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Eisai Co., Ltd.
Investor Relations Department
TEL: +81 (0)3-3817-5122

Biogen Inc.
Tim Power
+ 1-781-464-2442
IR@biogen.com

For more details, please visit: https://www.eisai.com/news/2025/news202584.html

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