TOKYO, Dec 2, 2025 - (JCN Newswire) - Eisai Co., Ltd. (Headquarters: Tokyo, CEO: Haruo Naito) today announced that new data on anti-tau antibody etalanetug (development code: E2814) was presented at the 18th Clinical Trials on Alzheimer’s Disease Conference (CTAD). Etalanetug is designed to bind to the microtubule-binding region (MTBR) of tau protein and prevent the seeding and propagation of tau pathology.

Anti-tau therapeutic antibody, etalanetug, reduces the novel biomarker plasma eMTBR-tau243 in patients with DIAD (Presentation: December 1, 4:35 PM PT)

This presentation is based on the Phase Ib/II study (E2814-103) conducted in individuals (n=7) with dominantly inherited Alzheimer’s disease (DIAD)*. In this study, as previously reported, tau aggregates in the brains of individuals (n=3) were measured using tau PET, and the results showed that the observed tau PET signals were stabilized or trended toward decrease following administration of etalanetug, suggesting that etalanetug inhibited tau propagation and suppressed or reduced the accumulation of tau aggregates in brains.1

The study evaluated eMTBR-tau243 as a specific biomarker of tau pathology progression and measured changes in cerebrospinal fluid (CSF) and plasma.

MTBR-tau243 is a CSF biomarker correlated with tau pathology, and eMTBR-tau243** has also been developed as a highly sensitive biomarker in plasma.

eMTBR-tau243 is a novel fluid biomarker consisting of tau fragments that include tau protein amino acid residue 243 and MTBR, with endogenous cleavage at the C-terminal side of residue 256. It is thought to arise during the formation of neurofibrillary tangles, a key pathological feature of Alzheimer’s disease (AD), and a strong correlation has been shown between tau PET and eMTBR-tau243 in both plasma and CSF.2 By using eMTBR-tau243, it becomes possible to easily measure changes in tau pathology using a blood test.

Study results show that etalanetug reduced CSF eMTBR-tau243 by 62% at 3 months and by 89% at 9 months. Similarly, plasma eMTBR-tau243 was reduced by 78% at 3 months and over 90% at 9 months. These findings support etalanetug’s mechanism of action to inhibit tau seeding and spreading in the brain and encourage further studies to determine its clinical potential as a disease-modifying therapy for AD.

Currently, etalanetug is being evaluated in two ongoing clinical studies: the Tau NexGen Phase II/III trial in DIAD, conducted under the Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU) and led by Washington University School of Medicine in St. Louis, added to a standard-of-care anti-Ab protofibril antibody lecanemab (brand name: LEQEMBI), and the Phase II Study 202, a global randomized trial in individuals with early sporadic AD, also assessing etalanetug added to lecanemab as the standard of care.

Media Inquiries:

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

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

* DIAD: Dominantly Inherited Alzheimer’s disease (DIAD) is a rare form of AD that causes memory loss and dementia in individuals - typically while they are in their 30s to 50s. The disease affects less than 1% of the total population of people with Alzheimer’s disease.

** eMTBR-tau243 is a novel fluid biomarker consisting of tau fragments that include tau protein amino acid residue 243 and MTBR, with endogenous cleavage at the C-terminal side of residue 256. It is thought to arise during the formation of neurofibrillary tangles, a key pathological feature of AD, and a strong correlation has been shown between tau PET and eMTBR-tau243 in both plasma and CSF.

For more details, please visit: https://www.eisai.com/news/2025/pdf/enews202583pdf.pdf

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