TOKYO, Oct. 23, 2024 /PRNewswire/ — Eisai Co. Ltd (Headquarters: Tokyo, CEO: Haruo Naito, “Eisai”) announced today that the company will present the latest findings on its Alzheimer’s disease (AD) pipeline and research, including our dual-acting, anti-amyloid beta (Aβ) protofibril* antibody for the treatment of AD, lecanemab (generic name, U.S. brand name: LEQEMBI®), at the Clinical Trials for Alzheimer’s Disease Conference (CTAD). The conference will be held in Madrid, Spain, and virtually from October 29 to November 1, 2024. Eisai will present data and research in 4 oral and 6 poster presentations at the meeting, and three symposiums on lecanemab will be held, including the importance of continued treatment of AD, a progressive neurodegenerative disease that begins before plaque deposition and continues after plaque removal. Additional findings from Eisai’s robust Alzheimer’s disease (AD) pipeline will be shared.
Blood BiomarkersLate Breaking Symposium 1: The AHEAD 3-45 Study: Design and Results of a Novel Screening Process for a Preclinical AD Trial
On October 29 (Tuesday) from 6:10 to 6:50 p.m. Central European Time (CET), this symposium will present the design of the AHEAD 3-45 trial focused on lecanemab AD and the findings on use of plasma biomarkers, amyloid and tau PET imaging in screening.
Lecanemab in Clinical PracticeLate Breaking Symposium 2: One-Year Experience on the Use of Lecanemab in Clinical Practice
On October 30 (Wednesday) from 3:30 to 4:10 p.m. (CET), this symposium will be discussed real-world evidence from clinical practice with lecanemab in the U.S. and Japan. Eisai will present Real World Settings in the U.S.
Lecanemab Long-Term BenefitsSymposium 1: Does the Current Evidence Base Support Continued Dosing with Lecanemab for Early Alzheimer’s Disease?
Keynote Presentation 1 ‘Lecanemab: From a Mutation to a Treatment for Alzheimer’s Disease’ by Professor emeritus Lars Lannfelt of Uppsala University, founder of BioArctic, will occur October 29 (Tuesday) at 4:30 p.m. (CET). Eisai and BioArctic have had a long-term collaboration regarding the development and commercialization of AD treatments.
“At CTAD 2024, Eisai will present the latest information on the use of dual-acting lecanemab in clinical practice, the use of plasma biomarkers in the AHEAD 3-45 trial to screen for preclinical AD, and the latest data on our anti-MTBR (Microtubule binding region) tau antibody E2814,” said Michael Irizarry, M.D., Deputy Chief Clinical Officer and Senior Vice President of Clinical Research at Eisai Inc. “Alzheimer’s disease is a relentlessly progressive disease caused by a continuous underlying neurotoxic process. There is an urgency to diagnose at the early symptomatic stages because appropriate and continuous treatment can slow the progression of Alzheimer’s disease. The earlier mild cognitive impairment due to AD and mild AD dementia are diagnosed and treated, the greater the opportunity for the patient to benefit.”
Key Presentation
■ Late Breaking Symposium 1:The AHEAD 3-45 Study: Design and Results of a Novel Screening Process for a Preclinical AD Trial From 6:10 to 6:50 p.m. (CET) on October 29 (Tuesday)
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Presentation Title |
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The AHEAD 3-45 Study: Adaptation to Challenges |
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Screening Plasma Biomarkers, Amyloid and Tau PET Imaging in the AHEAD 3-45 Study |
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Racial and Ethnic Differences in Plasma P-tau217 Biomarker Eligibility Rates in a Preclinical AD Trial |
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Q&A |
■ Late Breaking Symposium 2:One-Year Experience on the Use of Lecanemab in Clinical PracticeFrom 3:30 to 4:10 p.m. (CET), on October 30 (Wednesday)
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Presentation Title |
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Lecanemab Treatment in Real World Settings in the United States |
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Lecanemab Use in Clinical Practice at an Academic Medical Center (Independent to Eisai) |
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Lecanemab Use in Clinical Practice in Japan (Independent to Eisai) |
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Q&A |
■ Symposium 1Does the Current Evidence Base Support Continued Dosing with Lecanemab for Early Alzheimer’s Disease?From 9:40 to 10:20 a.m. (CET) on October 30 (Wednesday)
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Presentation Title |
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Mechanistic Rationale for Continued Lecanemab Dosing |
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Pharmacologic Support for a Maintenance Dosing Regimen with Lecanemab: An Update on the Latest Clinical Pharmacology Data and Modeling |
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Evidence for a Continued Benefit for Long-Term Lecanemab Treatment: A Benefit/Risk Update from Long-Term Efficacy, Safety and Biomarker Data |
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Q&A |
■ Roundtable:Advancing Combination Therapy: Discussion on Key Considerations, Perspectives, and Promising Avenues for the Future of Alzheimer’s Treatments
From 1:45 to 2:15 p.m. (CET) on October 30 (Wednesday)
■ Oral Presentations
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Asset/Project, Presentation Date and Time (CET) |
Presentation Number, Title |
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Lecanemab |
LB6 Lecanemab for the Treatment of Mild Cognitive Impairment and Mild Dementia Due to Alzheimer’s Disease in Adults That Are Apolipoprotein E ɛ4 Heterozygotes or Non-Carriers |
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Lecanemab |
LB18 AI-Derived Prognostic Covariates Enhance the Precision of Lecanemab Efficacy Assessments and Optimize Alzheimer’s Disease Clinical Trials |
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E2814 |
OC4 Anti-Tau Therapeutic Antibody, E2814, Reduces Early and Late Tau Pathology Biomarkers in Patients with DIAD |
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Biomarker |
LB29 The Use of Plasma Biomarkers for the Prediction of Amyloid Positivity |
■ Poster Presentations
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Asset/Project, Presentation Date |
Presentation Number, Title |
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Lecanemab Oct 29 (Tue) – Oct 30 (Wed) |
LP017 Transitioning from Clinical Trial to Clinical Practice for Long-Term Lecanemab Treatment in Early Alzheimer’s Disease: Perspectives from an Alzheimer’s Disease Treatment Center |
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Biomarker Oct 29 (Tue) – Oct 30 (Wed) |
P007 Using Plasma pTau217 to Forecast Longitudinal Progression Substantially Increases the Efficiency of AD Clinical Trials |
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Biomarker Oct 29 (Tue) – Oct 30 (Wed) |
P009 Assessing the Feasibility of Implementing Blood-Based Biomarkers as Confirmatory Diagnostic Tools for Early Alzheimer’s Disease in Real-World Clinical Practice: A Prospective, Multi-Clinic Implementation Science and Observational Study |
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Imaging/Biomarker Oct 31 (Thu) |
P098 Enhancing the Effectiveness of Alzheimer’s Disease Drug Development by Assessing Tau PET as a Promising Surrogate Endpoint Within the Pre-Competitive Critical Path for Alzheimer’s Disease (CPAD) Consortium |
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AD General Nov 1 (Fri) |
P206 Risk Prediction Models of Mild Cognitive Impairment Using Electronic Health Record Data |
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AD General Nov 1 (Fri) |
P217 All-Cause Mortality Increased with Intracerebral Hemorrhage in the United States Medicare Beneficiaries 65 Years or Older with Mild Cognitive Impairment or Alzheimer’s Dementia |
This release discusses investigational uses of agents in development and is not intended to convey conclusions about efficacy or safety. There is no guarantee that such investigational agents will successfully complete clinical development or gain health authority approval.
* Protofibrils are believed to contribute to the brain injury that occurs with AD and are considered to be the most toxic form of Aβ, having a primary role in the cognitive decline associated with this progressive, debilitating condition.1 Protofibrils cause injury to neurons in the brain, which in turn, can negatively impact cognitive function via multiple mechanisms, not only increasing the development of insoluble Aβ plaques but also increasing direct damage to brain cell membranes and the connections that transmit signals between nerve cells or nerve cells and other cells. It is believed the reduction of protofibrils may prevent the progression of AD by reducing damage to neurons in the brain and cognitive dysfunction.2
[Notes to editors]1. About Lecanemab (LEQEMBI®)Lecanemab is the result of a strategic research alliance between Eisai and BioArctic. It is a humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble (protofibril) and insoluble forms of amyloid-beta (Aβ). Lecanemab is approved in the U.S., Japan, China, South Korea, Hong Kong, Israel, the United Arab Emirates and Great Britain. Eisai has also submitted applications for approval of lecanemab in 10 countries and regions, including the European Union (EU).
LEQEMBI’s approvals in these countries were based on Phase 3 data from Eisai’s, global Clarity AD clinical trial, in which it met its primary endpoint and all key secondary endpoints with statistically significant results. The primary endpoint was the global cognitive and functional scale, Clinical Dementia Rating Sum of Boxes (CDR-SB). In the Clarity AD clinical trial, treatment with lecanemab reduced clinical decline on CDR-SB by 27% at 18 months compared to placebo.3,4 The mean CDR-SB score at baseline was approximately 3.2 in both groups. The adjusted least-squares mean change from baseline at 18 months was 1.21 with lecanemab and 1.66 with placebo (difference, −0.45; 95% confidence interval [CI], −0.67 to −0.23; P