FOR GLOBAL MEDIA AND JOURNALISTS OUTSIDE THE EMEA REGION
In Great Britain, lecanemab is indicated for the treatment of mild cognitive impairment and mild dementia due to Alzheimer’s disease (AD) in adult patients that are apolipoprotein E ε4 (ApoE ε4)* heterozygotes or non-carriers1
Great Britain becomes the first country in Europe to authorize the medicine, which targets an underlying cause of AD1
TOKYO and CAMBRIDGE, Mass., Aug. 22, 2024 /PRNewswire/ — 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 humanized amyloid-beta (Aβ) monoclonal antibody “Leqembi®” (brand name, generic name: lecanemab) has been granted a Marketing Authorization by the Medicines and Healthcare products Regulatory Agency (MHRA) in Great Britain.1 Lecanemab is indicated for the treatment of mild cognitive impairment (MCI) and mild dementia due to Alzheimer’s disease (AD) in adult patients that are apolipoprotein E ε4 (ApoE ε4)* heterozygotes or non-carriers.1 Lecanemab becomes the first treatment for early AD (MCI and mild dementia due to AD)2 that targets an underlying cause of the disease, to be authorized in a country in Europe.1
Lecanemab selectively binds to Aβ aggregate species, with preferential activity for toxic Aβ protofibrils** (as well as fibrils, which are a major component of Aβ plaques).2,3,4 It binds to these aggregate Aβ species to neutralize and clear them from the brain.2,3,4
The approval was primarily based on Phase 3 data from Eisai’s global, placebo-controlled, double-blind, parallel-group, randomized Clarity AD clinical trial, in which the medicine met its primary endpoint (change from baseline in the Clinical Dementia Rating Sum of Boxes [CDR-SB]† at 18 months) and all key secondary endpoints with statistically significant results.2 In the indicated population in Great Britain, the most common adverse reactions were infusion-related reaction, amyloid-related imaging abnormalities with hemorrhage (small spots of bleeding) (ARIA-H)‡, fall, headache and amyloid-related imaging abnormalities with cerebral edema (build-up of fluid) (ARIA-E)‡‡.1
In the United Kingdom, it is estimated that 982,000 people are living with dementia,5 and AD is the cause in 60-70% of people with dementia.6 These numbers are expected to rise, as the population ages.5,6
Eisai is working collaboratively with the National Institute for Health and Care Excellence (NICE), the Scottish Medicines Consortium (SMC) and the National Health Service (NHS) to make this medicine available to eligible people living with early AD as soon as possible.
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. In Great Britain, Eisai and Biogen will co-promote the medicine, with Eisai distributing the product as the Marketing Authorization holder.
*Apolipoprotein E is a protein involved in the metabolism of fats in humans. It is implicated in AD.
**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 damage in the brain, which can subsequently adversely affect cognitive function through multiple mechanisms.7 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.8
†CDR-SB is a commonly used diagnostic tool, which can help to stage dementia due to AD.9 It is a global cognitive and functional scale that measures six domains of functioning, including memory, orientation, judgement and problem solving, community affairs, home and hobbies, and personal care.9
‡ARIA-H: amyloid-related imaging abnormalities with hemorrhage (microhemorrhages, and superficial siderosis).
‡‡ARIA-E: amyloid-related imaging abnormalities with oedema (edema/effusion).
More information can be found in the Summary of Product Characteristics and Patient Information leaflets which will be published on the MHRA Products website within 7 days of approval.
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MEDIA CONTACTS |
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Eisai Co., Ltd. Public Relations Department TEL: +81 (0)3-3817-5120
Eisai Europe, Ltd. EMEA Communications Department +44 (0) 7974-879-419
Eisai Inc. (U.S.) Libby Holman 1-201-753-1945
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Biogen Inc. Jack Cox + 1-781-464-3260
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INVESTOR CONTACTS |
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Eisai Co., Ltd. Investor Relations Department TEL: +81 (0) 3-3817-5122 |
Biogen Inc. Chuck Triano + 1-781-464-2442 |
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).2,3
Lecanemab’s approval in Great Britain was primarily 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.1,2 Clarity AD was a Phase 3 global, placebo-controlled, double-blind, parallel-group, randomized study in 1,795 patients with early AD (MCI or mild dementia due to AD, with confirmed presence of amyloid pathology), of which 1,521 were in the indicated population in the label in Great Britain (ApoE ε4 heterozygotes or non-carriers).1 Of the total number of patients randomized 31% were non-carriers, 53% were heterozygotes and 16% were homozygotes.1 The treatment group was administered lecanemab 10 mg/kg bi-weekly, with participants allocated in a 1:1 ratio to receive either placebo or lecanemab for 18 months.1
The primary endpoint was the global cognitive and functional scale, CDR-SB.1 In the Clarity AD clinical trial, treatment with lecanemab, in the indicated population in Great Britain (ApoE ε4 heterozygotes or non-carriers), reduced clinical decline on CDR-SB by 33% at 18 months compared to placebo.1 The mean CDR-SB score at baseline was approximately 3.2 in both groups.1 The adjusted least-squares mean change from baseline at 18 months was 1.15 with lecanemab and 1.73 with placebo (difference, −0.58; 95% confidence interval [CI], −0.81 to −0.34; P