Leqembi®▼ (lecanemab) is the First Medicine that Slows Progression of Early Alzheimer’s Disease to be Authorised in the European Union

In the European Union (EU), lecanemab is indicated for the treatment of adult patients with a clinical diagnosis of mild cognitive impairment (MCI) and mild dementia due to Alzheimer’s disease (AD) (early AD) who are apolipoprotein E ε4 (ApoE ε4*) non-carriers or heterozygotes with confirmed amyloid pathology¹

Lecanemab is the first therapy that targets an underlying cause of the disease to be authorised in the EU for eligible people with early AD^1,2

Authorisation is primarily based on data from the global Phase 3 clinical trial, Clarity AD, which demonstrated that lecanemab slowed disease progression in early AD vs placebo at 18 months^1,2

The European Commission’s decision brings access to lecanemab one step closer for eligible people with early AD in the EU³

HATFIELD, HERTFORDSHIRE, UNITED KINGDOM, and CAMBRIDGE, Mass., 16 April, 2025 – Eisai Europe Ltd. and Biogen Inc. announced today that the European Commission (EC) has granted Leqembi^® (lecanemab) Marketing Authorisation (MA) in the European Union (EU).¹ This makes the medicine the first therapy that targets an underlying cause of Alzheimer’s disease (AD) to be granted a MA in the EU.^1,2

Lecanemab is indicated for the treatment of adult patients with a clinical diagnosis of mild cognitive impairment (MCI) and mild dementia due to AD (early AD) who are apolipoprotein E ε4 (ApoE ε4*) non-carriers or heterozygotes with confirmed amyloid pathology.¹ Early AD is usually the first stage of the disease, where symptoms become noticeable.⁴ Today’s MA applies to all 27 EU Member States as well as Iceland, Liechtenstein and Norway.⁵

Lecanemab is an amyloid-beta (Aβ) monoclonal antibody that preferentially binds and clears toxic protofibrils** (soluble Aβ aggregates), in addition to targeting and reducing Aβ plaques (insoluble Aβ aggregates).^1,2,6-10 Aβ protofibrils are a key toxic form of Aβ that accumulate in the brain and cause neuronal injury.^7,11,12

AD is a neurodegenerative disease that progresses in stages and increases in severity over time, and each stage of the disease presents different challenges for those living with AD and their care partners.^13,14 Early symptoms can include forgetting recent events or conversations.¹⁵ As AD progresses, everyday activities, hobbies and social engagements become more challenging, and independence is lost.^4,15 Early detection and diagnosis of AD can provide opportunities for interventions and support to be put in place for those in the early stages of the disease.^1,13,16

“Today’s decision makes lecanemab the first treatment option in the European Union that can slow the progression of early Alzheimer’s disease and is a key step to making the medicine available to eligible patients. This is important news for those in the clinical and research Alzheimer’s community who are dedicated to improving the management of a disease which poses a significant burden to healthcare systems and society,” said Gary Hendler, Regional Chairman and CEO, Eisai EMEA, Senior Vice President & Global Corporate Officer, Eisai Co. Ltd, Tokyo. “We are proud that our heritage of over 40 years in dementia has led to this milestone, as we aim to be part of the solution for a better future for those impacted by this disease.”

“The European Commission’s authorisation of lecanemab represents a significant milestone in addressing this progressive disease,” said Wolfram Schmidt, President and Head of Europe at Biogen. “We are proud there is now an approved treatment in the European Union that can slow the progression of early Alzheimer’s disease. Our team at Biogen remains dedicated to standing with the Alzheimer’s community, working collectively to achieve meaningful advancements in patient care.”

“Eisai will work collaboratively with national reimbursement authorities and healthcare providers to support access for eligible patients in European Union countries as soon as possible,” said Nick Burgin, President & COO, President Global Value & Access, Eisai EMEA. “Achieving optimal outcomes for people treated with the medicine is of paramount importance. To help achieve this, we are working with the European Medicines Agency and relevant national organisations to put measures in place to support the appropriate use of lecanemab as soon as it is introduced into each European Union country.”

The EC authorisation was primarily based on Phase 3 data from Eisai’s global, placebo-controlled, double-blind, parallel-group, randomised 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), demonstrating that lecanemab slowed disease progression in early AD vs placebo, and all key secondary endpoints.²

In the indicated population in the Clarity AD clinical trial, the most common adverse events in the treatment group (n=757) were infusion-related reaction, amyloid-related imaging abnormalities with haemorrhage (small spots of bleeding) (ARIA-H)^‡, headache and amyloid-related imaging abnormalities with cerebral oedema (build-up of fluid) (ARIA-E)^‡‡.^1,17

Eisai serves as the lead for lecanemab’s development and regulatory submissions globally with both Eisai and Biogen co-commercialising and co-promoting the product, and Eisai having final decision-making authority. In the EU (excluding the Nordic countries), Eisai and Biogen will co-promote the medicine, with Eisai distributing the product as the MA Holder. In the Nordic countries, Eisai and BioArctic will co-promote the medicine, with Eisai distributing the product as the MA Holder.

^*Apolipoprotein E is a protein involved in the metabolism of lipids in humans. It is implicated in AD.²

^**Protofibrils are believed to contribute to brain injury that occurs with AD and are considered to be a key toxic form of Aβ, having a primary role in the cognitive decline of this progressive, debilitating condition.¹¹ Protofibrils can cause injury to neurons in the brain which, in turn, can negatively impact cognitive function via multiple mechanisms,¹¹ 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.¹² It is believed the reduction of protofibrils may slow the progression of AD by reducing damage to neurons in the brain and cognitive dysfunction.¹²

^†CDR-SB is a disease staging tool used in clinical trials, which can help to stage dementia due to AD.¹⁵ 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.¹⁵

^‡ARIA-H: amyloid-related imaging abnormalities with haemorrhage (cerebral microhaemorrhages and superficial siderosis).

^‡‡ARIA-E: amyloid-related imaging abnormalities with oedema (oedema/effusion).

: This medicine is subject to additional monitoring. This will allow quick identification of new safety information. You can help by reporting any side effects you may get. If you get any side effects, talk to your healthcare professional. This includes any possible side effects not listed in the package leaflet. In the UK you can also report side effects directly via Yellow Card Scheme at www.mhra.gov.uk/yellowcard, for EU, via your EU national reporting system. By reporting side effects, you can help provide more information on the safety of this medicine.

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