Eisai Receives Regulatory Review Outcome for Lecanemab as a Treatment for Early Alzheimer’s Disease in Australia

TOKYO and CAMBRIDGE, Mass., March 3, 2025 – 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 Therapeutic Goods Administration (TGA) of Australia has confirmed the initial decision to decline the approval of humanized anti-soluble aggregated amyloid-beta (Aβ) monoclonal antibody lecanemab (generic name) as a treatment for early Alzheimer’s disease (AD) (mild cognitive impairment due to AD and mild AD dementia).

In October 2024, the TGA made the decision not to register lecanemab in Australia for the treatment of patients with early AD. In December 2024, Eisai requested reconsideration of the decision, proposing to the TGA the same apolipoprotein E4 (ApoE4) noncarrier and heterozygote indication that was agreed by the Medicines and Healthcare products Regulatory Agency (MHRA) and European Medicines Agency (EMA). In the course of the reconsideration of the initial decision, the TGA proposed an alternative narrow therapeutic indication only for ApoE4 noncarriers as an increasing number of ApoE4 alleles is a potential risk factor for ARIA. They did not agree that safety has been established for ApoE4 heterozygotes. Eisai proposed alternative indications, one of which was to maintain the ApoE4 noncarrier and heterozygote indication, but with heterozygotes treated in specialist centers and supervised by physicians with expertise in treatment of AD and monitoring for ARIA; however, the TGA rejected our proposal. 

“We are extremely disappointed and surprised by the TGA’s decision and understand that the AD community in Australia may also feel disheartened, especially given that eleven countries and regions across the globe have granted marketing authorization. We tried earnestly to reach a compromise with the TGA on an indication that would adequately represent the data in the application but were unfortunately unsuccessful at this time,” said Lynn Kramer, M.D., Chief Clinical Officer at Eisai. “The TGA proposed a narrow indication that would limit access to only ApoE4 noncarriers. This indication would deny approximately two-thirds (~70%) of all potentially eligible patients access to a treatment that could slow the progression of AD. Eisai believes ApoE4 heterozygote carriers should at least also have access to lecanemab given the similar benefit-risk profile to the noncarrier population. Therefore, we could not accept this restrictive indication as it is not patient-centric. Given this outcome, we are deeply concerned that Australians living with Alzheimer’s disease will not have access to a treatment that slows the progression of early Alzheimer’s disease by targeting its underlying causes. Eisai remains committed to ensuring eligible Australians with early Alzheimer’s disease can access lecanemab and is exploring options to achieve this, including potentially seeking review by the Administrative Review Tribunal.”

In Australia, the number of people living with dementia was estimated to be approximately 411,000 in 2023, and is reported to increase to approximately 849,000 by 2058.¹ AD is considered the most common cause of dementia, typically accounting for 60-70% of cases.² AD progresses over time in stages with increasingly severe symptoms that greatly impact not only those who are living with AD, but also their loved ones, care partners and society. There is a significant unmet need for new treatment options that slow down the progression of AD from its early stage.

Aβ which is involved in the onset of AD, gradually aggregates in the brain 15 to 20 years before symptoms appear, eventually forming insoluble plaques, a pathological feature of AD. AD is a progressive, relentless disease caused by a continuous underlying neurotoxic process that begins before and continues after plaque removal.^3,4,5 Only lecanemab works to fight AD in two ways: continuously clearing protofibrils* ,the most toxic Aβ species, and rapidly clearing plaque. This mechanism has been shown to reduce the rate of disease progression and to slow cognitive and functional decline. Lecanemab has been approved in the U.S., Japan, China, South Korea, Hong Kong, Israel, the United Arab Emirates, the United Kingdom, Mexico, Macau and Oman. Regulatory filings for the treatment have been made in the EU and 17 other countries and regions. In the EU, in February 2025, the Committee for Medicinal Products for Human Use reaffirmed its positive opinion for lecanemab in early AD, adopted in November 2024, and the European Commission is proceeding with the decision-making process for lecanemab’s marketing authorization.

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 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.⁶ 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.⁷