Eisai Co., Ltd. (Headquarters: Tokyo, CEO: Haruo Naito, “Eisai”) and Biogen Inc. (Nasdaq: BIIB, Corporate headquarters: Cambridge, Massachusetts, CEO: Christopher A. Viehbacher, “Biogen”) announced that the Federal Commission for the Protection Against Sanitary Risk (COFEPRIS) in Mexico has approved humanized anti-soluble aggregated amyloid-beta (Aβ) monoclonal antibody “LEQEMBI^®” (lecanemab) for the treatment of early Alzheimer’s disease (AD)*.

LEQEMBI selectively binds to soluble Aβ aggregates (protofibrils**), as well as insoluble Aβ aggregates (fibrils) which are a major component of Aβ plaques, thereby reducing both Aβ protofibrils and Aβ plaques in the brain. LEQEMBI is the first approved treatment shown to reduce the rate of disease progression and to slow cognitive and functional decline through this mechanism. LEQEMBI is also approved and being marketed in the U.S., Japan, China, South Korea, Hong Kong, Israel, the United Arab Emirates, and Great Britain.

LEQEMBI’s approval is based on the large global Phase 3 Clarity AD study. In the Clarity AD study, LEQEMBI met its primary endpoint and all key secondary endpoints with statistically significant results.^1,2

Approximately 1.3 million people in Mexico are estimated to suffer from AD, accounting for 60-70% of all dementia diagnoses.³  AD most commonly affects individuals over the age of 65.³  

Eisai serves as the lead of LEQEMBI development and regulatory submissions globally with both Eisai and Biogen co-commercializing and co-promoting the product and Eisai having final decision-making authority. Eisai and Biogen will co-commercialize and co-promote LEQEMBI in Mexico.

* Collectively referred to mild cognitive impairment due to AD or mild AD dementia.

** 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.⁴ 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.⁵