TOKYO, CAMBRIDGE - 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 Department of Health in Hong Kong has approved humanized anti-soluble aggregated amyloid-beta (A) monoclonal antibody 'LEQEMBI' for treatment of Alzheimer's disease (AD).
Treatment with LEQEMBI should be initiated in patients with mild cognitive impairment (MCI) or mild dementia stage of disease (collectively referred to as early AD), the population in which treatment was initiated in clinical trials.
LEQEMBI selectively binds to soluble A aggregates (protofibrils), as well as insoluble A aggregates (fibrils) which are a major component of A plaques, thereby reducing both A protofibrils and A 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. Hong Kong is the fifth approval, following approvals in the U.S., Japan, China, and South Korea.
LEQEMBI's approval in Hong Kong 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 In Hong Kong, 9.3% of people aged 70 years and older were living with dementia, increasing to 32% of those aged 85 years and older. Of whom with dementia, 73.5% were reported to have Alzheimer's disease.3, 4
Eisai serves as the lead of lecanemab 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 will distribute LEQEMBI in Hong Kong.
Protofibrils are believed to contribute to the brain injury that occurs with AD and are considered to be the most toxic form of A, having a primary role in the cognitive decline associated with this progressive, debilitating condition.5 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 A 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.6
Contact:
Jack Cox
Tel: 1-781-464-3260
Email: public.affairs@biogen.com
Chuck Triano
Tel: 1-781-464-2442
Email: IR@biogen.com
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 (A).
LEQEMBI's FDA approval was 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 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 LEQEMBI reduced clinical decline on CDR-SB by 27% at 18 months compared to placebo. 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 LEQEMBI and 1.66 with placebo (difference, 0.45; 95% confidence interval [CI], 0.67 to 0.23; P
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