Eisai and Biogen Jointly Announce Commercial Launch of Leqembi in South Korea
Lecanemab selectively binds to soluble Aβ aggregates (protofibrils*) and insoluble Aβ aggregates (fibrils), the main components of Aβ plaques in AD, thereby reducing Aβ protofibrils and Aβ plaques in the brain. Lecanemab is the first approved treatment drug that slows disease progression and cognitive and functional decline through this mechanism.
Reportedly, there were approximately 900,000 people with dementia in South Korea in 2021.1Among them, one in ten people aged 65 and over suffers from dementia, and one in five suffers from mild cognitive impairment.2Patients with Alzheimer's disease dementia account for about 70% of all dementia patients. It is estimated that the annual average cost of care/medical treatment for each dementia patient is 21.1 million Korean won (KRW), while the cost for severe dementia patients is as high as 33.1 million Korean won.1。
Eisai is leading the global development and registration application of lecanemab, while the product is co-commercialized and promoted by Eisai and Biogen. Among them, Eisai has the final decision-making power. Eisai Korea will be responsible for the distribution and information promotion activities of the product in Korea.
Eisai Korea has been a pioneer in the field of dementia for many years, dedicating itself to various activities to raise disease awareness. In recent years, Eisai Korea has collaborated with stakeholders including healthcare professionals, academic groups, patient communities, care centers, health examination companies, and diagnostic firms to build a dementia ecosystem that promotes Alzheimer’s disease (AD) awareness, early diagnosis, and early treatment. Eisai Korea will first launch the drug in the self-pay market and plans to establish a patient assistance program to provide lecanemab for patients awaiting treatment, bringing positive impacts not only to patients but also to their caregivers and Korean society as a whole.
*Fibrils are considered the culprit behind brain damage in AD patients, containing the highest toxicity among Aβ, and playing a major role in the cognitive decline associated with this progressively debilitating disease.3。Fibrils cause damage to brain neurons, and then negatively affect cognitive function through various mechanisms. They not only increase the formation of insoluble β plaques but also directly harm the connections that transmit signals between brain cell membranes and neurons or between neurons and other cells. Reducing fibrils can decrease damage to brain neurons and cognitive dysfunction, thereby halting the progression of Alzheimer's disease.4。
Media Contact
Eisai Co., Ltd. Public Relations Department Tel: 03-3817-5120
Biogen Public Affairs Department Email: public.affairs@biogen.com
References
- Korean dementia observatory 2022: National Institute of Dementia (Korean)
- Korean dementia observatory 2021: National Institute of Dementia (Korean)
- Amin L, Harris DA. Aβ receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers. Nat Commun. 2021;12:3451. doi:10.1038/s41467-021-23507-z
- Ono K, Tsuji M. Protofibrils of Amyloid-β are Important Targets of a Disease-Modifying Approach for Alzheimer’s Disease. Int J Mol Sci. 2020;21(3):952. doi: 10.3390/ijms21030952. PMID: 32023927; PMCID: PMC7037706.