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Lecanemab (Leqembi®) Approved in Hong Kong for Early Alzheimer’s Disease Treatment

Jul 11, 2024 10:49 CST Updated 10:49
Eisai

Pharmaceutical Product R&D and Manufacturer

Biogen

New Drug Developer

Eisai and Biogen Announce Approval of Leqembi® (Lecanemab), a Humanized Anti-Soluble Aggregating Amyloid-beta (Aβ) Monoclonal Antibody, by the Department of Health of the Hong Kong Special Administrative Region Government for the Treatment of Alzheimer's Disease. Leqembi® is indicated for patients with mild cognitive impairment or mild dementia stage, consistent with the population initiated in clinical trials.

 

Lecanemab selectively binds to soluble Aβ aggregates (protofibrils*) as well as insoluble Aβ aggregates (fibrils), the main component of Aβ plaques in AD, thereby reducing Aβ protofibrils and Aβ plaques in the brain. Lecanemab is the first fully approved treatment that slows disease progression and reduces cognitive and brain function decline through this mechanism. Hong Kong, China, is the fifth country/region to approve the drug, following the United States, Japan, China, and South Korea.

 

Leqembi (Lecanemab) Approved in Hong Kong, China, Based on the Global Large-Scale Phase III Clarity AD Study. In the Clarity AD study, Leqembi (Lecanemab) met the primary endpoint and all key secondary endpoints, with results statistically significant.1，2In Hong Kong, China, 9.3% of people aged 70 and above suffer from dementia, and this proportion increases to 32% among those aged 85 and above, with 73.5% reported to have Alzheimer's disease.3，4。

 

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 will be responsible for the commercial promotion of this product in Hong Kong, China.

 

*Fibrils are considered the culprit behind brain damage in AD patients, containing the highest toxicity within Aβ, and playing a major role in the cognitive decline associated with this progressively debilitating disease.5。Fibrils cause damage to brain neurons, and then negatively affect cognitive function through various mechanisms. This not only increases the formation of insoluble β plaques but also enhances direct damage to 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.6。

 

References

  1. Eisai presents full results of lecanemab Phase 3 confirmatory Clarity AD study for early Alzheimer’s disease at Clinical Trials on Alzheimer’s Disease (CTAD) conference. Available at: https://www.eisai.co.jp/news/2022/news202285.html
  2. van Dyck, H., et al. Lecanemab in Early Alzheimer’s Disease. New England Journal of Medicine. 2023;388:9-21. https://www.nejm.org/doi/full/10.1056/NEJMoa2212948.
  3. Department of Health – Press Release “Dementia Care Seminar cum Kick-off Ceremony for Dementia Care Campaign. Available at: https://www.dh.gov.hk/english/press/2006/061013.html
  4. Ruby Yu , et al. Trends in Prevalence and Mortality of Dementia inElderly Hong Kong Population: Projections, Disease Burden, andImplications for Long-Term Care. Int J Alzheimer’s Dis. 2012(7593):406852. doi: 10.1155/2012/406852
  5. 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
  6. 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.