“leqembi®” (lecanemab) approved for the treatment of alzheimer’s disease in the united arab emirates – eisai china lnc.-leyu手机版登录入口app

eisai and biogen announced today that the ministry of health and prevention in the united arab emirates (uae) has approved humanized anti-soluble aggregated amyloid-beta (aβ) monoclonal antibody “leqembi®” (lecanemab) for the 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 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 in the u.s., japan, china, south korea, hong kong, and israel, and is being marketed in the u.s., japan, and china.

 

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 in the uae, it is reported that 4.09% of those over 60 years old have dementia. 3 ad is considered the most common cause of dementia, typically accounting for 60-70% of cases.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. biogen will commercialize leqembi in the uae.

 

* 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. 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 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. 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. qassem t., et al, prevalence and economic burden of dementia in the arab world. bjpsych open. 2023 jul; 9(4): e126. https://doi.org/10.1192/bjo.2023.517
  4. world health organization. dementia fact sheet. march 2023. available at: https://www.who.int/news-room/fact-sheets/detail/dementia.
  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.