Lecanemab

在阿尔茨海默病治疗领域，药物研发与审批一直备受关注。经过漫长的等待和波折，卫材（Eisai）和渤健（Biogen）联合研发的药物 Leqembi 终于在欧洲获得了期待已久的批准，这一消息为该药物的发展带来了新的契机，也在医药行业引起了广泛关注。曲折获批路终迎曙光Leqembi 在欧洲的审批之路充满坎坷。去年夏天，欧洲药品管理局人用药品委员会（CHMP）曾不建议使用该药物，这让卫材大失所望。但几个月后，经过重新审查，在限制适用人群和制定特定治疗规则（患者在治疗过程中必须按特定间隔进行 MRI 扫描）的情况下，该药物迎来了转机。2024 年 11 月，Leqembi 获得了积极评价，但随后欧盟委员会（EC）要求 CHMP 对新出现的安全数据进行评估。今年 2 月，CHMP 在评估新数据后再次批准该药物。最终，作为欧洲药品审批的最高权力机构，欧盟委员会于本周二做出最终决定，批准 Leqembi 在欧洲 “严格条件” 下用于治疗早期阿尔茨海默病引起的轻度认知障碍。适用患者被严格限定为携带一个或不携带 ApoE4 基因拷贝且大脑中有淀粉样 β 斑块的人群，这是因为携带两个 ApoE4 基因拷贝的患者使用该药物时，出现脑肿胀或出血等淀粉样蛋白相关影像学异常（ARIA）副作用的风险较高。获批意义重大Leqembi 的获批是阿尔茨海默病治疗领域的一个重要里程碑。就在今年 3 月，礼来（Eli Lilly）的同类阿尔茨海默病药物 Kisunla 因类似的 ARIA 相关安全问题被欧洲药品管理局拒绝，Leqembi 成为首个在欧洲获批的此类药物。这一批准对于卫材和渤健来说至关重要，为 Leqembi 在欧洲市场的推广打开了大门。从市场角度来看，尽管 Leqembi 自 2023 年获得美国 FDA 批准后，在美国市场的推广速度较为缓慢，但欧洲市场的开放为其带来了新的增长机遇。卫材首席运营和增长官内藤圭介在 2 月的财报电话会议上就曾表示，Leqembi 即将进入 “增长扩张阶段”。随着人们对阿尔茨海默病认知的提高、诊断指南的完善以及美国新批准的给药方案，都有望推动 Leqembi 未来的市场增长。欧洲获批后，该药物将有机会触达更多患者，进一步提升其市场表现。Leqembi 在欧洲的获批为阿尔茨海默病患者带来了新的希望，也为卫材和渤健的这款药物注入了新的活力。未来，Leqembi 在欧洲市场的表现如何，以及它能否在全球范围内进一步拓展市场，助力更多患者，值得持续关注。同时，这一事件也将促使医药行业更加关注阿尔茨海默病药物的研发和安全性，推动整个领域不断向前发展。参考来源：https://www.fiercepharma.com/pharma/eisai-and-biogens-alzheimers-med-leqembi-wins-long-awaited-european-approval识别微信二维码，添加生物制品圈小编，符合条件者即可加入生物制品微信群！请注明：姓名+研究方向！版权声明本公众号所有转载文章系出于传递更多信息之目的，且明确注明来源和作者，不希望被转载的媒体或个人可与我们联系(cbplib@163.com)，我们将立即进行删除处理。所有文章仅代表作者观不本站。

In the European Union (EU), lecanemab is indicated for the treatment of adult patients with a clinical diagnosis of mild cognitive impairment and mild dementia due to Alzheimer’s disease (early AD) who are apolipoprotein E ε 4 (ApoE ε 4 * ) non-carriers or heterozygotes with confirmed amyloid pathology Lecanemab is the first therapy that targets an underlying cause of the disease to be authorized in the EU for eligible people with early AD TOKYO, Japan and CAMBRIDGE, MA, USA I April 15, 2025 I 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 European Commission (EC) has granted the amyloid-beta (Aβ) monoclonal antibody Leqembi ® (lecanemab) Marketing Authorization (MA) in the European Union (EU). This makes the medicine the first therapy that targets an underlying cause of Alzheimer’s disease (AD) to be granted a MA in the EU. 1,2 Lecanemab is indicated for the treatment of adult patients with a clinical diagnosis of mild cognitive impairment (MCI) and mild dementia due to AD (early AD) who are apolipoprotein E ε4 (ApoE ε4 * ) non-carriers or heterozygotes with confirmed amyloid pathology. 1 The lecanemab MA applies to all 27 EU Member States as well as Iceland, Liechtenstein, and Norway. 3 Lecanemab is the only approved Aβ monoclonal antibody that preferentially binds and clears toxic protofibrils ** (soluble Aβ aggregates), in addition to targeting and reducing Aβ plaques (insoluble Aβ aggregates). 1,2,4-7 Protofibrils are a key toxic form of Aβ that accumulate in the brain and cause neuronal injury. 4-10 MCI due to AD and AD dementia currently affects an estimated 15.2 million and 6.9 million people in Europe, respectively. 11 AD progresses in stages that increase in severity over time, and each stage of the disease presents different challenges for those living with AD and their care partners. There is a significant unmet need for new treatment options that slow down the progression of AD from its early stage and reduce the overall burden on people affected by AD and society. “Today’s decision makes lecanemab the first treatment option in the EU that can slow the progression of early Alzheimer’s disease. We are proud that our about 40-year heritage in dementia has led to this important milestone, as we aim to be part of the solution for a better future for those impacted by this disease globally,” said Haruo Naito, Chief Executive Officer at Eisai. “Eisai is working collaboratively with national reimbursement authorities and healthcare providers to support access for those eligible for lecanemab as soon as possible, aiming to make an impact not only on patients but also on their caregiving families and society in the EU.” “The approval of lecanemab by the European Commission marks the thirteenth approval of this important medicine, which has already benefitted thousands of patients in the United States, Japan and other regions of the world,” said Christopher A. Viehbacher, President and Chief Executive Officer at Biogen. “Lecanemab is the first treatment which showed that the reduction of the Aβ plaques in the brain is associated with the slowing of cognitive decline in patients at the early stage of the disease. This is a landmark advancement in a field where there has been no or little innovation in the past 20 years.” Eisai serves as the lead for lecanemab’s development and regulatory submissions globally with both Eisai and Biogen co-commercializing and co-promoting the product and Eisai having final decision-making authority. In the EU (excluding the Nordic countries), Eisai and Biogen will co-promote the medicine, with Eisai distributing the product as the MA Holder. In the Nordic countries, Eisai and BioArctic will co-promote the medicine, with Eisai distributing the product as MA Holder. * Apolipoprotein E is a protein involved in the metabolism of lipid in humans. It is implicated in AD. People with only one (heterozygous) or no copy (non-carriers) of the ApoE ε4 gene are less likely to experience ARIA than people with two ApoE ε4 copies (homozygous). 2 ARIA is a recognized important side effect with lecanemab that involves swelling and potential bleeding in the brain. 1,2 ** 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 of this progressive, debilitating condition. 7 Protofibrils cause injury to neurons in the brain which, in turn, can negatively impact cognitive function via multiple mechanisms, 7 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. 8 It is believed the reduction of protofibrils may slow the progression of AD by reducing damage to neurons in the brain and cognitive dysfunction. 8 ∇: This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. If you have any side effects, talk to your healthcare professional. This includes any possible side effects not listed in the package leaflet. You can also report side effects directly via your national reporting system. By reporting side effects, you can help provide more information on the safety of this medicine. Notes to Editors References SOURCE: Eisai