多奈单抗(Donanemab-AZBT) - 药物靶点：pGlu3Aβ_在研适应症：阿尔茨海默病引起的痴呆症，轻度认知障碍，阿尔茨海默症_专利_临床

概要

基本信息

药物类型

单克隆抗体

别名

Donanemab、Donanemab (USAN)、N3pG-AB-monoclonal-antibody-Eli-Lilly

+ [12]

靶点

pGlu3Aβ

作用方式

抑制剂

作用机制

焦谷氨酸 (3pE) 修饰型β-淀粉样蛋白抑制剂

治疗领域

神经系统疾病其他疾病

在研适应症

阿尔茨海默病引起的痴呆症轻度认知障碍阿尔茨海默症+ [3]

非在研适应症-

原研机构

Eli Lilly & Co.

在研机构

Eli Lilly & Co.Eli Lilly Nederland BVEli Lilly Australia Pty Ltd.

+ [2]

非在研机构-

权益机构-

最高研发阶段批准上市

首次获批日期

美国 (2024-07-02),

阿尔茨海默症

最高研发阶段(中国)批准上市

特殊审评优先审评 (美国)、突破性疗法 (美国)、优先审评 (中国)、突破性疗法 (中国)

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结构/序列

Sequence Code 190619L

来源: *****

Sequence Code 190621H

来源: *****

关联

16

项与多奈单抗相关的临床试验

NCT06996730

/ Not yet recruiting临床2/3期IIT

A Double-Blind, Placebo-Controlled, Double-Dummy Study of Donanemab and RG6289 in PSEN1 E280A Mutation Carriers, and in Non-Randomized, Placebo-Treated Non-Carriers From the Same Kindred, to Evaluate the Efficacy and Safety of Donanemab, RG6289, or the Combination of Donanemab and RG6289, in the Treatment of Autosomal-Dominant Alzheimer's Disease

The study will be conducted in 2 blinded parts (Part 1 and Part 2). In Part 1, study participants who are mutation carriers will receive active donanemab and non-mutation carriers will receive placebo-donanemab for up to 18 months (76 weeks), with a minimum treatment period of 9 months. Amyloid PET scans will be conducted at screening, 9, and 18 months in Part 1. Participants who are at or below 11 CL at screening or reach complete amyloid plaque clearance as measured by florbetapir F18 PET (defined as ≤11 CL) at 9 months will initiate Part 2. Participants who are ≤11 CL at screening may delay their entry into Part 2 for up to 6 months at the discretion of the Investigator. All remaining participants will start Part 2 after completing 18 months (76 weeks) in Part 1 independent of amyloid results. Non-carriers will receive placebo in both Parts 1 and 2.
In Part 2, study participants who are mutation carriers will be randomized 1:1:1:1 in a full factorial design to receive either RG6289 + placebo-donanemab (RG6289 alone group), donanemab + placebo-RG6289 (donanemab alone group), the combination of RG6289 and donanemab (combination group), or placebo-RG6289 and placebo-donanemab (placebo group). All non-carriers will be assigned to the placebo group. CDR-GS at the end of Part 1 and the amyloid level using the last completed amyloid PET scan in Part 1 will be used for stratification. All study participants will participate in a double-dummy design for the duration of Part 2 receiving both an intravenous (IV) infusion at the required interval for the donanemab or matching placebo as well as a daily oral treatment of RG6289 or matching placebo.
An exploratory outcome of Part 1 is a comparison of the amyloid clearance between this ADAD cohort and historical controls using propensity score matching. The primary outcome in Part 2 is change from the start of Part 2 through the end of Part 2 in brain amyloid load in PSEN1 E280A mutation carriers as measured by amyloid PET imaging. Other endpoints will include fluid and imaging biomarkers and measures of cognition and functioning. The maximum study duration for any individual participant will be 3 years, not including the screening or follow-up periods

开始日期2026-01-15

申办/合作机构

Banner Health

[+2]

NCT06911944

/ Not yet recruiting临床4期IIT

A Randomized, Double-Blind, Placebo-Controlled, Phase 4 Dose-Escalation Study Evaluating the Safety, Tolerability, and Efficacy of Donanemab in Adults With Down Syndrome

The goal of this clinical trial is to learn if donanemab can reduce levels of amyloid in the brain, and if donanemab is safe and well-tolerated in participants with Down syndrome.
The main questions it aims to answer are: Does donanemab reduce amyloid in the brain? Is donanemab safe and well-tolerated in people with Down syndrome? Researchers will compare donanemab to a placebo (a look-alike substance that contains no drug) to see if donanemab works to reduce levels of amyloid in the brain.
Participants in the study will be 35-50 years old and will be in the study for 12 months. Participants will then stay in the study for an additional 12 months in an long-term extension where all participants will receive donanemab. Participants who had a reduction in amyloid (measured by amyloid brain scan) by the end of the first 12 months will receive placebo for the long-term extension, while participants who did not have an amyloid reduction will receive study donanemab for the long-term extension. Everyone (participants and study staff) will remain blinded to treatment for the duration of the study.
Participants will:
* Have intravenous (IV) infusions of donanemab (or placebo) every 4 weeks
* Visit the clinic once every other month for checkups and tests. These tests will include brain scans (magnetic resonance imaging [MRI] and positron emission tomography [PET] ), blood draws and memory tests.
* Have a study partner who who can provide information about the participant and can join participant for some of the study visits.

开始日期2025-12-01

申办/合作机构

University of Southern California

[+3]

NCT06566170

/ RecruitingN/A

Long-Term Real-World Comparative Effectiveness of Donanemab Plus Usual Care Versus Usual Care Alone in US Patients With Early Symptomatic Alzheimer's Disease (TRAILBLAZER-REAL US)

The main purpose of this study is to evaluate the long-term effectiveness of donanemab plus usual care versus usual care alone in participants with early symptomatic AD. The study will employ a prospective, observational cohort design with participant management resembling real-world practice to the greatest extent possible via prospective assessments and linkage to historical and prospective electronic health records. The study will last about 273 weeks and may include up to 28 visits.

开始日期2024-10-07

申办/合作机构

Eli Lilly & Co.

100 项与多奈单抗相关的临床结果

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100 项与多奈单抗相关的转化医学

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100 项与多奈单抗相关的专利（医药）

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242

项与多奈单抗相关的文献（医药）

2026-02-01·Neural Regeneration Research

Recent advances in immunotherapy targeting amyloid-beta and tauopathies in Alzheimer’s disease

Article

作者: Guo, Wanshu ; Sha, Sha ; Ren, Lina ; Qu, Le ; Li, Ying ; Cao, Yunpeng ; Wang, Yan ; Xing, Xiaona

Alzheimer’s disease, a devastating neurodegenerative disorder, is characterized by progressive cognitive decline, primarily due to amyloid-beta protein deposition and tau protein phosphorylation. Effectively reducing the cytotoxicity of amyloid-beta42 aggregates and tau oligomers may help slow the progression of Alzheimer’s disease. Conventional drugs, such as donepezil, can only alleviate symptoms and are not able to prevent the underlying pathological processes or cognitive decline. Currently, active and passive immunotherapies targeting amyloid-beta and tau have shown some efficacy in mice with asymptomatic Alzheimer’s disease and other transgenic animal models, attracting considerable attention. However, the clinical application of these immunotherapies demonstrated only limited efficacy before the discovery of lecanemab and donanemab. This review first discusses the advancements in the pathogenesis of Alzheimer’s disease and active and passive immunotherapies targeting amyloid-beta and tau proteins. Furthermore, it reviews the advantages and disadvantages of various immunotherapies and considers their future prospects. Although some antibodies have shown promise in patients with mild Alzheimer’s disease, substantial clinical data are still lacking to validate their effectiveness in individuals with moderate Alzheimer’s disease.

2025-12-01·JPAD-Journal of Prevention of Alzheimers Disease

Add-on combination therapy with monoclonal antibodies: Implications for drug development

Review

Three anti-amyloid monoclonal antibodies (MABs) including aducanumab, lecanemab, and donanemab have been approved by the FDA and lecanemab and donanemab are available in the US market and a variety of other national markets. The increasing use of anti-amyloid MABs to treat early AD will require that development of novel agents occur as add-on treatment to MABs. There is limited experience with add-on therapy to anti-amyloid agents. In most cases, it is prudent to initiate novel agents after at least six-months exposure to the MAB at the highest dose. Agents with extensive data on pharmacokinetics and pharmacodynamics and well-known safety may employ alternative approaches. Anti-amyloid MABs have different mechanisms of action, titration, and side effect profiles suggesting that add-on trials include only one type of MAB if possible. Demonstration of clinical benefit with add-on therapy will require showing additional slowing beyond that provided by the anti-amyloid MAB. Anti-amyloid therapies have profound effects on biomarkers including amyloid positron emission tomography and plasma p-tau and plasma GFAP measures. Definition of the biomarker profile of a novel agent prior to initiation of add-on therapies, inclusion of target engagement biomarkers specific to the novel intervention, assessment of biomarkers not known to be affected by anti-amyloid MABs, and interrogation of the magnitude, timing, and trajectory of biomarker change in the add-on context compared to monotherapy with MABs will provide insight into the biological impact of the novel therapy on AD. Patient convenience in terms of formulation and timing of add-on therapies will be important to successful clinical implementation. Add-on therapies are an important step in addressing the complexity of AD and optimizing patient outcomes.

2025-11-01·JPAD-Journal of Prevention of Alzheimers Disease

Early Alzheimer’s disease (mild cognitive impairment or mild dementia): Prevalence, diagnostics, treatment options, and guidelines in Asia, Australasia, and Pacific nations countries

Review

作者: Shea, Yat Fung ; Park, Kee Hyung ; Tan, Lolita Stephanie ; Prusty, Vinay ; Hsu, Jung-Lung ; Panegyres, Peter K ; Eom, Young In ; Huang, Yao Hsien

Early diagnosis of mild cognitive impairment (MCI) and Alzheimer's disease (AD) with mild dementia is becoming increasingly important to enable patients to receive appropriate treatment with available amyloid-targeting therapies. Reviews of AD prevalence and diagnostic and treatment patterns typically focus on global or western populations, but the situation in Asia, Australasia, and Pacific Nations (AAPN) countries is less clear. We performed a narrative review of literature for AD in several AAPN countries, focusing on patients with MCI or mild dementia who may benefit from early treatment. Published information regarding AD incidence and prevalence and current practice in AAPN countries is limited and the nature of available information differs between countries. However, AAPN countries include some of the most rapidly aging populations and show the associated increasing trend of all-cause dementia prevalence observed globally. Although lecanemab and donanemab are now approved for AD with MCI and mild dementia in several AAPN countries, the most appropriate diagnostic pathway for patients with MCI and early AD is not established. Even though the AAPN region includes countries with routine access to advanced technologies, concerns have already been raised about the ability of healthcare systems in Australia, New Zealand, and Korea to respond to approvals of new AD therapies, including the need to ensure availability of biomarker testing and dementia specialists to allow patients to receive the early diagnosis required to enable appropriate treatment. Guidelines and national policies also need updating to differentiate between dementia subtypes and include amyloid-targeting therapies for eligible patients with early AD.

1,216

项与多奈单抗相关的新闻（医药）

2025-11-19

·新浪看点

一靶向Aβ国产「阿尔茨海默病」双抗获批临床

近日，康方生物宣布，公司独立自主研发的协同靶向Aβ和BBB高表达受体的双特异性抗体新药AK152，已正式获得国家药品监督管理局（NMPA）批准，开展用于治疗阿尔茨海默症（AD）的临床试验，该药也是中国首个用于阿尔茨海默症疾病修饰治疗的双特异性抗体新药。据康方新闻稿介绍，AK152是一种同时靶向Aβ和BBB高表达受体的双特异性抗体，一方面，其Aβ端不仅能结合Aβ斑块，还能够高选择性结合更具神经毒性的可溶性Aβ多聚体；另一方面，利用BBB高表达受体介导的胞吞-胞转运机制，显著提高AK152的入脑率。临床前研究结果表明，AK152具有显著的生物活性和良好的安全性特征，相比单抗可有效提高抗体入脑率，更快清除Aβ斑块，展现出显著优于单抗的治疗药效，有望为阿尔茨海默症患者带来新的希望。研究显示，β-淀粉样蛋白（Aβ）的异常聚集与沉积是阿尔茨海默症疾病发生发展的核心病理机制。目前全球已有数款Aβ单靶点抗体药物获批上市，如礼来（Eli Lilly）的多奈单抗（Donanemab）、卫材（Eisai）与渤健（Biogen）合作开发的仑卡奈单抗（Lecanemab）。截至2025年10月的公开信息，我国（含本土原研或已在国内申报/启动临床）处于“在研”阶段的阿尔茨海默病（AD）新药/新疗法，包可以SHR-1707（恒瑞医药）、琥珀八氢氨吖啶片（通化金马）、CM383（康诺亚生物）、RP902（润佳医药）、ZUNVEYL（β-分泌酶抑制剂+多奈哌齐复方，引进自Alpha Cognition，康哲药业）等。此外，9月石药集团（1093.HK）宣布，其自主开发的仑卡奈单抗注射液已获国家药品监督管理局（NMPA）批准，可在中国开展临床试验，适用于治疗由阿尔茨海默病（AD）引起的轻度认知障碍和阿尔茨海默病轻度痴呆。这些品种覆盖了抗-Aβ单抗、胆碱酯酶抑制剂、小分子Aβ抑制剂、肠-脑轴调节剂及改良剂型等多种机制，标志着我国阿尔茨海默病新药研发已进入“多靶点、多模态”并行推进的新阶段。新浪医药综合发布于：北京

上市批准申请上市临床结果

2025-11-19

·北京银丰鼎诚生物

超越淀粉样蛋白：阿尔茨海默病治疗的范式重构与多维干预新纪元

引言阿尔茨海默病（Alzheimer’s Disease, AD）作为全球最主要的神经退行性疾病，其研究与治疗策略长期受“淀粉样蛋白假说”主导。然而，即便抗Aβ单抗（如lecanemab、donanemab）在清除脑内Aβ斑块方面显示出一定生物学效应，其在认知功能改善方面效果有限，且伴随诸如ARIA（淀粉样蛋白相关影像学异常）等显著安全性风险。这促使科研与制药界重新审视AD的本质，并加速向更系统、更早期、更多维的干预策略转型。本文将从三大维度探讨当前AD防治的新趋势：（1）全球药物研发靶点从单一走向多元的结构性转变；（2）以FINGER研究为基石的“脑健康服务”在二级预防中的关键作用；（3）神经干细胞外泌体通过多机制协同在疾病修饰治疗中的前沿潜力。一、全球AD药物研发：从单一靶点到系统生物学导向的转变根据2024年ClinicalTrials.gov及阿尔茨海默病药物发现基金会（ADDF）年度报告数据，当前AD药物研发格局正在发生深刻变化。截至2024年，全球共有182项针对阿尔茨海默病的随机临床试验正在进行：其中30%的试验在测试疾病修饰生物制剂，43%在测试疾病修饰小分子药物，14%在测试认知增强剂，11%在测试神经精神药物。尤为关键的是，仅有33%的研究产品以β-淀粉样蛋白和tau蛋白为靶点；其余所有产品均以不同机制为靶点，如肠-脑轴、脉管系统、表观遗传学、昼夜节律、生长因子和激素、APOE状态、脂质代谢、神经发生、氧化应激、蛋白质代谢、生物能量学、突触可塑性、神经递质受体、炎症和免疫。这种多样性反映了人们对阿尔茨海默病的看法已从淀粉样蛋白级联假说的确定性观点转向更复杂、更具解释性的病理生理模型，这些模型可容纳共病和耐受性。二、脑健康服务：应对治疗困境的二级预防新策略尽管抗Aβ疗法取得一定进展，但淀粉样蛋白沉积与认知障碍之间的相关性并不始终一致，部分患者即便Aβ负荷显著降低，认知衰退仍未得到有效遏制。这一现实凸显了在症状出现前进行干预的必要性，预防因此成为当前最具成本效益的战略方向。芬兰FINGER研究（2015年发表于《The Lancet》）为此提供了关键循证依据。该研究显示，对60–77岁具有心血管风险的老年人实施为期2年的多领域干预（包括营养指导、体育锻炼、认知训练和血管风险管理），可显著改善或维持整体认知功能（效应量d=0.20），在执行功能和处理速度方面改善尤为显著。后续US POINTER及World-Wide FINGERS联盟进一步验证该模式在不同种族与文化背景下的普适性。基于FINGER研究成果，欧洲多个中心已构建“脑健康服务”（Brain Health Services, BHS）临床路径，其核心架构包括三大支柱： 1.精准风险分层：整合APOE基因型、血液生物标志物（如p-tau217、GFAP、NfL）、血管代谢指标及数字认知评估； 2.结构化风险沟通：利用可视化工具解释个体风险，强调可干预性，避免由基因信息带来的心理负担； 3.个性化多域干预处方：根据个体风险特征定制干预方案，例如： ○ APOE ε4携带者 + 高p-tau217 → 强化抗炎饮食 + 规律有氧运动； ○ 以血管风险为主 → 强化血压/血糖管理 + 认知储备训练。 BHS不仅是一种临床服务模式，更是一项公共卫生策略——它将AD的防控重心从“晚期专科诊治”转向“基层慢性病管理”，有望在人口老龄化背景下推迟疾病的发生高峰。三、神经干细胞外泌体：多机制协同的疾病修饰新载体神经干细胞来源的外泌体（NSC-derived exosomes）正成为AD治疗的新兴策略。这类直径30–150 nm的细胞外囊泡不仅继承了母体细胞的修复潜能，还具备穿越血脑屏障、低免疫原性和高生物相容性等优势。其作用机制不依赖细胞替代，而是通过多重通路协同干预AD的病理进程。近年研究表明，神经干细胞外泌体可通过以下机制发挥疾病修饰作用： 1.神经营养与突触保护：外泌体富含BDNF、GDNF、miR-124、miR-132等活性分子，可激活PI3K/Akt和CREB通路，增强突触可塑性并抑制神经元凋亡。在5×FAD小鼠模型中，静脉注射NSC外泌体显著提升空间记忆并增加树突棘密度。 2.调控神经炎症微环境：外泌体携带TGF-β、IL-10及抗炎miRNA（如miR-146a），推动小胶质细胞由促炎M1表型向修复性M2表型转化，降低脑内IL-1β、TNF-α水平，缓解慢性神经炎症损伤。 3.促进Aβ清除与Tau稳态：外泌体表面表达LRP1和neprilysin，可结合并转运Aβ肽；其内含miR-29c可下调BACE1表达，减少Aβ生成。同时，miR-132通过抑制GSK-3β活性，降低Tau蛋白过度磷酸化。 4.增强脑血管功能与代谢支持：外泌体传递VEGF、miR-126等因子，促进脑微血管内皮增殖与屏障完整性修复，改善脑血流并提升葡萄糖摄取与线粒体功能。 5.激活内源性修复机制：动物实验显示，外泌体可刺激海马齿状回神经干细胞巢增殖与分化，增强内源性神经发生，形成“外源引导–内源响应”的再生循环。

临床结果临床研究

2025-11-18

·ETPharma

Eli Lilly gets CDSCO nod for Alzheimer's drug Donanemab

New Delhi: US pharma major, Eli Lilly has secured CDSCO nod for its Alzheimer's drug Donanemab . The therapy is approved for adults with early symptomatic stages, particularly individuals with mild cognitive impairment (MCI) and those in the mild dementia stage of AD, with confirmed amyloid pathology. Before India, the therapy had secured marketing approval from the US FDA in 2024 and later in Japan and China as well. Donanemab , marketed under the brand name Kisunla, had initially faced reservations in Europe due to its limited efficacy in select patient group and its ability to ‘only delay the risk of serious adverse events’ such as brain swelling and bleeding. However, in July this year, the European Medicines Agency granted its approval following a re-examination bid from Lilly. Lilly’s drug is a disease modifying therapy that helps the body remove excessive buildup of amyloid plaques – a type of protein and slows the cognitive and functional decline. “The approval of Donanemab marks a significant milestone in our mission to address the urgent needs of people living with Alzheimer’s disease in India,” said Winselow Tucker, president and general manager, Lilly India. By Online Bureau ,

上市批准

100 项与多奈单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11500	多奈单抗	-	-

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
阿尔茨海默病引起的痴呆症	英国	Eli Lilly Nederland BV	2024-10-23
阿尔茨海默病引起的痴呆症	英国	Eli Lilly & Co.	2024-10-23
轻度认知障碍	英国	Eli Lilly Nederland BV	2024-10-23
轻度认知障碍	英国	Eli Lilly & Co.	2024-10-23
阿尔茨海默症	美国	Eli Lilly & Co.	2024-07-02

未上市

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适应症	最高研发状态	国家/地区	公司	日期
精神障碍	申请上市	加拿大	Eli Lilly Canada, Inc.	-
神经认知障碍	临床3期	中国	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	阿根廷	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	澳大利亚	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	波兰	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	韩国	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	西班牙	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	中国台湾	Eli Lilly & Co.	2022-10-10
神经认知障碍	临床3期	英国	Eli Lilly & Co.	2022-10-10
认知功能障碍	临床2期	美国	Eli Lilly & Co.	2020-11-23

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临床结果

适应症

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT05738486 (TRAILBLAZER-ALZ 6, CTgov)	临床3期	阿尔茨海默症 \| 神经认知障碍	1,175	Placebo+Donanemab (1400 mg Donanemab - Standard Regimen)	膚廠顧憲醖構艱鬱製鏇 = 遞淵簾鏇繭獵願製窪廠構築壓繭網鏇襯製顧蓋 (積遞淵蓋鹽鏇願衊鬱鬱, 鬱鏇選蓋選糧襯窪襯繭 ~ 鑰範鹹願壓繭範廠鏇觸) 更多	-	2025-11-14
				Placebo+Donanemab (1400 mg Donanemab - Dose Skipping)	膚廠顧憲醖構艱鬱製鏇 = 範艱艱製製願遞簾憲願構築壓繭網鏇襯製顧蓋 (積遞淵蓋鹽鏇願衊鬱鬱, 築淵廠積餘鬱網憲築淵 ~ 範廠簾鹹構觸襯廠鏇衊) 更多
NCT04437511 (TRAILBLAZER-ALZ 2, PRNewswire) 人工标引	临床3期	阿尔茨海默症	-	Kisunla	鏇醖鹹製網構鬱壓觸夢(膚憲憲壓顧襯窪蓋顧簾): Difference = -0.6 更多	积极	2025-07-30
				Neuroimaging Initiative (untreated external cohort)
NCT04437511 \| NCT03367403 (TRAILBLAZER-ALZ and ALZ 2, Pubmed \| JAMA Neurol)	N/A	阿尔茨海默症 APOE ε4 allele number \| amyloid levels	3,030	Donanemab	鹹夢醖簾淵觸鬱鏇願鏇(鬱鹽顧蓋製艱齋簾觸顧) = 壓鹽網構鏇願膚顧觸選鑰夢齋網壓觸簾鑰衊憲 (鬱觸構廠觸憲膚觸蓋網 ) 更多	积极	2025-05-01
				Placebo	鹹夢醖簾淵觸鬱鏇願鏇(鬱鹽顧蓋製艱齋簾觸顧) = 繭壓襯淵願壓築膚網製鑰夢齋網壓觸簾鑰衊憲 (鬱觸構廠觸憲膚觸蓋網 ) 更多
NCT05108922 (TRAILBLAZER-ALZ 4, Pubmed \| Alzheimers Dement)	临床3期	阿尔茨海默症 amyloid plaque clearance	148	Donanemab	窪網憲衊餘觸繭鬱衊憲(範製遞簾範構夢齋鬱繭) = 顧淵廠窪襯醖鬱憲窪鬱廠窪觸構餘蓋衊廠鏇鹹 (廠窪齋鏇糧鏇築壓膚鹽 ) 更多	积极	2025-05-01
				Aducanumab	窪網憲衊餘觸繭鬱衊憲(範製遞簾範構夢齋鬱繭) = 醖築鑰憲窪鹹窪夢鏇夢廠窪觸構餘蓋衊廠鏇鹹 (廠窪齋鏇糧鏇築壓膚鹽 ) 更多
NCT05738486 (TRAILBLAZER-ALZ 6, Company_Website 1 \| Company_Website 2) 人工标引	临床3期	阿尔茨海默症	843	received two vials (700 mg) of donanemab for the first three infusions, then four vials (1400 mg) thereafterdonanemab for the first three infusions, then four vials (1400 mg) thereafter (Standard Dosing Regimen)	網築鬱襯觸餘鬱構鏇鹽(廠襯膚襯鏇蓋積簾憲窪) = 淵憲襯醖壓觸積鏇積築壓網簾憲膚衊選願選鏇 (憲憲構夢淵窪衊鏇積築 ) 更多	积极	2024-10-29
				received 1 vial (350 mg) of donanemab for the first infusion, two vials (700 mg) for the second infusion, three vials (1,050 mg) for the third infusion,donanemab for the first infusion, two vials (700 mg) for the second infusion, three vials (1,050 mg) for the third infusion, and four vials (1400 mg) per infusion thereafter (Modified Titration)	網築鬱襯觸餘鬱構鏇鹽(廠襯膚襯鏇蓋積簾憲窪) = 憲淵鹹膚餘繭蓋衊窪襯壓網簾憲膚衊選願選鏇 (憲憲構夢淵窪衊鏇積築 ) 更多
NCT01837641 (CTgov)	临床1期	阿尔茨海默症 \| 认知功能障碍 \| 轻度认知障碍	63	Placebo (Placebo IV)	窪繭鏇襯壓餘積鏇顧顧 = 繭壓憲艱淵觸醖衊製築齋獵蓋積願願淵鏇憲願 (顧選蓋鹽網壓淵齋窪襯, 餘餘廠淵襯夢選窪淵鹹 ~ 簾鹹範膚遞簾願餘築鑰) 更多	-	2024-10-04
				LY3002813 (0.1 mg/kg / 0.3 mg/kg LY3002813 IV)	窪繭鏇襯壓餘積鏇顧顧 = 鹹遞膚壓顧範獵範積醖齋獵蓋積願願淵鏇憲願 (顧選蓋鹽網壓淵齋窪襯, 繭壓餘廠憲醖襯鬱廠積 ~ 願衊淵蓋積窪願獵憲顧) 更多
NCT05567159 (CTgov)	临床1期	-	42	Donanemab	積膚積膚製獵壓網齋醖(鹹衊窪簾獵鑰觸繭願積) = 窪鬱鑰糧蓋遞願鹽鏇觸範觸齋襯廠壓壓構蓋艱 (鏇窪獵糧願衊夢顧積壓, 23) 更多	-	2024-10-04
NCT05533411 (CTgov)	临床1期	-	36	Placebo (Placebo)	鑰鏇顧糧鏇夢淵觸衊繭 = 構夢構廠製遞範蓋選鏇築顧製遞顧醖醖築網選 (積構鹹襯鹽襯淵鹽選鬱, 艱餘蓋醖窪壓鑰蓋鹹鬱 ~ 夢獵觸膚壓選選餘齋構) 更多	-	2024-10-04
				Donanemab (700 mg Donanemab)	鑰鏇顧糧鏇夢淵觸衊繭 = 膚衊遞廠簾淵齋觸築鹽築顧製遞顧醖醖築網選 (積構鹹襯鹽襯淵鹽選鬱, 廠窪簾願淵鏇夢糧衊築 ~ 網網壓蓋繭夢鹹窪製獵) 更多
NCT04437511 (FDA_CDER) 人工标引	临床3期	阿尔茨海默症	1,736	KISUNLA	鑰積積獵獵遞憲艱壓夢(膚簾餘鹹醖網鹽繭窪構): Difference = 2.92, P-Value = <0.0001 更多	积极	2024-07-02
				Placebo
NCT04437511 \| NCT03367403 (TRAILBLAZER-ALZ \| TRAILBLAZER-ALZ2, AAN2024)	临床2/3期	number of microhemorrhages \| cortical superficial siderosis \| mean arterial pressure ... 更多	2,031	Donanemab	淵積鏇觸醖範鏇選鬱築(鏇積繭觸鏇憲鏇餘顧鏇) = 鹽襯襯廠餘齋鏇築膚範觸憲願廠積夢廠繭顧鏇 (願積製蓋糧範觸衊簾淵 )	积极	2024-04-09