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更新于：2026-02-27
Gantenerumab
甘特鲁单抗
更新于：2026-02-27
概要
基本信息
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)终止 |
特殊审评突破性疗法 (美国) |
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结构/序列
Sequence Code 65473H
来源: *****
Sequence Code 65501L
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关联
19
项与 甘特鲁单抗 相关的临床试验NCT05256134
A Phase III, Multicenter, Randomized, Parallel-Group, Double-Blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Gantenerumab in Participants at Risk for or at the Earliest Stages of Alzheimer's Disease
A study to evaluate the efficacy and safety of gantenerumab in amyloid-positive, cognitively unimpaired participants at risk for or at the earliest stages of AD. The planned number of participants for this study is approximately 1200 participants randomized in a 1:1 ratio to receive either gantenerumab or placebo (600 participants randomized to gantenerumab and 600 participants randomized to placebo).
开始日期2022-04-19 |
申办/合作机构 |
CTR20210207
一项在健康中国受试者中考察单次腹部皮下注射GANTENERUMAB高浓度液体制剂后药代动力学、安全性和耐受性的单中心、开放性、I期研究
本研究将在健康中国受试者中评价G4工艺生产的gantenerumab在单次皮下注射510 mg剂量后的药代动力学、安全性和耐受性特征。
1. 药代动力学目的：根据以下终点，描述健康中国受试者单次SC注射（510 mg）gantenerumab的药代动力学特征：
● 主要PK参数：AUCinf和Cmax
● 次要PK参数：AUC0-672h、AUC0-last、t1/2（如下方法计算：ln 2/消除速率常数[λz]）、表观清除率（CL/F）、非静脉给药后的终末期分布容积（Vz/F）
2. 安全性目的
根据以下终点，评价健康中国受试者单次SC注射（510 mg）gantenerumab的安全性和耐受性：
● 不良事件的性质、发生率、严重程度和因果关系
● 使用视觉模拟量表（VAS）和言语评定量表（VRS）进行局部疼痛评估
● 异常实验室检查结果、异常生命体征和异常心电图的发生率
● ISR的发生率（局部和全身）
3. 免疫原性目的
根据以下终点评价受试者对gantenerumab的免疫应答：
● 研究期间gantenerumab抗药抗体（ADA）发生率相对基线时ADA发生率的变化
开始日期2021-06-02 |
申办/合作机构 |
NCT04374253
An Open-Label, Multicenter, Rollover Study to Evaluate the Safety, Tolerability, and Efficacy of Long-Term Gantenerumab Administration in Participants With Alzheimer's Disease
This is an open-label, multicenter, rollover study to evaluate the safety, tolerability, and efficacy of long-term administration of open-label gantenerumab in participants with AD who completed Study WN29922 or WN39658, either the double-blind or open-label extension (OLE) part.
开始日期2021-01-26 |
申办/合作机构 |
100 项与 甘特鲁单抗 相关的临床结果
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100 项与 甘特鲁单抗 相关的转化医学
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100 项与 甘特鲁单抗 相关的专利（医药）
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114
项与 甘特鲁单抗 相关的文献（医药）2026-02-01·JOURNAL OF ALZHEIMERS DISEASE
Severe symptomatic amyloid-related imaging abnormalities in Alzheimer's disease: Two case reports and systematic review of reported cases
Review
作者: Muñoz-García, Mariana I ; González-Sánchez, Marta ; Blanco-Palmero, Víctor Antonio ; Llamas-Velasco, Sara ; Hilario, Amaya ; Villarejo Galende, Alberto ; Pérez-Martínez, David A ; Morenas-Rodríguez, Estrella ; Ramos-González, Ana
Background:
Amyloid-related imaging abnormalities (ARIA) are a recognized complication of anti-amyloid monoclonal antibodies for Alzheimer's disease (AD). While typically asymptomatic, a subset of patients develops severe clinical symptoms and radiological findings requiring intensive management. Data on their presentation, treatment, and outcomes remain limited.
Objective:
We report two cases and analyze the clinical features of all published cases of severe symptomatic ARIA, with a focus on associated risk factors, therapeutic approaches, and patient outcomes.
Methods:
We report two cases of severe symptomatic ARIA in patients treated with gantenerumab. A systematic review was conducted following PRISMA guidelines using MEDLINE, Web of Science, and manual reference screening. We included case reports and series providing individual-level data on symptomatic ARIA episodes classified as severe by clinical criteria. Demographic, genetic, clinical, radiological, therapeutic, and outcome data were extracted.
Results:
Thirty-six cases were included (2 new and 34 from 21 publications). Fifteen cases were associated with lecanemab, 10 with gantenerumab, 6 with donanemab, and 5 with other antibodies.
APOE
ε4 was present in 62.5%, including 10 ε4/ε4 homozygotes. Baseline MRI showed hemorrhagic markers in 10 cases, including superficial siderosis in 2 of the 5 patients with isolated macrohemorrhages. Most episodes occurred within 6 months of treatment. Symptoms included altered consciousness (75%), focal deficits (66.7%), seizures (38.9%), and headache (36.1%). ARIA-E resolved in all non-fatal cases. Corticosteroids were used in 72%. Among the patients whose outcome data were available, 15 patients recovered completely, 10 had persistent deficits, and 10 died.
Conclusions:
Severe symptomatic ARIA is a rare but serious adverse effect of anti-amyloid therapy. Standardized diagnostic and therapeutic guidelines are needed to minimize ARIA-related morbidity and mortality.PROSPERO registration no. CRD420251055067
2026-02-01·CNS DRUGS
Hippocampal Atrophy on Magnetic Resonance Imaging as a Surrogate Marker for Clinical Benefit and Neurodegeneration in Early Symptomatic Alzheimer’s Disease: Synthesis of Evidence from Observational and Interventional Trials
Review
作者: Porsteinsson, Anton ; Dickson, Sam ; Hey, John A ; Tosun, Duygu ; Yu, Jeremy ; Albayrak, Adem ; Kesslak, J Patrick ; Petrella, Jeffrey ; Flint, Susan ; Bracoud, Luc ; Durrant, Abe ; Ritchie, Craig ; Doraiswamy, P Murali ; McLaine, Rosalind ; McSweeney, Emer ; Schaefer, Jean F ; Tolar, Martin ; Abushakra, Susan ; Sabbagh, Marwan ; Gauthier, Serge ; Bray, Margaret ; Barakos, Jerome ; Barkhof, Frederik ; Liang, Earvin ; Hendrix, Suzanne ; Boada, Merce ; Watson, David ; Cohen, Sharon ; Power, Aidan
Amyloid-plaque reduction is currently the only recognized surrogate outcome for Alzheimer's disease (AD) trials, allowing accelerated approval of plaque-clearing amyloid antibodies. However, plaque reduction does not facilitate the development of new non-plaque-clearing treatments. The hippocampus is among the first brain regions affected by AD pathology, exhibiting synaptic dysfunction and neurodegeneration that manifests as hippocampal atrophy and memory decline. We evaluated hippocampal volume (HV) as a potential surrogate outcome that can predict clinical benefit in disease-modification trials. Using published data from observational and interventional studies that examined both cognition and HV on volumetric magnetic resonance imaging (vMRI), we evaluated the cross-sectional correlations of HV to cognitive performance, the longitudinal correlations of HV atrophy to cognitive decline, HV sensitivity to drug effects, and the correlations between drug effects on HV atrophy and cognitive decline. We also examined the magnitude of HV protection that corresponds to meaningful clinical benefit. Analyses from 30 observational studies encompassing 13,187 individuals (2633 cognitively normal; 10,554 early AD) showed significant cross-sectional correlations between baseline HV and cognition, and longitudinal correlations between HV atrophy and cognitive decline over ≥ 1 year. The relationship of HV-cognitive drug effects was examined at the group level in nine placebo-controlled trials of five antiamyloid agents that evaluated HV in early AD trials of at least 18 months' duration. These trials included four amyloid antibodies (aducanumab, lecanemab, donanemab, and gantenerumab) and one oral anti-oligomer agent (valiltramiprosate). Individual-level HV-cognition relationships were examined in two valiltramiprosate studies, one of which included diffusion tensor imaging (DTI) providing microstructural correlates of HV drug effects and helping distinguish neuroprotection from brain edema. Across these anti-amyloid drug trials (total N ~10,000), there was a linear relationship between drug effects on slowing of cognitive decline and slowing of HV atrophy. Two anti-oligomer trials (valiltramiprosate) reported significant subject-level correlations between drug effects on HV and cognition over 18-24 months (r = -0.40 to -0.44, p < 0.005, N = 50/69), with significant correlations of drug effects on brain microstructure (decreased mean diffusivity) with both HV and cognitive benefits, supporting reduced neurodegeneration. The minimal HV preservation at the mild cognitive impairment (MCI) stage that is associated with clinical benefit is estimated to be ≥ 40 mm3 or ≥ 10% of atrophy in the placebo arm over 18 months. Our findings demonstrate that hippocampal atrophy is an early indicator of cognitive decline in AD, linked to amyloid and tau-related neurodegeneration. HV on standardized vMRI is sensitive to anti-amyloid treatments, demonstrating strong correlations between slowed hippocampal atrophy and slowed cognitive decline. Data from over 23,000 subjects over three decades support HV as a surrogate marker for predicting clinical benefit in early symptomatic AD.
2026-02-01·Clinical Pharmacology in Drug Development
Bioequivalence Between a Gantenerumab Disposable Syringe and an Autoinjector: A Randomized Controlled Trial in Healthy Volunteers
Article
作者: Hofmann, Carsten ; Keshavarz, Ali ; Schwab, Dietmar ; Bittner, Beate ; Martens, Kimberly ; Dickerson, Daniel S. ; van Iersel, Thijs ; Justies, Nicole
Abstract:
Gantenerumab, a monoclonal antibody targeting amyloid beta plaques in the brain, reduces plaque accumulation and was developed to slow Alzheimer's disease progression. Results from the pivotal GRADUATE I and II studies evaluating gantenerumab in people with early Alzheimer's disease were announced in 2022. The studies did not meet their primary endpoint of slowing clinical decline. This study evaluated the pharmacokinetics, immunogenicity, and safety of a high concentration liquid formulation of gantenerumab administered subcutaneously as a single dose using an autoinjector (AI) or a disposable syringe (DS). The DS was employed in pivotal clinical trials, while the AI was developed in parallel to ease SC administration. The study aimed to demonstrate bioequivalence (BE) between AI and DS administration in healthy participants, defined by 90% confidence intervals (CIs) for geometric least square (LS) mean ratios being within the 0.80‐1.25 range for maximum observed plasma concentration (C
max
) and area under the plasma concentration–time curve (AUC). Among the 266 healthy participants, 135 received 255 mg gantenerumab via AI and 131 received 255 mg via DS in a parallel group design. BE between AI and DS SC administration was demonstrated with geometric LS mean ratios (90% CIs) for C
max
, AUC
0‐inf
, and AUC
0‐last
of 1.078 (1.006, 1.155), 1.053 (0.986, 1.124), and 1.054 (0.992, 1.121), respectively, all within the 0.80‐1.25 BE range. Safety findings were consistent with the known safety profile of gantenerumab.
345
项与 甘特鲁单抗 相关的新闻（医药）2026-02-04
*仅供医学专业人士阅读参考
2025年AD十项关键研究拼出未来。
撰文丨医学界报道组
阿尔茨海默病（AD）作为全球老龄化进程中最棘手的神经退行性疾病之一，长期以来面临诊断滞后、治疗手段有限、安全性挑战等多重困境。2025年，该领域迎来了多项里程碑式进展。在此背景下，医学界特邀复旦大学附属华山医院郁金泰教授与崔梅教授，围绕2025年度AD领域十大关键研究、以及混合病理鉴别、生物制剂突破等核心议题，展开系统梳理与深度对话。
2025年度核心关键词：从研究成果到领域趋势的浓缩
郁金泰教授指出，2025年AD领域的进展，可凝练为十个具有代表性的关键词，其中，八个关键词集中体现了核心研究突破的方向，包括：血浆p-tau217、Donanemab、Trontinemab、同种异体间充质干细胞疗法、靶向Tau、大数据新药研发革命、中国实践（仑卡奈单抗真实世界研究）、ARIA安全性管理。
此外，还有两项体系性的关键进展：血液生物标志物（BBMs）指南的发布，首次在全球层面明确了血液检测作为分诊工具与病理鉴定手段的双重角色，为标准化诊断流程提供了关键依据；而仑卡奈单抗皮下注射的给药方式革新，通过每周500mg的治疗方式，在确保与静脉输注相当药物暴露水平的同时，显著提升了治疗的可及性、便利性与长期依从性。
2025年度TOP10研究：从临床数据到诊疗变革的实践突破
2025年AD领域的研究在诊断、药物、技术与预防等多个维度均取得了关键进展，其核心突破体现在以下十个研究中。郁金泰教授分别详细介绍了这十大研究。
➤ 研究一：中国实践——仑卡奈单抗的真实世界验证
由复旦大学附属华山医院牵头的首个仑卡奈单抗中国多中心真实世界研究[1]，纳入了全国7家医院共407例患者，平均随访5.6个月。结果显示，治疗6个月后，患者的生物标志物显著改善，认知功能保持稳定。在接受MRI复查的患者中，淀粉样蛋白相关影像异常（ARIA）发生率为12%，其中89.74%为无症状，58.97%的影像学表现为轻度。
在安全性方面，不良事件发生率低且可控。22%的患者出现输注相关症状，10%报告输液相关反应（IRRs），经对症处理后均能缓解。该研究为中国人群应用仑卡奈单抗提供了真实世界有效性和安全性数据，不仅填补了本土证据空白，也为临床制定个体化治疗方案提供了直接参考。
➤ 研究二：Donanemab改良滴定方案——实现疗效与安全的平衡
TRAILBLAZER-ALZ6 Ⅲb期临床试验[2]直接比较了Donanemab标准方案（700mg起始）与改良滴定方案（350/700/1050mg起始）的安全性和疗效。结果显示，改良方案将24周内ARIA-E（水肿型）发生幅度降低达40.5%，且严重程度显著减轻。同时，两种方案的Aβ清除效果无统计学差异，疗效相当。
➤ 研究三：Trontinemab——基于脑穿梭技术的双特异性抗体
Trontinemab是一种采用创新“脑穿梭（Brainshuttl）”技术的双特异性抗体。临床试验初步数据[3]显示其强大的病理清除能力。接受3.6mg/kg剂量治疗28周后，92%的患者达到Aβ-PET阴性标准（≤24 centiloids）。在探索性临床终点方面，包括CDR-SB、MMSE、CSF Aβ40/42等指标均显示出改善趋势，但尚未达到统计学显著性。该药物的核心价值在于其作用机制所带来的双重潜在优势：一方面大幅提升了药物在脑内的有效浓度，另一方面减少对血管壁的非特异性作用，从而从源头上降低ARIA的发生风险。
➤ 研究四：DIAD长期抗体治疗随访研究——病理清除与临床获益的落差
针对显性遗传性阿尔茨海默病（DIAD）人群的首项长期抗体治疗研究[4]公布了3年随访数据。该研究评估了高剂量Gantenerumab在此类预计中年发病的明确遗传人群中的效果。结果显示，长期治疗能显著清除大脑Aβ斑块，最高清除率达71%，并伴随部分下游生物标志物的有益变化。但这一显著的病理改善未能转化为具有统计学意义的临床认知功能延缓。在安全性方面，高达53%的参与者出现ARIA，这一高发生率限制了高剂量方案的临床应用。
➤ 研究五：靶向转铁蛋白受体的抗体递送策略——提升脑内暴露，降低ARIA风险
新一代ATVcisLALA抗体通过结构双重优化，在增强疗效与提升安全性方面取得关键突破。该抗体首先利用靶向转铁蛋白受体（TfR）的抗体传输载体（ATV）结构，显著提升穿越血脑屏障的效率，使脑内抗体浓度增加5~8倍；同时通过LALA突变（亮氨酸替换为丙氨酸），降低其免疫激活潜力，从而减少血管炎症反应[5]。动物实验[6]进一步证实，该抗体在有效清除Aβ沉积的同时，能显著降低ARIA发生风险。
➤ 研究六：血浆p-tau217揭示AD病理分布——早诊人群的精准定位
一项针对超1.1万名挪威社区老年人的大规模研究[7]，通过检测血浆p-tau217，首次明确了AD神经病理改变（ADNC）的社区流行率。数据显示，ADNC患病率随年龄呈现显著递增：在58~69岁人群中低于8%，而90岁以上人群则高达65.2%。在70岁及以上人群中，33.4%存在ADNC，其中10%为临床前AD，10.4%为前驱期AD，9.8%为AD痴呆。2025年5月，美国FDA正式批准了基于p-tau217/Aβ42比值的血液检测体外诊断工具[8]，其临床价值在于实现了病理早期无创筛查，为精准定位、早期干预人群提供了革命性工具。
➤ 研究七：抗癌药“跨界”AD——多靶点联合治疗的新可能
单细胞图谱技术揭示了AD患者大脑中存在的细胞类型异质性，包括抑制性神经元比例降低、细胞通讯失衡，提示治疗可能需要多靶点干预。为此，该研究通过药物重定位与电子病历分析筛选，预测来曲唑与伊立替康两种药物可以协同逆转神经元的异常基因表达[9]。在AD动物模型中，该联合治疗方案不仅显著改善了记忆功能衰退，还减轻了Aβ沉积、Tau病理及神经炎症水平[9]。
➤ 研究八：异体干细胞疗法Laromestrocel——脑萎缩的“减速阀”
一项Ⅱa期随机对照临床试验[10]首次评估了静脉输注异体间充质干细胞Laromestrocel在轻度AD患者中的有效性与安全性。结果显示，治疗39周后，与安慰剂组相比，高剂量组的全脑萎缩速度减缓48.4%，左侧海马体积萎缩速度降低61.9%；同时，该疗法表现出良好的安全性特征，未报告ARIA等严重不良事件，整体耐受性良好。该疗法被认为通过抗炎、免疫调节及神经保护等多重机制发挥作用，为AD治疗提供了一种全新的非药物干预路径。
➤ 研究九：内源性锂缺乏——AD早期的关键驱动因素
近期研究[11]发现，AD及轻度认知障碍（MCI）患者脑内锂水平显著降低，而Aβ斑块可螯合锂离子，导致其生物利用度进一步下降，从而加剧病理进程。动物实验证实，锂缺乏会直接加速Aβ沉积、Tau蛋白磷酸化、神经炎症及认知衰退。而一种经过优化设计、不易被Aβ斑块捕获的新型锂盐——正清酸锂，在AD小鼠模型中表现出预防与逆转上述关键病理及记忆损伤的潜力。
➤ 研究十：带状疱疹疫苗——AD全病程的保护作用
基于威尔士地区带状疱疹疫苗接种政策中严格的出生日期分界，该研究[12]构建准实验设计，比较了生日相近（仅间隔一周）、基线特征相似但接种资格不同的两组人群。分析显示，在基线无认知障碍的个体中，接种疫苗可使9年内新发MCI的诊断率降低3.1%；而在已确诊痴呆的患者中，接种可使9年内痴呆相关死亡风险下降29.5%。此外，所有保护效应在女性群体中均更为显著。
尚待解决的问题：突破与争议并存的发展之路
郁金泰教授认为尽管2025年AD领域在多个方面取得显著进展，但仍存在诸多尚未解决的挑战，这些瓶颈也提示着未来研究的关键方向。
▌全球治疗格局不均
AD药物治疗不仅受临床证据和科学进展的影响，还与社会、文化、环境等多种因素密切相关。目前，各国在认知改善类药物和疾病修饰药物的批准及临床可及性方面仍存在显著差异[13]。如何推动AD治疗药物的全球公平分配，已成为公共卫生与政策制定中亟待协调的课题。
▌生物制剂的受益人群局限
当前以Aβ为核心的精准诊疗体系，其主要获益人群是相对年轻、病因单一的早期AD患者。然而，在真实临床场景中，多数患者年龄较高，常伴有多种共病与混合病理，其临床表现复杂且非典型，在现有诊疗趋势下面临被忽视或边缘化的风险。由于临床试验通常纳入高度同质化的受试人群，其结果外推至真实世界患者的能力有限。若严格遵循临床试验入组标准，仅约8%–15%的早期AD患者符合单抗治疗条件[14]。
▌研发管线的多元探索与持续挑战
2025年AD药物研发呈现鲜明的多元化特征[15]：在182项临床试验涉及138种药物中，33%直接靶向Aβ或Tau蛋白，其余大多聚焦于炎症、代谢、神经保护等更多样的病理机制。
然而该领域挑战同样存在：部分靶向Tau的药物在随机对照阶段未能达主要临床终点，仅在开放标签延伸阶段显示出减轻Tau负担的趋势[16]；此外，司美格鲁肽用于AD治疗的两项Ⅲ期研究均未达主要终点，未能延缓早期AD患者的认知与功能衰退[17]。这些结果提示，AD的病理机制可能比想象中复杂，单一靶点干预或直接跨界应用的成功路径仍需更深入的探索与验证。
圆桌讨论：混合病理的鉴别与年度突破性进展
在AD与血管性认知障碍（VCI）常常交织的临床现实中，如何精准鉴别并制定策略至关重要。针对混合性病理患者的临床鉴别要点，崔梅教授指出，新版VasCog-2-WSO指南及中国指南均强调了对“临床前/高危期VCI”概念的重视。鉴别的核心在于，不能仅凭影像学显示的血管损伤就诊断为血管性痴呆，必须评估其是否达到足以解释认知障碍的“阈值”。同时，应积极利用血浆p-tau217等生物标志物，明确AD病理的共存情况。因为“单纯”VCI患者预后相对良好，而AD与血管病理共存时，预后显著更差，且治疗与管理策略截然不同。
当被问及2025年疾病修饰治疗的重要进展时，郁金泰教授提及了Trontinemab的Ⅱ期临床数据。该研究之所以关键，在于其创新的“脑穿梭”技术有效解决了抗体药物穿越血脑屏障的核心瓶颈。数据显示，其在快速强效清除Aβ病理的同时，显著降低了ARIA相关副作用的发生率。这一突破为未来所有需要入脑治疗的生物制剂指明了全新的研发方向。
结语：
本次年度盘点不仅是对过去一年AD领域成就的梳理，更是对未来方向的眺望。从Aβ到Tau，从单靶点到多机制，从治疗到预防，AD诊疗正在多条战线同步推进。2025年的进展告诉我们，这是一场需要科学创新、临床智慧与人文关怀共同支撑的持久战，而每一步扎实的突破，都在为最终胜利积累着希望。
专家简介
郁金泰 教授
复旦大学附属华山医院
主任医师、博士生导师
复旦大学科学技术研究院副院长
复旦大学附属华山医院神经内科副主任
复旦大学附属华山医院神经内科认知障碍亚专科带头人
中华医学会神经病学分会神经心理和行为学组副组长
长期从事神经内科一线临床和科研工作，主要围绕认知障碍疾病的临床和基础进行系列研究工作，主持多项国家级研究项目，在Science,Cell,Lancet Neurology等本专业顶级期刊发表多篇学术论文。
专家简介
崔梅 教授
复旦大学附属华山医院
主任医师，博士研究生导师
上海市东方英才、上海市青年科技启明星、上海市医苑新星杰出医学人才
中华医学会神经病学分会脑血管病学组青年委员
中国医师学会阿尔茨海默病与认知障碍学组委员
中国卒中学会多组学分会副主任委员
中华中医药学会络病分会委员
中国微循环学会神经变性委员会委员
中国卒中学会脑小血管病分会委员
上海市青年科技启明星、上海市东方英才、上海市医苑新星杰出医学人才
近五年以第一作者或通讯作者在发表SCI论文50余篇
执笔撰写2024版《中国血管性认知障碍诊治指南》
承担科技创新2030“脑科学与类脑研究”重大项目子课题、国自然面上项目4项。
参考文献：
[1]Ling-Ling Li, Rong-Ze Wang, Zhen Wang, Hua Hu, Wei Xu, Lin Zhu, Yan Sun, Ke-Liang Chen, Shu-Fen Chen, Xiao-Yu He, Ming-Yang Yuan, Yu-Yuan Huang, Xiao-yan Liu, Ping Liu, Qin-Yong Ye, Jie Wang, Zi-Zhao Ju, Wei Zhang, Bin Hu, Yu Guo, Xiao-Yun Cao, Yu-Xin Li, Chuan-Tao Zuo, Wei Cheng, Teng Jiang, Lan Tan, Xiao-Chun Chen, Qian-Hua Zhao, Mei Cui, Guo-Ping Peng, Jia-Wei Xin, Jin-Tai Yu. Safety and short-term outcomes of lecanemab for Alzheimer's disease in China: a multicentre study. Brain. 2025 Nov 11:awaf427. doi: 10.1093/brain/awaf427. Epub ahead of print. PMID: 41215623.
[2]Wang H, Serap Monkul Nery E, Ardayfio P, et al. Modified titration of donanemab reduces ARIA risk and maintains amyloid reduction. Alzheimers Dement. 2025;21(4):e70062.
[3]Luka Kulic, Fabien Alcaraz, Gregory Klein, et al.Brainshuttle AD: new interim results of a randomized, placebo-controlled Phase Ib/IIaproof-of-concept study with trontinemab, a novel anti-amyloid monoclonal bispecific antibody for the treatment of Alzheimer’s disease. CTAD 2025.
[4]Bateman RJ, Li Y, McDade EM, et al. Safety and efficacy of long-term gantenerumab treatment in dominantly inherited Alzheimer's disease: an open-label extension of the phase 2/3 multicentre, randomised, double-blind, placebo-controlled platform DIAN-TU trial. Lancet Neurol. 2025;24(4):316-330.
[5]Pizzo ME, Plowey ED, Khoury N, et al. Transferrin receptor-targeted anti-amyloid antibody enhances brain delivery and mitigates ARIA. Science. 2025;389(6760):eads3204.
[6]Xing M, Song W. Improving Alzheimer's disease immunotherapy. Science. 2025;389(6760):571-572.
[7]Aarsland D, Sunde AL, Tovar-Rios DA, et al. Prevalence of Alzheimer's disease pathology in the community. Nature. Published online December 17, 2025.
[8]https://wrap.wisc.edu/2025/05/28/uw-madison-research-helps-launch-first-fda-cleared-blood-test-for-alzheimers/
[9]Li Y, Pereda Serras C, Blumenfeld J, et al. Cell-type-directed network-correcting combination therapy for Alzheimer's disease. Cell. 2025;188(20):5516-5534.e18.
[10]Rash BG, Ramdas KN, Agafonova N, et al. Allogeneic mesenchymal stem cell therapy with laromestrocel in mild Alzheimer's disease: a randomized controlled phase 2a trial. Nat Med. 2025;31(4):1257-1266.
[11]Aron L, Ngian ZK, Qiu C, et al. Lithium deficiency and the onset of Alzheimer's disease. Nature. 2025;645(8081):712-721.
[12]Xie M, Eyting M, Bommer C, Ahmed H, Geldsetzer P. The effect of shingles vaccination at different stages of the dementia disease course. Cell. 2025;188(25):7049-7064.e20.
[13]European Dementia Monitor - Comparing and benchmarking national dementia policies and strategies. https://www.alzheimer-europe.org/resources/publications/european-dementia-monitor-comparing-and-benchmarking-national-dementia?language_content_entity=en (2023).
[14]Frisoni GB, Aho E, Brayne C, et al. Alzheimer's disease outlook: controversies and future directions. Lancet. 2025;406(10510):1424-1442.
[15]Cummings JL, Zhou Y, Lee G, et al. Alzheimer's disease drug development pipeline: 2025. Alzheimers Dement (N Y). 2025;11(2):e70098. Published 2025 Jun 3.
[16]Saori Shimizu, et al. Results from the open-label extension periodof TOGETHER, a Phase II study evaluatingefficacy,safety and tolerability of bepranemabin prodromal-mild Alzheimer's disease. CTAD 2025.
[17]Jeffrey Cummings. TOPLINE RESULTS from Evoke and Evoke+: Two Phase 3 Randomized Placebo-Controlled Trials of Semaglutide in Participants with Early-Stage Symptomatic Alzheimer’s Disease. CTAD 2025.
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临床结果细胞疗法临床成功
2026-02-03
Early and Consistent Decreases in P-tau
217
Plasma Levels Were Associated with Improvements in Cognition, Function, and Brain Atrophy Measures
MCI Subjects Receiving Valiltramiprosate Showed Significant Correlations Between Decreases in Plasma P-tau
217
and Improvements on ADAS-Cog (r = 0.28, p = 0.039), CDR-SB (r = 0.38, p = 0.005), and Hippocampal Volume (r = 0.35, p = 0.013)
High Rates of Alzheimer’s Disease Positivity Were Confirmed Across Phase 3 and 2 Trials Using FDA-Approved P-tau
217
/Aβ1-42 Biomarker Threshold
Results Validate Upstream Molecular Mechanism of Inhibiting Formation of Neurotoxic Soluble Amyloid Oligomers – A Key Driver of Alzheimer’s Pathology
Valiltramiprosate Has Potential to Become the First Oral Agent to Slow Alzheimer’s Pathology in Patients
FRAMINGHAM, Mass.--(BUSINESS WIRE)--
#ALZ801
--
Alzheon, Inc.
, a clinical-stage biopharmaceutical company developing a broad portfolio of investigational therapies and diagnostic assays for patients with Alzheimer’s disease (AD) and other neurodegenerative disorders, today announced plasma biomarker analyses from its APOLLOE4 Phase 3 and Phase 2 clinical studies of valiltramiprosate/ALZ-801. New results offer robust evidence supporting the biological activity of valiltramiprosate’s, its novel mechanism of action, and effects in therapeutic studies, while validating the Alzheimer’s disease pathology in trial participants through FDA-approved plasma biomarker thresholds.
“Valiltramiprosate has emerged as the only late-stage oral treatment with a potential to materially change the Alzheimer’s therapeutic landscape in the near future, and this data completes the picture showing how valiltramiprosate’s action leads to positive effects on cognition, daily function, and brain protection against atrophy,” said Martin Tolar, Founder, President, and CEO of Alzheon. “In 2026, we will move forward with our plans for the next Phase 3 study based on analyses from the APOLLOE4 Phase 3 trial and its long-term extension. These efforts put us in a strong position as we focus on expanding the valiltramiprosate platform, developing new candidates, and investigating additional target groups.”
Alzheon will continue to use these biomarker insights to advance the valiltramiprosate platform, improve patient selection, and guide clinical development for genetically defined and high-risk Alzheimer’s disease groups.
“These findings underscore the usefulness of plasma biomarkers in connecting Alzheimer’s disease pathology with clinically relevant outcomes,” stated Robert Rissman, PhD, Professor of Physiology and Neurosciences at the University of Southern California. “The robust associations between decreases in plasma p-tau
217
, benefits on cognition and function, and protection from brain atrophy, offer valuable insights into disease mechanisms and further justify the advancement of valiltramiprosate as a potential disease-modifying therapy.”
Across both studies, the majority of participants satisfied criteria for AD positivity in accordance with the recently FDA-approved plasma p-tau
217
/Aβ1-42 ratio. In the Phase 3 APOLLOE4 trial involving APOE4/4 homozygotes, 94% of enrolled subjects were confirmed as AD positive, and in the Phase 2 trial targeting APOE4 carriers that utilized CSF biomarkers as inclusion criteria, 97% of homozygote and 96% of heterozygote patients met the AD positivity threshold. These results demonstrate substantial enrichment for amyloid-driven disease across both clinical trials.
Biomarker analyses of Phase 3 and 2 studies examining the effects of valiltramiprosate revealed consistent and early decreases in plasma p-tau
217
, which is a biomarker linked to beta amyloid and early tau pathology. In the Phase 3 trial, participants who received valiltramiprosate for 78 weeks showed reductions in p-tau
217
starting at 26 weeks that continued throughout the treatment period, with even greater benefits seen in patients at the Mild Cognitive Impairment (MCI) stage.
For those with MCI in the placebo group, p-tau
217
increased
by about 17% from baseline over 78 weeks, while those given valiltramiprosate experienced a
decrease
in p-tau
217
of approximately 36%, translating to a 53% difference vs. placebo. Among the MCI group receiving valiltramiprosate, there were significant and meaningful relationships between decreases in plasma p-tau
217
and benefits on clinical outcomes ADAS-Cog (r = 0.28, p = 0.039), CDR-SB (r = 0.38, p = 0.005), as well as protection of hippocampal volume (r = 0.35, p = 0.013).
Baseline plasma p-tau
217
levels were strongly correlated with both clinical and neuroimaging outcomes throughout the Phase 3 study, providing further biological support for the discovery that valiltramiprosate benefits are tied to treatment at the appropriate disease stage. Within the Phase 3 MCI cohort, baseline p-tau
217
demonstrated significant and consistent associations in valiltramiprosate–treated participants with ADAS-Cog at baseline (r = 0.31, p = 0.019), CDR-SB (r = 0.40, p = 0.002), hippocampal volume (r = -0.532, p <0.0001), and cortical thickness (r = -0.60, p <0.0001). Notably, significant correlations were also identified in the overall Phase 3 population, including both active and placebo arms.
"Our new biomarker results offer robust biological validation for valiltramiprosate's upstream molecular mechanism, designed to inhibit formation of neurotoxic soluble amyloid oligomers, which are considered pivotal drivers of Alzheimer’s disease pathology,” said John Hey, Chief Scientific Officer of Alzheon, Inc. “The consistent demonstration of Alzheimer’s positivity, early and sustained reductions in p-tau
217
, and strong correlations with cognitive, functional, and imaging outcomes highlight the importance of p-tau
217
as a marker for disease progression and treatment efficacy, particularly in patients at earlier stages of Alzheimer’s disease."
About ALZ-801
Valiltramiprosate/ALZ-801
is an investigational oral agent currently in
Phase 3 development
as a potential first-in-class, disease-modifying treatment for Alzheimer’s disease.
3-7,9,12
Valiltramiprosate is designed to inhibit the formation of neurotoxic soluble beta amyloid oligomers that contribute to cognitive decline in individuals with AD.
4-8,10,15
Preclinical mechanism-of-action studies have demonstrated that ALZ-801 can completely block the formation of these neurotoxic oligomers at the dosage used in Phase 3 clinical trials.
3,9,12,14
Valiltramiprosate employs an
enveloping molecular mechanism of action
intended to prevent the aggregation of soluble amyloid oligomers in the human brain,
14
which are associated with the onset and progression of cognitive impairment in AD patients.
3,4,7,9,10
In recognition of its therapeutic promise, valiltramiprosate received Fast Track designation from the U.S. Food and Drug Administration in 2017 for the treatment of Alzheimer’s disease.
Clinical trial data indicate that valiltramiprosate exhibits strong clinical efficacy at the MCI stage, and a favorable safety profile, with no observed increase in the risk of brain vasogenic edema.
5-1-10,13,15
The initial
Phase 3 program for valiltramiprosate
targets Early AD patients who are homozygous for the apolipoprotein ε4 allele (APOE4/4), with plans to expand future research to include AD treatment and prevention in individuals carrying one copy of the APOE4 gene.
3–10
Valiltramiprosate APOLLOE4 Phase 3 Trial
An Efficacy and Safety Study of Valiltramiprosate in APOE4/4 Early Alzheimer's Disease Subjects (
NCT04770220
): This trial was designed to evaluate the efficacy, safety, biomarker and imaging effects of 265 mg twice daily oral dose of valiltramiprosate in Early AD subjects with two copies of the apolipoprotein ε4 allele (APOE4/4 homozygotes), who constitute approximately 15% of Alzheimer's patients. This double-blind, randomized trial compared oral valiltramiprosate to placebo treatment over 78 weeks. The APOLLOE4 trial was supported by a
grant from the National Institute on Aging
to Alzheon, with Susan Abushakra as the principal investigator.
Valiltramiprosate APOLLOE4 Long Term Extension Trial (Phase 3 LTE)
An ongoing long-term extension of the trial, APOLLOE4-LTE, evaluates valiltramiprosate in subjects who complete the core APOLLOE4 study for an additional 104 weeks of treatment for a total of 182 weeks or 3.5 years over the core and LTE study. This LTE study is currently ongoing in the US, UK, and Canada (
NCT06304883
).
Valiltramiprosate Phase 2 Biomarker Trial
Biomarker Effects of Valiltramiprosate in APOE4 Carriers with Early Alzheimer's Disease (
NCT04693520
): This trial was designed to evaluate the effects of 265 mg twice daily oral dose of valiltramiprosate on biomarkers of AD pathology in subjects with Early AD, who have either the APOE4/4 or APOE3/4 genotype and constitute 65-70% of Alzheimer's patients. The primary outcome was the change from baseline in plasma p-tau
181
. The trial also included evaluation of clinical efficacy, safety, tolerability, and pharmacokinetic pro valiltramiprosate over 104 weeks of treatment. A completed long-term extension of the trial evaluated the same dose of valiltramiprosate for an additional 104 weeks of treatment for a total of 208 weeks.
3,7,8
About Alzheon
Alzheon, Inc.
is a clinical-stage biopharmaceutical company dedicated to advancing a diverse portfolio of product candidates and diagnostic assays for individuals affected by Alzheimer’s disease and other neurodegenerative disorders. The company is focused on innovating therapeutic solutions that directly target the underlying pathology of neurodegeneration. Its lead Alzheimer's clinical candidate,
valiltramiprosate/ALZ-801
, is a first-in-class oral agent currently in
Phase 3 clinical development
as a potentially disease-modifying treatment for Alzheimer’s disease. Valiltramiprosate is an orally administered small molecule shown in preclinical studies to completely inhibit the formation of neurotoxic soluble amyloid oligomers. Leveraging clinical expertise and a robust technology platform, Alzheon pursues drug discovery and development using a
precision medicine approach
that incorporates individual genetic and biomarker pro aiming to advance therapies with meaningful benefits for patients.
Alzheon Scientific Publications
1
Abushakra S, et al:
Hippocampal Atrophy on Magnetic Resonance Imaging as a Surrogate Marker for Clinical Benefit and Neurodegeneration in Early Symptomatic Alzheimer’s Disease: Synthesis of Evidence from Observational and Interventional Trials,
Drugs
2026;40(2):199-214.
2
Abushakra S, et al:
Clinical Efficacy, Safety and Imaging Effects of Oral Valiltramiprosate in APOEε4/ε4 Homozygotes with Early Alzheimer’s Disease: Results of the Phase III, Randomized, Double-Blind, Placebo-Controlled, 78-Week APOLLOE4 Trial
,
Drugs
2025; 85, 1455-1472.
3
Pearson D, et al:
Polymorph Analysis of ALZ-801 (Valiltramiprosate), a Valine-Conjugated Oral Prodrug of Tramiprosate in Late-Stage Clinical Development for Alzheimer’s Disease,
Journal of
Chemical
Crystallography
2025; 55, 206-215.
4
Hey JA, et al:
Clinical Pharmacokinetics of Oral ALZ-801/Valiltramiprosate in a Two-Year Phase 2 Trial of APOE4 Carriers with Early Alzheimer’s Disease,
Clinical Pharmacokinetics
2025; 64, 407-424.
5
Aye S, et al:
Point of View: Challenges in Implementation of New Immunotherapies for Alzheimer’s Disease,
The Journal of Prevention of Alzheimer’s Disease
2025;12(1):100022.
6
Abushakra S, et al:
APOLLOE4 Phase 3 Study of Oral ALZ-801/Valiltramiprosate in APOE
ε
4/
ε
4 Homozygotes with Early Alzheimer’s Disease: Trial Design and Baseline Characteristics,
Alzheimer’s & Dementia
2024; 10(3): e12498.
7
Tolar M, et al:
The Single Toxin Origin of Alzheimer’s Disease and Other Neurodegenerative Disorders Enables Targeted Approach to Treatment and Prevention,
International Journal of Molecular Sciences
2024; 25(5), 2727.
8
Hey JA, et al:
Analysis of Cerebrospinal Fluid, Plasma
β
Amyloid Biomarkers, and Cognition from a 2-Year Phase 2 Trial Evaluating Oral ALZ-801/Valiltramiprosate in APOE4 Carriers with Early Alzheimer’s Disease Using Quantitative Systems Pharmacology Model,
Drugs
2024; 84(7), 825-839.
9
Hey JA, et al:
Effects of Oral ALZ-801/Valiltramiprosate on Plasma Biomarkers, Brain Hippocampal Volume, and Cognition: Results of 2-Year Single Arm, Open Label, Phase 2 Trial in APOE4 Carriers with Early Alzheimer’s Disease,
Drugs
2024; 84(7), 811-823.
10
Tolar M, et al:
Neurotoxic Soluble Amyloid Oligomers Drive Alzheimer’s Pathogenesis and Represent a Clinically Validated Target for Slowing Disease Progression
,
International Journal of Molecular Sciences
2021; 22(12), 6355.
11
Abushakra S, et al:
APOE ε4/ε4 Homozygotes with Early Alzheimer’s Disease Show Accelerated Hippocampal Atrophy and Cortical Thinning that Correlates with Cognitive Decline
,
Alzheimer’s & Dementia
2020; 6(1): e12117.
12
Tolar M, et al:
Aducanumab, Gantenerumab, BAN2401, and ALZ-801—the First Wave of Amyloid-Targeting Drugs for Alzheimer’s Disease with Potential for Near Term Approval,
Alzheimer’s Research & Therapy
2020; 12(1): 95.
13
Tolar M, et al:
The Path Forward in Alzheimer’s Disease Therapeutics: Reevaluating the Amyloid Cascade Hypothesis
,
Alzheimer’s & Dementia
2020; 16(11):1553-1560.
14
Hey JA, et al:
Discovery and Identification of an Endogenous Metabolite of Tramiprosate and Its Prodrug ALZ-801 that Inhibits Beta Amyloid Oligomer Formation in the Human Brain
,
CNS Drugs
2018; 32(9): 849-861.
15
Hey JA, et al:
Clinical Pharmacokinetics and Safety of ALZ-801, a Novel Prodrug of Tramiprosate in Development for the Treatment of Alzheimer’s Disease
,
Clinical Pharmacokinetics
2018; 57(3): 315-333.
16
Abushakra S, et al:
Clinical Effects of Tramiprosate in APOE4/4 Homozygous Patients with Mild Alzheimer’s Disease Suggest Disease Modification Potential
,
Journal of Prevention of Alzheimer’s Disease
2017; 4(3): 149-156.
17
Kocis P, et al:
Elucidating the A
β
42 Anti-Aggregation Mechanism of Action of Tramiprosate in Alzheimer’s Disease: Integrating Molecular Analytical Methods
,
Pharmacokinetic and Clinical Data
,
CNS Drugs
2017; 31(6): 495-509.
18
Abushakra S, et al:
Clinical Benefits of Tramiprosate in Alzheimer’s Disease Are Associated with Higher Number of APOE4 Alleles: The “APOE4 Gene-Dose Effect,”
Journal of Prevention of Alzheimer’s Disease
2016; 3(4): 219-228.
Contacts
Media Contact
Yasemin Khakian, Alzheon, Inc.
508.808.2301
yasemin.khakian@alzheon.com
Investor Contact
Erwan de Naurois, Alzheon, Inc.
802.735.8789
erwan.denaurois@alzheon.com
临床2期临床结果临床3期快速通道
2026-01-29
AD_Drug_Development_2021-2026.xlsx
关键词：阿尔茨海默病、药物、临床、研发、Phase
25年的AD药物统计还没看到，AI先做了一个汇总表
阿尔茨海默病(AD)药物研发汇总报告
2021-2026年全球AD药物研发管线分析
数据摘要
已上市药物
3个 (Lecanemab, Donanemab, Aduhelm[退市])
Phase 3在研
18个
Phase 2/3在研
8个
Phase 2在研
22个
Phase 1在研
10个
研发失败/终止
19个
总计
80个药物
说明
本报告汇总了2021-2026年间全球阿尔茨海默病药物研发情况，包括已上市药物、在研药物（Phase 1-3）以及研发失败的药物。数据来源于ClinicalTrials.gov、PubMed、FDA等权威机构。涵盖Aβ靶向、tau靶向、神经炎症、老药新用等多种机制。
23/24年大佬整理的药物研发情况汇总：
参考文献
ClinicalTrials.gov
https://clinicaltrials.gov
PubMed
https://pubmed.ncbi.nlm.nih.gov
FDA
https://www.fda.gov
Alzheimer's & Dementia (Journal)
https://alz-journals.onlinelibrary.wiley.com
Nature Reviews Drug Discovery
https://www.nature.com/nrd
New England Journal of Medicine
https://www.nejm.org
JAMA Neurology
https://jamanetwork.com/journals/jamaneurology
Lancet Neurology
https://www.thelancet.com/neurology
Cummings et al. 2025 Pipeline Report
Alzheimer's Dement 2025;11:e70098
Alzforum
https://www.alzforum.org
Alzheimers Dement (N Y). 2023 May 25;9(2):e12385.
Alzheimers Dement (N Y). 2024 Apr 24;10(2):e12465.
本文内容来自公开信息及研究文献，不代表临床建议。
如需投稿、转载、商务合作后台留言，回复有一定延迟敬请谅解。
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药品名称
进展阶段
临床试验编号
所属公司/机构
开发起始时间
备注
GV-971 (Sodium Oligomannate)
中国已上市/全球Phase 3终止
NCT04520412 (Green Memory)
Green Valley Pharma (China)
2019
中国2019年批准，国际III期2022年终止
Lecanemab (Leqembi)
已上市 (FDA 2023.1加速批准, 2023.7完全批准)
NCT03887455 (Clarity AD)
Eisai / Biogen / BioArctic
2020
抗Aβ原纤维抗体，减缓认知下降27%
Donanemab (Kisunla)
已上市 (FDA 2024.7批准)
NCT04437511 (TRAILBLAZER-ALZ 2)
Eli Lilly
2020.6
抗Aβ抗体，低/中tau患者减缓下降60%
Remternetug
Phase 3 (进行中)
NCT05463731 (TRAILRUNNER-ALZ1)
Eli Lilly
2022.8
第三代抗Aβ抗体，皮下/静脉给药
ALZ-801 (Valiltramiprosate)
Phase 3 (进行中)
NCT04770220 (APOLLOE4)
Alzheon
2021.5
口服Aβ寡聚体抑制剂，针对APOE4/4纯合子
Semaglutide
Phase 3 (进行中)
NCT04777396 / NCT04777409 (EVOKE/EVOKE+)
Novo Nordisk
2021.5
GLP-1受体激动剂，老药新用
Nilotinib
Phase 3 (进行中)
NCT05143528
Novartis
2022.2
酪氨酸激酶抑制剂，老药新用
Masitinib
Phase 3 (进行中)
NCT05564169
AB Science
2022
酪氨酸激酶抑制剂，抗炎
KarXT (Xanomeline-Trospium)
Phase 3 (进行中)
NCT05511363
Karuna Therapeutics / Bristol-Myers Squibb
2022
毒蕈碱受体激动剂组合
Masupirdine (SUVN-502)
Phase 3 (进行中)
NCT05397639
Suven Pharmaceuticals
2022
5-HT6受体拮抗剂，用于激越症状
Nabilone
Phase 3 (进行中)
NCT04516057
University of Toronto
2020
大麻素受体激动剂，老药新用，用于激越
Dextromethorphan/Quinidine
Phase 3 (进行中)
NCT03389922
Otsuka / Avanir
2018
用于AD相关激越
NE3107
Phase 3 (进行中)
NCT04669028
BioVie
2021
口服抗炎胰岛素增敏剂
AR1001
Phase 3 (进行中)
NCT05531526
AriBio
2022
PDE5抑制剂，老药新用
ATH-1017 (Fosgonimeton)
Phase 3 (进行中)
NCT04488419
Athira Pharma
2020
肝细胞生长因子增强剂
AXS-05 (Dextromethorphan/Bupropion)
Phase 3 (进行中)
NCT05526968
Axsome Therapeutics
2022
用于AD相关激越
Trontinemab (RO7126209)
Phase 3 (进行中)
NCT06385072
Roche / Genentech
2024
Brainshuttle技术抗Aβ抗体，基于gantenerumab
ALZ-801 (Long-term Extension)
Phase 3扩展 (进行中)
NCT06304883
Alzheon
2023
APOLLOE4试验长期扩展
Blarcamesine (ANAVEX 2-73)
Phase 2/3 (完成)
NCT03790709
Anavex Life Sciences
2019
Sigma-1受体激动剂，已提交欧洲上市申请
Piromelatine
Phase 2/3 (进行中)
NCT05267535
Neurim Pharmaceuticals
2022.5
褪黑素受体激动剂
Buntanetap
Phase 2/3 (进行中)
NCT05686044
Annovis Bio
2023
神经毒性聚集蛋白翻译抑制剂
Metformin
Phase 2/3 (进行中)
NCT04098666
University of Pennsylvania
2021.3
降糖药，老药新用
E2814 (Etalanetug)
Phase 2/3 (进行中)
NCT05269394 (DIAN-TU Tau NexGen)
Eisai / UCL
2022.1
抗tau抗体，靶向MTBR，获FDA快速通道资格
Rotigotine + Rivastigmine
Phase 2/3 (进行中)
NCT04185099
University of California
2019
多巴胺激动剂+胆碱酯酶抑制剂
Lecanemab + E2814
Phase 2/3 (进行中)
NCT05269394 (DIAN-TU-001)
Eisai
2022
抗Aβ+抗tau组合疗法
ABBV-916
Phase 2 (进行中)
NCT05291234
AbbVie
2022
抗Aβ抗体，靶向N3pG-Aβ
CT1812 (Zervimesine)
Phase 2 (进行中)
NCT03507790 (SHINE) / NCT05531656 (START)
Cognition Therapeutics
2018
Sigma-2受体调节剂
Bepranemab (UCB0107)
Phase 2 (进行中)
NCT04867616
Roche / UCB
2021
抗tau抗体，靶向tau中央区域
JNJ-63733657
Phase 2 (进行中)
NCT04619420 (AUTONOMY)
Janssen
2020
抗tau抗体，靶向p-tau217
LY3372689
Phase 2 (进行中)
NCT05063539
Eli Lilly
2021.9
O-GlcNAcase抑制剂，小分子
BIIB080 (IONIS-MAPTRx)
Phase 2 (进行中)
NCT05399888 (CELIA)
Biogen / Ionis
2022
Tau反义寡核苷酸
ACI-35
Phase 2 (进行中)
NCT04445831
AC Immune / Janssen
2020
抗tau疫苗
Hydralazine Hydrochloride
Phase 2 (进行中)
NCT04842552
University of Colorado
2021
老药新用，激活Nrf2通路
Caffeine
Phase 2 (进行中)
NCT04570085
University of Miami
2020
腺苷受体拮抗剂，老药新用
Sildenafil
Phase 2 (进行中)
NCT05403764
Cleveland Clinic
2022
PDE5抑制剂，老药新用
Dasatinib + Quercetin
Phase 2 (进行中)
NCT04063124
Mayo Clinic
2019
衰老细胞清除剂，老药新用
Liraglutide
Phase 2 (进行中)
NCT05653675
Novo Nordisk
2023
GLP-1受体激动剂，老药新用
Foralumab
Phase 2 (进行中)
NCT06382623
Tiziana Life Sciences
2024
抗CD3单抗，鼻内给药，针对神经炎症
PRX005
Phase 2 (进行中)
NCT06126686
Prothena
2023
抗tau抗体
Exenatide
Phase 2 (进行中)
NCT04269349
University of Oxford
2020
GLP-1受体激动剂，老药新用
Lixisenatide
Phase 2 (进行中)
NCT05837287
Sanofi
2023
GLP-1受体激动剂，老药新用，帕金森病
Tirzepatide
Phase 2 (进行中)
NCT06556289
Eli Lilly
2024
GLP-1/GIP双受体激动剂，老药新用
Dulaglutide
Phase 2 (进行中)
NCT05844971
Eli Lilly
2023
GLP-1受体激动剂，老药新用
Tadalafil
Phase 2 (进行中)
NCT05422885
University of California
2022
PDE5抑制剂，老药新用
Vardenafil
Phase 2 (进行中)
NCT05575076
University of Pennsylvania
2022
PDE5抑制剂，老药新用
Ibudilast
Phase 2 (进行中)
NCT05549530
MediciNova
2022
PDE4/PDE3抑制剂，抗炎
Saracatinib
Phase 2 (进行中)
NCT05256052
AstraZeneca
2022
Src/Fyn激酶抑制剂
AZD0530
Phase 2 (进行中)
NCT05256052
AstraZeneca
2022
Src激酶抑制剂
Posdinemab (ACI-35-028)
Phase 2 (进行中)
NCT06126686
AC Immune / Janssen
2023
抗磷酸化tau抗体
AADvac1
Phase 2完成 (未达主要终点)
NCT04170891 (ADAMANT)
Axon Neuroscience
2020
抗tau疫苗，未达主要终点
ASN51
Phase 2终止 (2025)
NCT05544431
Asceneuron
2022
tau靶向药物，战略调整终止
Lu AF87908
Phase 1 (完成)
NCT04149860
Lundbeck
2019
抗磷酸化tau抗体
PNT001
Phase 1 (完成)
NCT05059380
Pinteon Therapeutics
2021
抗cis-pT231 tau抗体
MK-2214
Phase 1 (进行中)
NCT05544431
Merck
2022
抗tau抗体
APNmAb005
Phase 1 (进行中)
NCT05575076
Applied NeuroSolutions
2022
抗tau寡聚体抗体
Denali TVD (Transferrin Receptor)
Phase 1 (进行中)
NCT05712223
Denali Therapeutics
2023
脑穿梭技术平台，抗体递送
DNL919
Phase 1 (进行中)
NCT05544431
Denali Therapeutics
2022
TREM2激活剂，脑穿梭技术
AL101 (GSK4527226)
Phase 1 (进行中)
NCT05575076
Alector / GSK
2022
Progranulin增强单抗
NI006
Phase 1 (进行中)
NCT05575076
University Hospital Zurich
2022
抗Aβ纳米抗体
ATN-101
Phase 1 (进行中)
NCT05575076
Aton Pharma
2022
抗Aβ抗体
RG7345
Phase 1终止 (2015)
NCT01952637
Roche / Genentech
2015
抗tau抗体
BIIB076
Phase 1终止 (2022)
NCT03113815
Biogen / Neurimmune
2017
抗tau抗体
AL002
Phase 2 (失败)
NCT04592874 (INVOKE-2)
Alector
2020
TREM2激动剂抗体，INVOKE-2试验未达终点
Ponezumab
Phase 2失败
NCT00960531
Pfizer
2012
抗Aβ抗体
Gosuranemab (BIIB092)
Phase 2失败 (2021终止)
NCT03352557
Biogen / Bristol-Myers Squibb
2018
抗tau抗体，未达主要终点
Tilavonemab (ABBV-8E12)
Phase 2失败 (2021终止)
NCT03413319
Bristol-Myers Squibb / AbbVie
2018
抗tau抗体，未达主要终点
Zagotenemab (LY3303560)
Phase 2失败 (2021终止)
NCT03518073
Eli Lilly
2018
抗tau抗体，未达主要终点
Varoglutamstat (PQ912)
Phase 2失败 (2024终止)
NCT03919162 (VIVA-MIND) / NCT04498650 (VIVIAD)
Vivoryon Therapeutics
2019
QPCT抑制剂，VIVIAD试验失败，已转向糖尿病肾病
Semorinemab
Phase 2失败 (TAURIEL/LAURIET)
NCT03289143 (TAURIEL) / NCT03828747 (LAURIET)
Genentech / Roche
2018
TAURIEL未达终点，LAURIET部分终点阳性但功能终点阴性
Idalopirdine
Phase 3失败
NCT01955143
Lundbeck / Otsuka
2015
5-HT6受体拮抗剂
Intepirdine
Phase 3失败
NCT02585934
Axovant
2017
5-HT6受体拮抗剂
Bapineuzumab
Phase 3失败
NCT00575055 / NCT00574132
Pfizer / Janssen
2014
抗Aβ抗体，未达临床终点
Verubecestat (MK-8931)
Phase 3失败 (2017终止)
NCT01739348
Merck
2017
BACE1抑制剂，因无效提前终止
Lanabecestat (AZD3293)
Phase 3失败 (2018终止)
NCT02245737
AstraZeneca / Eli Lilly
2018
BACE1抑制剂
Atabecestat (JNJ-54861911)
Phase 3失败 (2018终止)
NCT02569398
Janssen
2018
BACE1抑制剂，肝毒性
Crenezumab
Phase 3失败 (2019终止/2022发表)
NCT02670083 (CREAD) / NCT03114657 (CREAD2)
Roche / Genentech
2019
CREAD/CREAD2试验因无效提前终止
Gantenerumab
Phase 3失败 (2022.11)
NCT03444870 (GRADUATE I) / NCT03443973 (GRADUATE II)
Roche / Genentech
2018
GRADUATE试验未达主要终点，未能减缓认知下降
Solanezumab
Phase 3失败 (2023年A4研究失败)
NCT02008357 (A4 Study)
Eli Lilly
2014
EXPEDITION 1/2及A4研究均未达终点
Simufilam (PTI-125)
Phase 3失败 (2024-2025)
NCT04994483 (RETHINK-ALZ) / NCT05026177 (REFOCUS-ALZ)
Cassava Sciences
2021.11
Filamin A抑制剂，两项Phase 3均未达终点，已停止开发
Aduhelm (Aducanumab)
已退市 (FDA 2021.6加速批准, 2024.1停产)
NCT02484547 (EMERGE)
Biogen / Neurimmune
2021.6
2024年1月Biogen宣布停产，非安全/疗效原因
临床3期上市批准抗体药物偶联物加速审批申请上市
100 项与 甘特鲁单抗 相关的药物交易
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 遗忘 | 临床3期 | 意大利 | - | 2020-08-07 |
| 阿尔茨海默症 | 临床3期 | 西班牙 | 2008-12-15 | |
| 疼痛 | 临床1期 | 美国 | 2016-08-31 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
| 研究 | 分期 | 人群特征 | 评价人数 | 分组 | 结果 | 评价 | 发布日期 |
|---|
临床2/3期 | 74 | (any gantenerumab) | 製網憲衊鬱窪願齋獵窪(簾鹽鑰獵獵積築鏇蓋範) = At the interim analysis, the hazard ratio for clinical decline of CDR-SB in asymptomatic mutation carriers was 0·79 (n=53 [95% CI 0·47 to 1·32]) for participants who were treated with gantenerumab in either the double-blind or OLE period (Any Gant), and 0·53 (n=22 [0·27 to 1·03]) for participants who were treated with gantenerumab the longest (Longest Gant). 繭鹽鏇選膚繭製鹽膚淵 (製鑰膚餘壓築鬱壓選衊 ) 更多 | 积极 | 2025-04-01 | ||
(Longest gantenerumab) | |||||||
临床2/3期 | 73 | OLE+Gantenerumab (Double-blind Placebo - OLE Gantenerumab) | 醖襯遞膚窪獵膚壓簾簾(積壓窪憲鹹選願醖蓋廠) = 鏇鏇鬱願鏇壓壓淵積願 壓築廠網築餘構醖鏇衊 (鬱願鹹鹽築窪艱憲壓廠, 0.22606) 更多 | - | 2025-02-04 | ||
Gantenerumab+Solanezumab (Double-blind Solanezumab - OLE Gantenerumab) | 醖襯遞膚窪獵膚壓簾簾(積壓窪憲鹹選願醖蓋廠) = 製壓鏇夢選醖選鹽廠鏇 壓築廠網築餘構醖鏇衊 (鬱願鹹鹽築窪艱憲壓廠, 0.40538) 更多 | ||||||
临床3期 | 1,939 | 範膚遞選選艱齋選鏇積(鬱廠簾選鹹餘範蓋膚繭) = 壓糧醖餘鑰鬱廠壓顧鹽 鹽齋膚糧範願夢醖齋範 (製艱鹽顧選壓襯壓齋醖 ) 更多 | 积极 | 2024-11-18 | |||
临床3期 | 25 | Placebo (Placebo) | 遞選廠壓憲構鹹壓襯壓(鹽夢鹽憲顧鹽鏇遞糧艱) = 窪網餘構壓獵積遞網鹽 鬱網蓋積壓範齋觸鏇鹽 (積遞廠觸築鏇網鹽膚壓, 0.5790) 更多 | - | 2024-07-09 | ||
(Gantenerumab) | 遞選廠壓憲構鹹壓襯壓(鹽夢鹽憲顧鹽鏇遞糧艱) = 鹹蓋壓膚繭淵餘齋鹹選 鬱網蓋積壓範齋觸鏇鹽 (積遞廠觸築鏇網鹽膚壓, 0.6038) 更多 | ||||||
临床3期 | 1,382 | Placebo (Placebo: Participated in Graduate OLE) | 鹹獵壓製製鹹壓製願餘 = 獵糧鹽網製廠顧網衊蓋 醖憲夢鏇憲壓遞襯鑰鏇 (鏇網鑰憲夢壓鬱艱淵願, 觸淵獵鹹鏇製顧範餘構 ~ 獵衊鹽鹽襯觸壓顧繭壓) 更多 | - | 2024-05-08 | ||
Placebo (Placebo: No Participation in Graduate OLE) | 鹹獵壓製製鹹壓製願餘 = 膚製願鹽蓋鬱鹹餘製醖 醖憲夢鏇憲壓遞襯鑰鏇 (鏇網鑰憲夢壓鬱艱淵願, 繭構鑰範淵齋鬱鏇繭獵 ~ 遞簾餘壓遞夢鏇膚鬱艱) 更多 | ||||||
临床2/3期 | - | 鹹製齋鬱醖鹹網鏇製夢(鏇簾觸鹹壓築憲廠鏇簾) = 齋餘壓窪遞積鹹淵鏇願 糧顧壓夢膚範蓋繭願淵 (醖鑰鹹築簾鑰鏇艱積範, 0.43) | - | 2024-04-29 | |||
临床2期 | 192 | 憲構襯鏇窪淵醖積鑰襯(獵顧廠膚顧網憲願艱壓) = 範網壓壓鬱觸憲築膚簾 廠艱選衊餘築網願膚艱 (醖簾廠壓積醖餘鬱繭廠, 29.80) 更多 | - | 2024-03-27 | |||
临床3期 | 1,053 | placebo+gantenerumab (Global - DBT Period: Placebo) | 構願願衊鏇製艱蓋觸蓋(製範鑰膚獵築鑰夢窪觸) = 鑰願艱觸顧壓醖積鏇鑰 夢簾憲夢夢範範鹽製膚 (醖製範範膚鹹蓋觸簾鬱, 0.16) 更多 | - | 2024-01-30 | ||
(Global - DBT Period: Gantenerumab) | 構願願衊鏇製艱蓋觸蓋(製範鑰膚獵築鑰夢窪觸) = 選憲範醖衊築窪構膚鬱 夢簾憲夢夢範範鹽製膚 (醖製範範膚鹹蓋觸簾鬱, 0.14) 更多 | ||||||
临床3期 | 116 | (SCarlet RoAD) | 夢簾鬱構膚壓觸襯繭齋 = 醖觸選獵鬱憲積願繭齋 醖繭鹹壓獵遞願壓餘範 (簾鏇鹽憲夢鹹窪鬱夢淵, 衊鹹顧顧繭鹹鹽淵窪構 ~ 製醖襯構蓋衊淵艱憲顧) 更多 | - | 2024-01-18 | ||
(Marguerite RoAD) | 夢簾鬱構膚壓觸襯繭齋 = 簾鏇蓋壓網鹽願範繭網 醖繭鹹壓獵遞願壓餘範 (簾鏇鹽憲夢鹹窪鬱夢淵, 鏇鹽窪製遞窪襯製醖選 ~ 簾淵積蓋鏇觸簾鑰糧選) 更多 | ||||||
临床3期 | 975 | placebo+gantenerumab (Placebo: DBT) | 衊製願壓遞觸繭醖鬱憲(夢鏇範壓壓遞鹹鏇衊膚) = 餘窪願醖鑰顧壓襯襯範 壓繭簾艱觸齋襯繭糧網 (艱壓艱齋繭網積齋築窪, 0.15) 更多 | - | 2024-01-17 | ||
(Gantenerumab: DBT) | 衊製願壓遞觸繭醖鬱憲(夢鏇範壓壓遞鹹鏇衊膚) = 襯鏇遞壓選遞膚鹹願選 壓繭簾艱觸齋襯繭糧網 (艱壓艱齋繭網積齋築窪, 0.14) 更多 |
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