A Patient- and Investigator-Blind, Placebo-Controlled Study to Evaluate the Efficacy, Safety, and Tolerability of Bepranemab (UCB0107) in Study Participants With Prodromal to Mild Alzheimer's Disease (AD), Followed by an Open-Label Extension Period

The purpose of the study is to investigate the effect of bepranemab versus (vs) placebo on the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) up to Week 80 in study participants with prodromal or mild Alzheimer's Disease (AD).

开始日期2021-06-09

申办/合作机构

UCB Biopharma SRL

NCT04658199

/ Active, not recruiting临床1期

An Open-Label Extension Study to Evaluate the Safety and Tolerability of Long-Term UCB0107 Administration in Study Participants With Progressive Supranuclear Palsy

The purpose of the study is to assess the long-term safety and tolerability of UCB0107 in study participants with progressive supranuclear palsy (PSP).

开始日期2020-11-16

申办/合作机构

UCB Biopharma SRL

NCT04185415

/ Completed临床1期

A Participant-Blind, Investigator-Blind, Placebo-Controlled, Phase 1b Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of UCB0107 in Study Participants With Progressive Supranuclear Palsy (PSP)

The purpose of the study is to assess the safety and tolerability of UCB0107 in study participants with Progressive Supranuclear Palsy (PSP).

开始日期2019-12-03

申办/合作机构

UCB Biopharma SRL

100 项与 Bepranemab 相关的临床结果

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100 项与 Bepranemab 相关的转化医学

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100 项与 Bepranemab 相关的专利（医药）

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项与 Bepranemab 相关的文献（医药）

2025-12-01·Alzheimers & Dementia

Establishing bepranemab posology through exposure‐response modeling and simulation for TOGETHER, a double‐blind, placebo‐controlled Phase II study of bepranemab in prodromal–mild Alzheimer’s disease (AD)

Article

作者: Sidhu, Jagdev S ; Gallais, Fanny ; Ewen, Colin ; Mesa, Irene Rebollo ; Sardu, Maria Luisa ; Khandelwal, Akash ; Byrnes, William ; Dua, Pinky ; Björnsson, Marcus A ; Barton, Matthew E

Abstract:

Background:

Bepranemab is a recombinant, humanized, full‐length immunoglobulin G4 monoclonal antibody that targets a mid‐region epitope of human tau considered essential for aggregation. TOGETHER (NCT04867616), a Phase II participant‐ and investigator‐blind, randomized, placebo‐controlled study, assessed efficacy and safety of bepranemab in people with prodromal–mild Alzheimer’s disease (AD). The relationships between clinical measures and systemic bepranemab exposure, in conjunction with placebo response, were investigated through modeling and simulation, to support bepranemab dosing for further clinical development.

Methods:

Pharmacokinetic, demographic, and efficacy data from a low tau burden or apolipoprotein ε4 (APOε4) genotype non‐carrier subpopulation (N=189; age range: 69.7–72 years), a “responder” population to bepranemab in the TOGETHER study (in which participants received 45 mg/kg bepranemab, 90 mg/kg bepranemab, or placebo every 4 weeks [Q4W] for <76 weeks), were modeled using non‐linear mixed‐effect models. Disease progression models, assessing Baseline scores and the influence of selected clinical covariates, were developed separately for Clinical Dementia Rating Sum of Boxes (CDR‐SB), Alzheimer's Disease Assessment Scale‐Cognitive subscale (ADAS‐Cog) 14, and tau‐positron emission tomography (PET; whole cortical gray and jack temporal meta), with each model characterizing the time‐course of placebo response and a change of response due to bepranemab exposure. Model‐based simulations were conducted to predict improvements in the 80‐week time course of each endpoint due to bepranemab dosing at 45, 60, and 90 mg/kg Q4W, versus placebo, in larger study participant cohorts with low and high tau burdens.

Results:

The time courses of CDR‐SB, ADAS‐Cog 14, and tau‐PET were best described by linear disease progression models. In each model, bepranemab exposure (concentrations) in all dose cohorts was found to reduce clinical markers of AD progression. For all models, simulations predicted that higher bepranemab doses (ie, >45 mg/kg) may result in improved clinical outcomes versus placebo in prodromal–mild AD.

Conclusions:

Exposure‐response modeling and simulation of TOGETHER study data confirmed improvement in clinical outcomes with bepranemab in a prodromal–mild AD population with low tau burden or APOε4 non‐carriers. The modeling also predicted that higher bepranemab doses are likely to be therapeutically beneficial (vs placebo) in future clinical trials.

2025-12-01·Alzheimers & Dementia

Tau positron emission tomography results from TOGETHER, a double‐blind, placebo‐controlled Phase II study of bepranemab in prodromal–mild Alzheimer’s disease

Article

作者: Ewen, Colin ; Barton, Matthew E ; Taiyari, Katie ; Bloemers, Jos ; Byrnes, William ; Buchanan, Tim J ; Tricht, Hans L.G Van ; Mesa, Irene Rebollo ; Famodimu, Omobola ; Einstein, Steve ; Steen, Bart Van Den ; Maguire, Ralph P

Abstract:

Background:

Bepranemab is a recombinant, humanized, full‐length immunoglobulin G4 monoclonal antibody that targets a mid‐region epitope of human tau. TOGETHER (NCT04867616), a Phase II participant‐ and investigator‐blinded, randomized, placebo‐controlled study, assessed efficacy and safety of bepranemab in people with prodromal–mild Alzheimer’s disease (AD). Previously presented data from TOGETHER indicate a clinical benefit with bepranemab. Here, we describe the effect of bepranemab on tau accumulation in the brain in study participants with prodromal or mild AD.

Methods:

Participants (aged 50–80 years) received bepranemab (45 mg/kg or 90 mg/kg, intravenously every 4 weeks) or placebo over an 80‐week treatment period. Participants received [ 18 F] Genentech tau probe 1 (GTP1) and underwent positron emission tomography (PET) imaging at Baseline, Week 56, and Week 80. Eligibility criteria included prodromal–mild AD (National Institute on Aging and the Alzheimer's Association 2018 Stage 3/4); cerebral amyloid beta presence (PET or cerebrospinal fluid); global Clinical Dementia Rating (CDR) score of 0.5; CDR‐Memory Box score ≥0.5. Secondary objectives included investigating the effect of bepranemab on tau‐PET imaging at Weeks 56 and 80. PET images were analyzed by a central imaging laboratory to determine the standardized uptake value ratio relative to cerebellum in multiple brain regions.

Results:

In total, 466 participants were randomized 1:1:1 across three arms (90 mg/kg bepranemab, 45 mg/kg bepranemab, placebo). Bepranemab slowed tau accumulation (by 33–58% vs placebo, across both bepranemab arms) in the whole cortical gray (n=scanned/total: 90 mg/kg bepranemab [n=113/152], 45 mg/kg bepranemab [n=104/152], and placebo [n=97/156]) and jack temporal meta regions (n=scanned/total: 90 mg/kg bepranemab [n=114/152], 45 mg/kg bepranemab [n=105/152], and placebo [n=97/156]) at Week 80 in the initial analysis of the full trial population (those who received at least a partial dose of study medication and had at least one valid post‐Baseline clinic visit and efficacy assessment). Data on tau accumulation in regions based on Braak staging will be presented.

Conclusion:

TOGETHER provides the first clinical demonstration of slowing of tau accumulation with an antibody targeting the tau mid‐region, as evidenced by tau PET imaging, and marks the first time that any tau‐directed therapy has demonstrated a clinical benefit.

2023-07-03·Expert opinion on investigational drugs

Clinical development of passive tau-based immunotherapeutics for treating primary and secondary tauopathies

Review

作者: Sardone, Rodolfo ; Dibello, Vittorio ; Castellana, Fabio ; Bellomo, Antonello ; Damiani, Christian ; Bortone, Ilaria ; Altamura, Mario ; Daniele, Antonio ; Lozupone, Madia ; Zupo, Roberta ; Solfrizzi, Vincenzo ; Lampignano, Luisa ; Panza, Francesco ; Stallone, Roberta ; Cirillo, Nicoletta

INTRODUCTION:

Tauopathies are clinicopathological entities with increased and pathological deposition in glia and/or neurons of hyperphosphorylated aggregates of the microtubule-binding protein tau. In secondary tauopathies, i.e. Alzheimer's disease (AD), tau deposition can be observed, but tau coexists with another protein (amyloid-β). In the last 20 years, little progress has been made in developing disease-modifying drugs for primary and secondary tauopathies and available symptomatic drugs have limited efficacy.

AREAS COVERED:

The present review summarized recent advances about the development and challenges in treatments for primary and secondary tauopathies, with a focus on passive tau-based immunotherapy.

EXPERT OPINION:

Several tau-targeted passive immunotherapeutics are in development for treating tauopathies. At present, 14 anti-tau antibodies have entered clinical trials, and 9 of them are still in clinical testing for progressive supranuclear palsy syndrome and AD (semorinemab, bepranemab, E2814, JNJ-63733657, Lu AF87908, APNmAb005, MK-2214, PNT00, and PRX005). However, none of these nine agents have reached Phase III. The most advanced anti-tau monoclonal antibody for treating AD is semorinemab, while bepranemab is the only anti-tau monoclonal antibody still in clinical testing for treating progressive supranuclear palsy syndrome. Further evidence on passive immunotherapeutics for treating primary and secondary tauopathies will come from ongoing Phase I/II trials.

项与 Bepranemab 相关的新闻（医药）

2026-01-01

·生物通

综述：Tau蛋白在阿尔茨海默病中的作用：塑造未来患者诊疗路径

摘要阿尔茨海默病（Alzheimer’s disease, AD）是一种复杂的神经退行性疾病，其两大核心病理特征为β-淀粉样蛋白（Aβ）斑块和Tau蛋白神经原纤维缠结（neurofibrillary tangles, NFTs）。近年来，靶向Aβ的疾病修正疗法（disease-targeted therapies, DTTs），如单克隆抗体lecanemab和donanemab，已获批准用于早期AD患者。然而，研究表明，要最大化临床疗效，可能需要同时干预多种病理驱动因素。越来越多的证据指出，Tau蛋白在AD病理生理中扮演着关键角色，与神经退行性变和认知衰退密切相关。目前，已有多种靶向Tau的治疗药物进入临床研发阶段。本综述旨在探讨Tau研究的进展如何塑造未来的AD患者诊疗路径，强调Tau作为治疗靶点和生物标志物的双重潜力，并思考其对已处于演变中的患者护理模式（包括更早诊断、工作流程改变和决策复杂化）可能带来的影响。 1. 引言 AD是导致晚发性认知衰退最常见的原因。其病理生理涉及Aβ和Tau蛋白的异常聚集，此外还包括突触功能障碍、炎症等。尽管疾病负担沉重，但AD治疗领域在近二十年曾面临瓶颈。近五年来，随着靶向Aβ的单克隆抗体获批，AD治疗格局发生了转变。这些疗法能延缓早期症状性AD的认知衰退，但认知功能仍会随时间恶化，提示需要同时针对其他病理靶点（如Tau）进行干预。 Aβ病理出现最早，而新皮层Tau缠结的积累更接近临床症状出现的时间，并且与症状的严重程度和进展的相关性比Aβ斑块沉积更强。Tau生物标志物在AD临床前和轻度认知障碍（mild cognitive impairment, MCI）阶段已显示出预测未来认知衰退的潜力。研究表明，治疗开始时通过Tau正电子发射断层扫描（positron emission tomography, PET）成像的Tau NFTs水平会影响抗Aβ单克隆抗体的治疗反应幅度。因此，Tau是一个有前景的治疗靶点，也是有价值的预后和药效学生物标志物。 2. Tau在AD病理生理中的作用在生理状态下，Tau是一种高度可溶的微管相关蛋白，对维持神经元正常功能至关重要。Tau由微管相关蛋白Tau（MAPT）基因编码，通过选择性剪接产生6种亚型，根据微管结合域重复序列的数量可分为3R和4R Tau。在AD等病理状态下，Tau会发生异常翻译后修饰（post-translational modifications, PTMs），如过度磷酸化（hyperphosphorylation），导致其功能失调、聚集形成NFTs。 Tau磷酸化是研究最深入的PTM。在AD大脑的病理环境中，Tau激酶和磷酸酶活性失衡，导致Tau过度磷酸化。这会使Tau从微管上解离，引起轴突运输失调、突触功能障碍和神经退行性变。过度磷酸化的Tau单体可自我聚集形成二聚体、寡聚体、前缠结，最终形成NFTs。Tau寡聚体具有神经毒性，可破坏基因组、线粒体功能、细胞信号传导等，并能引发强烈的神经胶质反应，加剧神经炎症。较大的Tau聚集体和NFTs则作为细胞质内的物理屏障，损害正常细胞代谢。除磷酸化外，其他PTMs如乙酰化、泛素化等也在Tau调控中起作用。Tau病理的扩散遵循可预测的模式（Braak分期），最初出现在脑干，然后逐步累及内侧颞叶（medial temporal lobe, MTL）、边缘系统，最后波及新皮层。这种神经元间病理Tau的传播被认为是通过一种“朊病毒样”播种机制实现的。 3. Tau作为未来AD治疗格局中的治疗靶点靶向Tau具有坚实的理论基础，可能减少Tau的传播和聚集，并减轻Aβ相关的毒性。多种作用机制不同的Tau靶向疗法正在临床研发中，包括抑制异常Tau产生、防止Tau错误折叠和聚集、阻断Tau在神经元间传播等。靶向病理性Tau经突触传播的细胞外阶段是一个有前景的策略。早期针对Tau蛋白N末端的抗体试验未达终点，可能与靶点表位有关。目前，针对Tau中段表位的药物（如单抗bepranemab）和靶向微管结合域的单抗（如etalanetug，正在与lecanemab联合试验）已进入后期临床试验阶段。细胞内抑制Tau产生也是重要策略。例如，BIIB080是一种鞘内给药的反义寡核苷酸，可选择性靶向MAPT信使RNA以减少Tau蛋白合成。其早期试验显示，可剂量依赖性地降低脑脊液（cerebrospinal fluid, CSF）中的磷酸化Tau（p-tau）181和总Tau水平，并减少Tau-PET显示的聚集Tau病理。其他有潜力的靶点包括减少Tau磷酸化（如激酶抑制剂）、Tau聚集抑制剂、微管稳定剂和Tau降解剂等。 4. Tau生物标志物在未来患者旅程中的作用 Tau生物标志物在药物研发中作用关键，并有望过渡到临床使用。最成熟的检测方法包括PET和CSF检测，而新兴的血液生物标志物（blood-based biomarkers, BBMs）因其成本较低、可及性好，有潜力改变临床护理路径。 Tau聚集体可通过Tau-PET在体可视化和量化。目前已有[18F]flortaucipir等Tau-PET示踪剂获批用于评估AD患者的Tau负荷。Tau-PET在临床研究中可用于根据Tau负荷水平对患者人群进行富集或分层，并作为试验终点。Tau病理沿Braak分期的进展与认知障碍的发生和进展相关。研究提出了“caTAUstrophe”概念，指当存在Aβ时，MTL区的Tau增殖加速并扩散至新皮层，这与认知恶化密切相关，是AD病理过程中的关键事件。在donanemab的III期试验中，根据基线Tau-PET水平（标准化摄取值比，standardized uptake value ratio, SUVr）对患者进行分层，结果显示低至中等Tau负荷的患者获益更大，凸显了Tau-PET在识别可能对治疗反应最佳患者方面的潜在效用。 CSF和血浆中的Tau生物标志物，如不同的磷酸化Tau异构体（p-tau181, p-tau217, p-tau231），可在AD临床前和MCI阶段出现异常，早于Tau-PET可检测到的显著变化。其中p-tau217在预测Aβ病理方面表现出高准确性。此外，CSF中与不溶性Tau聚集体病理更相关的标志物，如微管结合区Tau物种（MTBR-tau243），以及与早期可溶性Tau组装体相关的磷酸化位点（如p-tau serine262和356）也显示出前景。这些生物标志物在诊断、预测、确定最佳治疗窗口和提供预后见解方面具有潜在价值。 5. 不断演变的AD患者旅程 DTTs的出现使得理想的AD患者旅程概念发生范式转变，重心转向在疾病最早临床阶段实现生物标志物确认的诊断。未来若有靶向Tau的DTTs问世，可能会加速这一转变，增加更早寻求评估的患者数量，并使治疗决策、实施和监测更加复杂化。 5.1. 治疗决策随着不同类别DTTs的出现，治疗决策将趋向个体化，但也增加了复杂性，包括治疗类型、起始时机以及联合或序贯疗法的获益风险考量。临床医生可能需要构建包括个体生物标志物谱在内的全面临床图像，以确定最合适的药物和方案。未来Tau靶向疗法可能作为单药、与抗Aβ单抗联合使用或作为序贯/附加治疗。考虑到AD的多因素性质，联合治疗或序贯策略可能是必要的。此外，AD患者常合并其他病理（如α-突触核蛋白、TDP-43），这会影响治疗选择。对于已接受抗Aβ治疗并达到“治疗相关Aβ清除”（treatment-related amyloid clearance, TRAC）状态的患者，附加或序贯DTTs的决策还需考虑生物标志物谱的改变。 5.2. 治疗实施与监测新的DTTs可能具有独特的给药途径。例如，一些在研Tau靶向疗法采用鞘内给药，可能给药频率较低。新类别的DTT将有独特的风险谱和安全考量，需要特定的监测方案。抗Aβ单抗需要MRI监测淀粉样蛋白相关影像学异常（amyloid-related imaging abnormalities, ARIA）。未来若有两类DTTs可用，针对不同病理，治疗效果的监测以及联合用药背景下生物标志物的解读将变得更加复杂。需要制定基于数据的标准来指导治疗调整或停止。 6. 结论 Tau蛋白既是AD领域有前景的治疗靶点，也是宝贵的生物标志物。AD是一种多因素疾病，针对多种病理驱动因素可能是最大化临床效果所必需。Tau在AD病理生理中至关重要，与Aβ斑块沉积相比，它与症状严重程度和认知衰退的相关性更强。多种作用机制不同的Tau靶向药物正在研发中。Tau生物标志物正在深化我们对AD病理过程的理解，并在临床研究中发挥越来越大的作用。有效Tau靶向DTT的潜在问世，将推动AD诊疗向更早期、更个体化的方向发展，同时也对医疗系统应对复杂决策和监测的能力提出了更高要求。

2025-12-16

·EndPoints

Sanofi licenses Korean biotech’s tau-targeting Alzheimer’s drug for $80M upfront

In its second deal this week, Sanofi is spending $80 million upfront to license an Alzheimer’s drug candidate developed by the South Korean biotech ADEL. The French drugmaker will get global rights to ADEL-Y01, a monoclonal antibody designed to stop the buildup and spread of a toxic form of tau protein, which plays a key role in Alzheimer’s pathology. The pact could be worth up to $1.04 billion when factoring in milestones. ADEL is also eligible for tiered royalties ranging up to the double digits. ADEL has been advancing ADEL-Y01 with another South Korean biotech called Oscotec, which will be eligible for 47% of all the proceeds from the pact, according to Oscotec’s press release in Korean. The drug is currently in first-in-human development in the US. ADEL shared Phase 1a results at the Clinical Trials on Alzheimer’s Disease annual congress earlier this month. The buildup of toxic “tangles” of tau protein inside neurons is one of the hallmarks of Alzheimer’s disease. But many drug candidates that have targeted tau have ended up failing in mid-stage trials, including Johnson & Johnson’s posdinemab and UCB’s bepranemab . ADEL-Y01 targets a specific form of tau that is acetylated at a location called Lysine-280, ADEL said. The biotech hopes that by taking this more selective approach, it can slow disease progression while sparing other, healthy forms of tau that help neurons remain structurally stable. Sanofi’s ADEL pact follows a separate deal on Monday between the French drugmaker and California startup Dren Bio. Sanofi is paying $100 million upfront and up to $1.7 billion in milestones for rights to Dren’s unnamed B cell depleting therapy for autoimmune diseases. Also on Monday, Sanofi announced that its BTK inhibitor for multiple sclerosis called tolebrutinib flunked a Phase 3 trial in a severe form of MS and had its PDUFA date delayed for a different MS indication.

临床1期引进/卖出临床2期临床结果临床3期

2025-12-11

·同写意

药王折戟，AD研发迷雾难散

100+全球先锋领袖现场开讲、50+顶尖新基建机构抢先入驻、1000+产业精英面对面链接，中国ADC和核药产业界规格最高、影响力最大、汇聚创新力量最全的年度品牌盛会！近日，丹麦制药巨头诺和诺德宣布，其口服司美格鲁肽治疗早期阿尔茨海默病的两项III期临床试验未能达到主要终点。这款在糖尿病和肥胖症领域创造奇迹的药物，在神经退行性疾病领域遭遇重大挫折。就在同一周，强生也宣布终止其抗Tau蛋白抗体药物Posdinemab的II期临床试验。这款曾获FDA快速通道资格、峰值销售额被寄予厚望的药物，同样未能在早期阿尔茨海默病患者中显示出显著的临床益处。这些最新的受挫，让业界进一步体会到阿尔茨海默病“研发黑洞”之名所言非虚。过去数十年间，已有数百项临床试验在此领域折戟沉沙。但在阿尔茨海默病研发的“死亡谷”中，失败从未阻止冒险者。 TONACEA 01 跨界受挫在12月召开的阿尔茨海默病临床试验会议（CTAD）上，诺和诺德公布了详细数据。通过测量患者脑脊液，研究人员发现某些神经退行性变、炎症以及与阿尔茨海默病相关的Tau蛋白的标志物水平降低了10%或更低。然而，在分析的30种生物标志物中，大多数未观察到变化。这些试验是为诺和诺德明星成分司美格鲁肽开辟新市场的尝试。令人注意的是，研究显示，虽然临床终点未达标，但司美格鲁肽在试验中确实改善了阿尔茨海默病相关的生物标志物。诺和诺德临床药物开发国际医学副总裁Peter Johannsen表示：“司美格鲁肽确实对某些生物标志物产生了影响。”但他也承认，这些结果与罗氏未成功的候选药物甘特珠单抗大致相当，而已获批的阿尔茨海默病药物对生物标志物的影响幅度通常在30%左右。诺和诺德的尝试，是一场高风险的“跨界奇袭”，试图利用其在代谢疾病领域的王牌，开辟神经退行性疾病的新战场。这次尝试并非空穴来风。2020年，诺和诺德在针对司美格鲁肽在心血管适应症的临床研究数据事后分析中发现，15820名患者中，GLP-1治疗组发生痴呆的风险比安慰剂组降低53%。这一惊艳数据，促使诺和诺德采取了一项极为大胆的策略：跳过II期临床试验，直接进入III期研究。公司内部将这一策略形容为“彩票式布局”，即风险极高，但一旦成功，回报也将是变革性的。阿尔茨海默病被称为“3型糖尿病”的理论，为这一尝试提供了科学依据。研究表明，阿尔茨海默病患者大脑中存在胰岛素抵抗，导致神经元因缺乏能量受损。司美格鲁肽凭借其抗炎和改善代谢的特性，有望从这一机制入手干预疾病进程。超过3800名患者参与的大型研究最终显示，尽管部分生物标志物有所改善，但药物未能转化为患者临床获益。诺和诺德股价应声下跌，今年以来累计跌幅约51%。摩根士丹利此前估算，诺和诺德试验成功概率仅约25%，但是如果成功，预计可为公司带来高达50亿美元的年收入增长。这对于面临礼来激烈竞争的诺和诺德来说，意义重大。 Johannsen表示，公司仍在深入分析数据，现在谈论下一步计划为时过早。 TONACEA 02 传统路径未能幸免与诺和诺德的“跨界”尝试不同，强生的失败发生在阿尔茨海默病研发更传统的Tau蛋白靶点上。Posdinemab是一种精准靶向磷酸化Tau蛋白（pT217）的单克隆抗体，其设计意图是清除细胞外的病理性Tau蛋白，阻止其在神经元间的传播。强生对Posdinemab曾寄予厚望。公司曾预测该药最早于2028年上市，峰值销售额有望突破50亿美元。然而，这项名为Autonomy的II期研究显示，药物无法显著减缓患者的临床衰退。在礼来和卫材凭借靶向β淀粉样蛋白（Aβ）的药物确立市场领先地位后，针对Tau蛋白被认为是下一个最有希望的突破口。然而，强生的IIb期研究再次证明，即便能够降低大脑中某些Tau蛋白病理信号，也未必能减缓患者的临床衰退。强生的失败并非孤例。近年来，抗Tau蛋白疗法领域已接连多次受挫。UCB公司的bepranemab、罗氏的semorinemab以及礼来的LY3372689等多项Tau靶向疗法，均未能在临床试验中展现出稳定疗效。卫材首席临床官Lynn Kramer对近期一批抗Tau候选药物失败的原因有自己的见解。他指出，那些失败了的抗Tau候选药物未能成功是因为“没有正确的靶点”，阻止阿尔茨海默病发展的“关键”区域是Tau蛋白中一个参与其自身扩散“种子”的区域，而强生的药物并未击中那个种子区域。卫材之外，BMS、默沙东等公司仍在继续他们的抗Tau战役。 BMS的BMS-986446与MTBR内的R1-R3区域结合，主要用于治疗早期阿尔茨海默病。而默沙东的MK-2214靶向磷酸化丝氨酸413（pS413）Tau蛋白，于本月初获得FDA快速通道资格。 TONACEA 03 “百花齐放” 行业的视线正在从Aβ和Tau这两大传统靶点上挪开。根据Alzheimer's disease drug development pipeline: 2025报告，2025年有182项相关临床试验正在进行，比2024年增加了11%。这些试验涵盖了138种不同的药物，针对15种不同的病理过程。当前研发管线中，靶向Aβ的治疗方案仅占18%，而针对免疫炎症和Tau蛋白的分别占17%和11%。越来越多的企业开始探索脑肠轴、神经保护等非主流靶点，寻求颠覆性突破。阿尔茨海默病药物发现基金会联合创始人兼首席科学官Howard Fillit指出，炎症靶点正成为新的研究热点。“我个人的观点是，无论是系统性炎症还是神经炎症，都是这种疾病中一个非常重要的靶点。”目前，有超过30项针对炎症靶点的阿尔茨海默病临床试验正在进行。根据Roots Analysis预计，2025年AD全球诊断和治疗市场规模为124亿美元，2035年达到294亿美元，CAGR达到9%。巨大的市场潜力吸引着更多企业前赴后继地投入这一领域。在全球阿尔茨海默病研发格局中，中国药企正展现出日益活跃的态势。行业数据显示，中国针对阿尔茨海默病的药物研发活跃度已位居全球第二。恒瑞医药的SHR-1707（人源化抗Aβ单抗）针对早期阿尔茨海默病的II期临床试验正在进行中，成为国内第一款完全自主开发的抗淀粉样蛋白的抗体。康诺亚的CM383，靶向Aβ原纤维单抗，目前已启动I期临床试验。康方生物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，于今年11月获NMPA批准开展阿尔茨海默病临床试验，成为中国首个用于阿尔茨海默病疾病修饰治疗的双特异性抗体新药。石药集团于9月宣布，其自主开发的仑卡奈单抗注射液已获NMPA批准，可在中国开展临床试验，适用于治疗由AD引起的轻度认知障碍和阿尔茨海默病轻度痴呆。创新路径也在不断涌现。泰恩康旗下创新药CKBA在阿尔茨海默病的基础研究阶段达成阶段性成果，相关研究内容发表于国际学术期刊Nature Aging。CKBA相关研究的核心价值在于，其首次从机制层面揭示了“脂质代谢—小胶质细胞活化—神经炎症”这一全新的“脂—炎”轴在AD发病中的关键作用。 10月，CDE公示，再鼎医药引进的口服M1/M4型毒蕈碱乙酰胆碱受体激动剂KarXT胶囊（呫诺美林曲司氯铵胶囊）临床申请再获受理。根据药物临床试验登记与信息公示平台查询，推测此次拟定适应症为阿尔茨海默病相关的精神行为症状。参考文章： 1、https://mp.weixin.qq.com/s/f3GCcz6qk9fj2J3U6AJ2rg 2、https://view.inews.qq.com/k/20251204A05HJI00?web_channel=wap&no-redirect=1 3、https://www.biospace.com/drug-development/eisai-still-confident-in-anti-tau-asset-as-j-j-becomes-latest-victim-in-spiraling-space 4、https://www.bloomberg.com/news/articles/2025-12-04/novo-not-ready-to-quit-alzheimer-s-after-ozempic-pill-setback?srnd=phx-industries-health

100 项与 Bepranemab 相关的药物交易

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研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
轻度认知障碍	临床2期	荷兰	UCB Biopharma SRL	2021-05-26
阿尔茨海默症	临床2期	荷兰	UCB Biopharma SRL	2021-05-26
进行性核上性麻痹	临床1期	比利时	UCB Biopharma SRL	2019-12-03
进行性核上性麻痹	临床1期	德国	UCB Biopharma SRL	2019-12-03
进行性核上性麻痹	临床1期	西班牙	UCB Biopharma SRL	2019-12-03
进行性核上性麻痹	临床1期	英国	UCB Biopharma SRL	2019-12-03

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临床结果

适应症

分期

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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


NCT04867616 (TOGETHER, PipelineReview) 人工标引	临床2期	阿尔茨海默症	466	Low-dose bepranemab (45mg/kg)	觸憲願願獵鏇願繭選選(衊淵範遞築鬱簾網獵範) = no beneficial effect of low- or high-dose bepranemab compared with placebo was observed on the primary endpoint, Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) total score at Week 80 (CDR-SB is a measure of cognition and function). 壓觸鹽製範鏇築顧觸齋 (醖窪鏇簾鏇糧膚餘網壓 ) 未达到更多	积极	2024-10-31
				high-dose bepranemab (90mg/kg)bepranemab (90mg/kg)