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）

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.

2023-01-01·Handbook of clinical neurology

Passive tau-based immunotherapy for tauopathies.

Review

作者: Solfrizzi, Vincenzo ; Daniele, Antonio ; Panza, Francesco ; Lozupone, Madia

Tauopathies are heterogeneous clinicopathological entities characterized by abnormal neuronal and/or glial inclusions of the microtubule-binding protein tau. In secondary tauopathies, i.e., Alzheimer's disease (AD), tau deposition can be observed, but tau may coexist with another protein, i.e., 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. Treatments are being developed to interfere with the aggregation process or to promote the clearance of tau protein. Several tau-targeted passive immunotherapy approaches are in development for treating tauopathies. At present, 12 anti-tau antibodies have entered clinical trials, and 7 of them are still in clinical testing for primary tauopathies and AD (semorinemab, bepranemab, E2814, JNJ-63733657, Lu AF87908, PNT00, and APNmAb005). However, none of these seven 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. Two other anti-tau monoclonal antibodies have been discontinued for the treatment of primary tauopathies, i.e., gosuranemab and tilavonemab. Further evidence will come from ongoing Phase I/II trials on passive immunotherapeutics for treating primary and secondary tauopathies.

2020-08-01·Current opinion in neurology2区 · 医学

Immunotherapy in progressive supranuclear palsy

2区 · 医学

Review

作者: Olsen, Abby L ; Vaswani, Pavan A

Purpose of review:

Progressive supranuclear palsy (PSP) is a progressive adult-onset neurodegenerative disease. Abnormally, phosphorylated forms of the microtubule-associated protein tau containing four repeat domains (4R-tau) aggregate in neurons. Additionally, increasing evidence suggests that secretion and uptake of fragments of abnormal 4R-tau may play a role in disease progression. This extracellular tau is a natural target for immunotherapy.

Recent findings:

Three monoclonal antibodies targeting extracellular tau are in clinical stages of development. ABBV-8E12 and BIIB092 were safe in Phase 1, but both Phase two studies recently failed futility analyses. UCB0107 recently reported (in abstract form) Phase 1 safety results, and a Phase 2 study is under consideration. Stem cell therapy and the infusion of plasma are also being explored clinically.

Summary:

The likely role of extracellular tau in the progression of PSP makes tau a natural target for targeted immunotherapy. Clinical trials are still in early stages, and although tau immunotherapy has largely been shown to be safe, efficacy has yet to be demonstrated.

项与 Bepranemab 相关的新闻（医药）

2025-02-13

·BioSpace

Roche’s Evrysdi Becomes First Pill Cleared for Spinal Muscular Atrophy

iStock, Robert Way Evrysdi is the first, and so far only, noninvasive disease-modifying treatment for spinal muscular atrophy. The FDA on Wednesday approved the industry’s first-ever tablet treatment for spinal muscular atrophy— Roche ’s SMN2 splicing modifier Evrysdi—offering patients a more convenient and flexible dosing option. With the approval, granted to Roche subsidiary Genentech, Evrysdi remains the only noninvasive disease-modifying therapy for spinal muscular atrophy (SMA), according to Genentech’s news release. The tablet, which can be taken whole orally or dissolved in water, will be available in the coming weeks, the company said, and can be given to patients aged 2 years and up who weigh over 20 kgs (44 lbs). Genentech chief medical officer Levi Garraway called the approval a “significant step forward” for SMA patients. “Evrysdi has robust potential to modify the SMA disease trajectory, and has already been used to treat thousands of patients to date,” Garraway said, adding that the tablet formulation “combines established efficacy with convenience.” Everysdi’s active ingredient is risdiplam, a small-molecule drug that promotes the production of full-length and functional SMN protein in the brain. SMN—also known as survival of motor neuron—is involved in repairing DNA, managing cellular stress and preserving overall neuromuscular function. In SMA, genes encoding for SMN are typically mutated, leading to dysfunctional protein expression. The drug was first approved in 2020 , but as an oral solution that must be constituted by a healthcare provider before being dispensed to patients, according to its label . The drug is administered once daily after a meal through an oral syringe. Data from a bioequivalence study supported the approval of the pill form. Results showed that a 5-mg tablet could elicit comparable exposure to risdiplam, suggesting that patients taking the tablet will see “the same established efficacy and safety” as the oral solution of Evrysdi, according to Wednesday’s release. The pill approval for Evrysdi bucks Roche’s recent losing streak in the neurodegenerative space. In December 2024, the pharma announced that its Prothena-partnered Parkinson’s disease candidate prasinezumab failed its Phase IIb trial. The pharma pointed to “potential clinical efficacy” on the primary endpoint—time to confirmed motor progression—though the effect was not statistically significant. In October 2024, Roche let go of an Alzheimer’s disease prospect, sending rights to bepranemab back to UCB. Elsewhere in the SMA space, Biogen last month announced that the FDA had accepted a supplemental filing for Spinraza that proposes a higher dose of the Ionis-partnered asset for SMA. In October, Scholar Rock aced Phase III testing for its myostatin blocker apitegromab, which elicited significant improvements in motor function in kids with SMA.

上市批准临床2期临床3期

2025-02-08

·CPHI制药在线

病入新年感物华，2025年能否迎来阿尔茨海默病疗法突破？

关注并星标CPHI制药在线同样作为拥有广大患者数量的适应症，阿尔茨海默病与肥胖症的医药开发似乎处于完全不同的两条赛道之上，给人一种“君向潇湘我向秦”的感觉。减肥药市场一片百舸争流的大干快上景象，不仅已经上市的Wegovy和Zepbound令诺和诺德和礼来两大制药商领略到了“山顶千门次第开”的感受，为数众多的追随者也在“一波才动万波随”地争取跻身这个庞大的市场。而另一边，以阿尔茨海默病为代表的中枢神经系统疾病，尽管面对着同样庞大的商业机会，制药商们却一直在“多歧路，今安在”的道路上龃龉其中。2025年，阿尔茨海默病疗法开发能像肥胖症药物一样迎来“花开堪折直须折”的自由境界吗？ 1. 阿尔茨海默病疗法开发的2024困顿阿尔茨海默病与肥胖症疗法开发的一个相似点，就是这两种适应症的致病机理人们仍然没有完全搞清楚，在开发过程中都给人一种摸着石头过河的感觉。索性肥胖症疗法的开发得益于二型糖尿病GLP-1疗法开发过程中的“意外”发现，实现了截弯取直的快速发展。同样作为病理复杂的适应症，阿尔茨海默病不仅在生物标志物方面还存在争议，还面临着如何实现脑部递送的巨大的挑战。除此之外，以Aduhelm，Leqembi和Kisunla为代表的靶向脑部Aβ (β-amyloid，β淀粉样蛋白)的抗体药物，还存在着ARIA (Amyloid-Related Imaging Abnormalities，淀粉样蛋白相关的成像异常)的黑框警告，包括脑水肿和脑出血，这为阿尔茨海默病疗法的开发增加了极大的挑战。反观GLP-1药物，副作用大多数恶心和呕吐这样相对轻微的表现，在安全性方面的门槛要低很多。 2024年，阿尔海默病疗法开发遭遇的挫折几乎就是减肥药成功的镜相对照。 2024年1月底，当年顶着巨大争议上市的首款抗Aβ抗体阿尔茨海默病药物Aduhelm (aducanumab) 被其开发商渤健宣布撤市，而此前渤健已经撤回了Aduhelm向EMA递交的上市申请。Aduhelm“其兴也勃焉，其亡也忽焉”的故事为制药行业留下了众多的话题和思考。 2021年6月，FDA在先前的专家咨询委员会会议压倒性的1票支持、8票反对，2票弃权的情况下，仍然一意孤行地批准了Aduhelm的上市申请（专家咨询委员会投票结果对于FDA最终决定不具备约束性影响）。顶着巨大争议上市的Aduhelm的商业化效果并不理想，不仅过高的标价成为了业界诟病的问题（渤健最初将Aduhelm的年度治疗成本定价为56000美元），而且在有效性和安全性方面的争议已然不绝于耳，最终渤健做出了将Aduhelm撤市的决定，转而重点运作另一款获得FDA批准的阿尔茨海默病抗Aβ抗体疗法Leqembi（lecanemab）上。渤健强调，撤市的决定并不在于Aduhelm的安全性和有效性，而是出于战略考量，有一点“此天意，非战之罪”的姿态。 Aduhelm的“尔曹身与名俱灭”，似乎是很多兴勃亡忽的中枢神经系统疾病疗法殊途同归的命运。罗氏在2024年10月宣布了终止与UCB共同开发阿尔茨海默病候选药物bepranemab的决定，这也是罗氏2024年第三次放弃阿尔茨海默病项目。早在1月，罗氏就将两项合作开发的阿尔茨海默病资产归还给了AC Immune。罗氏与UCB于2020年达成的合作原本包括1.2亿美元的预付款和高达20亿美元的潜在里程碑付款。这项合作的关注点，在于靶向tau蛋白的bepranemab。Tau蛋白同β-淀粉样蛋白一样被视为阿尔茨海默病的生物标志物。tau蛋白的水平和磷酸化状态常被用作生物标志物。Tau蛋白不仅是阿尔茨海默病的关键生物标志物，也是开发新治疗方法的潜在靶点，其靶向药物的命运在一定程度也昭示着目前阿尔茨海默病疗法开发能够走出Aβ的圭臬樊笼。然而bepranemab的IIa期临床试验结果却令罗氏兴致阑珊，最终决定将该药物的开发权交还给UCB。值得注意的是，虽然罗氏终止了与UCB的合作，但他们仍对tau靶向疗法开发保持了浓厚兴趣。罗氏仍在试图针对 tau 蛋白开发阿尔茨海默病疗法，包括与 Sangamo Therapeutics Inc. 建立的临床前合作，两家公司于 2024年8 月签署了一项价值5000 万美元预付款的协议。在罗氏的管线中，有一款“嫡出”的抗tau蛋白抗体资产trontinemab。它采用罗氏的“脑穿梭（Brainshuttle）”技术，以蛋白质之躯跨越血脑屏障，靶向并抑制β淀粉样蛋白。这种技术允许大分子在不触发对周围细胞的免疫反应的情况下穿过血脑屏障。 2. 阿尔茨海默病疗法开发，病入新年感物华虽然阿尔茨海默病疗法在过往岁月更多以“命运多舛”的形象示人，但在这个领域仍然给众多开发者“桃花又是一年春”的希冀，包括渤健、卫材、礼来、罗氏和诺和诺德在内的制药公司依然加大了这个领域的投资力度，任何临床试验的成功或药物批准的突破都可能对股价产生重大影响。投资者高度重视以阿尔茨海默病为代表的中枢神经系统疾病的潜在商业价值。根据Bloomberg预测，到 2030 年阿尔茨海默病的市场规模可能达到 130 亿美元。渤健和卫材的上市药物Leqembi 目前的递送方式为静脉输注，但他们也在开发一种能够在家给药的Leqembi皮下注射版本。渤健和卫材已于2024年11月向FDA递交了这款Leqembi的BLA申请。皮下自动注射器用于每周维持给药，此前已获得 FDA 快速通道资格。这款皮下注射版本的Leqembi如果获得 FDA 批准，患者可以在家中或者医疗机构中完成给药，注射过程只需要15秒钟。相比之下，Leqembi的静脉输注制剂每两周给药一次，每次的注射时间大约在1小时左右。根据卫材公布的数据，皮下注射Leqembi治疗产生的淀粉样斑块清除率高于每两周静脉注射。Leqembi皮下注射版本是否能在2025年获得FDA的批准，这成为了阿尔茨海默病开发领域和投资者关注的焦点之一。礼来公司的抗Aβ抗体药物Kisunla（donanemab） 2024 年 7 月获得 FDA 批准，Kisunla未来是否将与Leqembi颉颃前行还是脱颖而出，也是阿尔茨海默病疗法投资者关注的重点。除了Kisunla之外，礼来的管线中还有一款阿尔茨海默病资产remternetug，可以通过静脉或皮下的途径给药。Remternetug是一款抗焦谷氨酸Aβ抗体药物正处于临床III期阶段。据Bloomberg称，Remternetug的III期试验将评估其淀粉样斑块清除率和安全性，以判断其在有效性上是否胜过已上市的donanemab。Remternetug 的试验结果可能会在今年年底或 2026 年初公布。罗氏在做出了终止了与USB共同开发bepranemab的合作之后，并没有在开发阿尔茨海默病疗法的道路上选择“行至水穷处，坐看云起时”的姿态，而是独自开发了他们自己的trontinemab。值得注意的是，罗氏在开发trontinemab的项目中使用了可穿越血脑屏障的技术平台Brainshuttle，如果成功，将为中枢神经系统疾病疗法的开发引入革命性的影响。巴克莱银行认为罗氏针对trontinemab的开发不会半途而废，而将继续进行中后期的研究。之所以这么说，是因为trontinemab本质上是 gantenerumab 的更新版本，gantenerumab 是罗氏之前对阿尔茨海默病的重大赌注，但最终未能减缓认知能力下降。尽管罗氏从bepranemab的合作项目中抽身而出，但开发它的比利时制药巨头UCB预计仍将在bepranemab的开发道路中继续上下求索。在去年的一项II期临床研究中，bepranemab未能达到主要临床终点，但的确减缓了认知能力的下降和生物标志物tau蛋白在大脑中的积累速度。一些分析师指出，bepranemab 具有相对较强的安全性数据，应该具备与其它疗法组成联合疗法治疗阿尔茨海默病的潜力。 3. GLP-1药物能否“达则兼济天下”？阿尔茨海默病未来疗法开发的一个重要看点，在于病理机制的深入研究是否能够突破目前囿于Aβ蛋白清除的樊笼。除了Aβ蛋白之外，tau蛋白也是一个重要的生物标志物，但也有很多公司在开发道路上选择了与这两个“部分存疑”的生物标志物不同的途径。进行GLP-1药物开发的公司，包括诺和诺德在内的几家制药商已经押注于此类药物治疗阿尔茨海默症的潜力。例如丹麦公司Kariya 正在开发 KP405，这是一种GLP-1/GIP双受体共激动剂，与礼来的tirzepatide师出同门。KP405最初用于治疗帕金森病，未来可能针对阿尔茨海默病进行研究。KP405的特别之处在于，它并没有使用semaglutide和tizepatide的脂化技术，而是在药物结构中添加了细胞膜受体识别的 TAT 序列，这使得药物分子可能穿越血脑屏障而进入大脑病灶。诺和诺德在2型糖尿病和肥胖症上大获成功的GLP-1药物semaglutide也在针对阿尔茨海默病进行研究。去年的一项研究表明，服用semaglutide的患者被诊断出患有阿尔茨海默病的风险显著降低。诺和诺德目前正在测试semaglutide是否能使早期阿尔茨海默病患者受益，预计将从两项大型 III 期试验 EVOKE 和 EVOKE Plus 中读取结果，测试semaglutide对阿尔茨海默病患者的作用。预计EVOKE将于 2025 年 9 月公布顶线数据，而EVOKE Plus则将在2026年10月读数。使用 GLP-1 治疗阿尔茨海默病的想法并非空穴来风。人们一直对用于治疗糖尿病和针对代谢疾病和内分泌疾病途径的药物是否会对阿尔茨海默病产生影响感兴趣。虽然关于阿尔茨海默病的真正病因存在很多争论，糖尿病和肥胖症与阿尔茨海默病之间可能存在交集。事实上，有几项研究表明胰岛素抵抗与阿尔茨海默病之间存在联系。导致有些人将阿尔茨海默病称为“3 型糖尿病”。多项观察性研究和荟萃分析也建立起了 2 型糖尿病与阿尔茨海默病的风险增加。随着年龄的增长，整个身体的胰岛素抵抗都会增加，这意味着细胞无法吸收足够的葡萄糖。当葡萄糖水平不理想而且高度活跃的神经元无法获得足够的能量时，它们就会出现功能障碍并最终慢性死亡。这种内在关联是具有一定道理的。如果胰岛素抵抗确实是阿尔茨海默病的一个诱因，那么 GLP-1 可能有助于延缓这种疾病，因为它通过刺激胰岛素分泌和减缓胰高血糖素释放来发挥作用。此前GLP-1药物利拉鲁肽（liraglutide）的一项II 期试验的结果支持了这样的假设。那项研究在英国多个地点随机对 204 名受试者进行安慰剂或利拉鲁肽治疗。结果发现，在一年的治疗中，利拉鲁肽组的认知功能下降速度比安慰剂组慢 18%。研究人员指出，脑容量损失速度较慢表明利拉鲁肽可以保护大脑，就像他汀类药物可以保护心脏一样。利拉鲁肽可以减少脑部炎症、降低胰岛素抵抗、改善神经细胞通讯并限制淀粉样蛋白β和 tau 的危害。尽管某些研究出现了积极的迹象，但专家们一致认为，GLP-1 仍有很长的路要走，才能证明其在阿尔茨海默病治疗中的价值，这需要在随机对照试验中对大量患者进行分析，这其实是一项非常艰巨的工作。 4. 直捣黄龙，药物递送的突破相对于稍显踯躅的病理研究，阿尔茨海默病疗法递送领域的开发已经取得了明显的突破，最主要的表现在于新一代的药物分子开始注重直接穿越血脑屏障的能力。例如前面提到的罗氏开发的trontinemab，就利用了最新技术平台Brainshuttle技术。Brainshuttle是凭借与TfR（Transferrin Receptor转铁蛋白受体）的作用实现血脑屏障的跨越。Trontinemab将抗TfR抗体模块与阿尔茨海默病抗体Gantenerumab（罗氏上一代的阿尔茨海默病抗体候选药）融合，与血脑屏障上皮细胞上的TfR受体结合。这种结合产生内体隔室，内体隔室穿过细胞质并通过转胞吞作用进入大脑（图1）。因此从本质上说，trontinemab是一款2 + 1 双特异性单体，可双价结合 Aβ蛋白，单价结合人 TfR1。图1. Brainshuttle技术支持的trontinemab穿越血脑屏障机制。（图片来源：Neuron）艾伯维通过14亿美元收购Aliada Therapeutics获得的关键资产阿尔茨海默病候选药物ALIA-1758也利用了类似的递送机制。ALIA-1758是一款抗β淀粉样蛋白（焦谷氨酸β淀粉样蛋白（3pE-Aβ））抗体药物。ALIA-1758通过专有技术Modular Delivery (MODEL) 平台设计，可以穿越血脑屏障而不触发神经毒性。 MODEL平台将抗TfR抗体模块与阿尔茨海默病抗体融合，与血脑屏障上皮细胞上的TfR受体结合。这种结合产生内体隔室，内体隔室穿过细胞质并通过转胞吞作用进入大脑。MODEL平台不仅可以携带抗体，也可以携带寡核苷酸、多肽、酶和其它蛋白，通过结合TfR或CD98的方式跨越血脑屏障。礼来与卫材最近也在利用各自的专有技术开发可穿越血脑屏障的中枢神经系统疾病疗法。礼来使用的是QinoTrans平台，通过工程化蛋白结合血脑屏障上的受体，以此穿越该屏障。卫材去年与瑞典生物技术公司BioArctic达成协议，获得了后者的BioArctic BrainTransporter技术的使用权限，开发通过与血脑屏障受体结合而抵达大脑的阿尔茨海默病药物。 5. 面壁十年图破壁阿尔茨海默病疗法的开发虽然面临巨大挑战，但与当前方兴未艾的减肥药领域有相似之处。减肥药市场在过去几年中因肥胖问题日益严重而加速发展，相关药物的需求不断攀升，促使制药公司加大研发力度，推出了如GLP-1受体激动剂等新型疗法，取得了显著成果。同样，阿尔茨海默病的全球影响力随着人口老龄化迅速扩大，使得开发有效疗法的需求愈发迫切。然而，阿尔茨海默病疗法的开发复杂性远超减肥药，因为其涉及多种致病机制，且有效治疗手段尚不成熟。尽管如此，正如减肥药领域通过技术突破和市场推动取得了进展，阿尔茨海默病疗法也有望迎来关键性突破，推动其开发进入新的高度，为患者带来实际疗效。精准医学的发展以及生物标志物的应用，将使早期诊断和个性化治疗成为可能，大幅提高治疗的有效性。同时，全球老龄化加剧意味着市场对阿尔茨海默病疗法的需求日益增长，类似减肥药市场的繁荣景象或将在阿尔茨海默病领域重现。尽管开发过程中仍存在诸多科学和临床障碍，但通过创新技术、跨学科合作以及更有效的临床研究设计，未来阿尔茨海默病疗法有望实现重大突破，实现面壁十年图破壁的真正飞跃。 Ref.Constantino, A. K. Biogen drops controversial Alzheimer’s drug Aduhelm to focus on Leqembi, experimental treatments. CNBC. 31. 01. 2024.Merrill, J. Biogen Closes The Book On The Aduhelm Saga. Pink Sheet. 31. 01. 2024.Armstrong, A. Roche Trims Another Alzheimer’s Prospect, Ending UCB Collabortion. Biospace. 22. 10. 2024.Jackson, M. UCB Assessing Bepranemab’s Future After Roche/Genentech Ends Partnership. Scrip. 22. 10. 2024.Kresge, N. et al. Roche CEO Is Optimistic on Coming Alzheimer’s Trial Results. Bloomberg. 23. 10. 2024.Eisai Completes Rolling Submission to US FDA for LEQEMBI® (lecanemab-irmb) Biologics License Application for Subcutaneous Maintenance Dosing for the Treatment of Early Alzheimer’s Disease Under the Fast Track Status. Eisai Press Release. 01. 11. 2024.McKenzie, H. Evidence Mounts for Potential of GLP-1s in Alzheimer’s Disease.Taylor, N. P. AbbVie inks $1.4B Aliada buyout, landing ex-J&J Alzheimer's drug to leap the blood-brain barrier. Fierce Biotech. 28. 10. 2024.Alpert, B. AbbVie’s Deal for Alzheimer’s Antibody Raises Curtain for Roche News on Wednesday. Barron’s. 29. 10. 2024.Qinotto and Lilly Enter Research Collaboration and License Agreement. Globe Newswire. 08. 10. 2024. 扫码领取CPHI & PMEC China 2025展会门票【智药研习社近期直播】来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com ▼更多制药资讯，请关注CPHI制药在线▼ 点击阅读原文，进入智药研习社~

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2024-11-05

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UCB shares ‘encouraging’ data for Alzheimer’s disease candidate bepranemab

UCB has announced “encouraging data” from a phase 2a study of its investigational anti-tau antibody bepranemab in Alzheimer’s disease (AD) patients. The TOGETHER study has been evaluating the safety, efficacy and tolerability of two dose levels of the drug in patients with prodromal-to-mild cases of the neurodegenerative disorder. Results presented at this year’s Clinical Trials on AD meeting showed that the primary endpoint of Clinical Dementia Rating Scale Sum of Boxes (CDR-SB), a measure of cognition and function, total score at week 80 was not met. However, the company highlighted benefits across key secondary endpoints, with bepranemab slowing the rate of tau accumulation versus placebo in key brain regions by 33% to 58% at week 80, and the drug slowed cognitive decline by 21% to 25% versus placebo in the same period. Improvements also were observed in patients with low tau burden at baseline and APOε4 non-carriers, who represent approximately 50% of the full study population. A post-hoc analysis of these two predefined subgroups showed that high-dose bepranemab slowed the rate of tau accumulation versus placebo in key brain regions by 63% to 67% at week 80, and slowed clinical disease progression by 29%, as measured by the change in CDR-SB, at week 80. The subgroup analysis also showed that bepranemab slowed disease progression according to secondary/exploratory endpoints, including measures of Activities of Daily Living by 41% to 54% at week 80. An estimated 982,000 people are living with dementia in the UK, with AD accounting for up to 75% of cases. The disease slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks. Bepranemab specifically targets a mid-region epitope of human tau, which is thought to be essential for tau aggregation and is a key driver of neurodegeneration in AD. UCB’s chief scientific officer, Alistair Henry, said: “We are deeply encouraged by the proof-of-concept data for bepranemab, which highlight its potential to impact early AD progression. This strengthens our belief in the value of targeting the mid-region of tau as an important strategy in altering the trajectory of the disease.” The company said it is now “evaluating next steps” in the bepranemab development programme.

临床2期临床结果

100 项与 Bepranemab 相关的药物交易

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研发状态

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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	美国	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	比利时	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	加拿大	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	法国	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	德国	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	意大利	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	荷兰	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	波兰	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	西班牙	UCB Biopharma SRL	2021-06-09
轻度认知障碍	临床2期	英国	UCB Biopharma SRL	2021-06-09

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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)	簾壓鏇襯鹹憲憲觸醖鏇(艱網醖積壓齋鏇艱繭觸) = 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). 餘艱憲鑰鬱膚淵糧襯廠 (廠襯鑰艱製艱積壓願網 ) 未达到更多	积极	2024-10-31
				high-dose bepranemab (90mg/kg)