A Multi-center, Double-blind, Randomized, Placebo Parallel Controlled, Safety and Tolerability Phase I Clinical Trial of Recombinant Novel Coronavirus Vaccine (CHO Cells) in Healthy People Between 18 and 59 Years of Age

In this trial, a total of 50 subjects were recruited; the test vaccines were divided into 3 groups, low-dose vaccine groups, high-dose vaccine groups, and placebo groups. The first-stage randomized participants in the low-dose group (20 cases) and the placebo group (5 cases) were evaluated for 7 days. After the 7-day safety data was evaluated and agreed by the DSMB, the second-stage study was conducted. Into the high-dose group (20 cases) and placebo group (5 cases) subjects; follow-up to 30 days, after the safety assessment by the investigator and consent, then inoculate the second dose. Observation was performed for 1.0 hour after the second dose. The researchers conducted a safety evaluation and agreed to follow-up after discharge.

开始日期2020-06-22

申办/合作机构

安徽智飞龙科马生物制药有限公司

[+2]

NCT03531710

/ Terminated临床2期

An Extension Study of a Phase IIa Study in Patients With Mild Alzheimer's Disease to Evaluate the Safety, Tolerability, Immunogenicity, and Efficacy of UBITh® AD Immunotherapeutic Vaccine (UB-311)

To evaluate the long-term safety, tolerability and potential efficacy, patients who previously participated in V203-AD study (NCT02551809) will be eligible to participate in the extension study and will receive 3 or 5 doses of UB-311 within a 96-week treatment period followed by a 12-week follow-up period.

开始日期2018-08-10

申办/合作机构

United Neuroscience Ltd.

NCT02551809

/ Completed临床2期

A Randomized, Double-blind, Placebo-controlled, 3-arm Parallel-group, Multicenter, Phase IIa Study to Evaluate the Safety, Tolerability, Immunogenicity, and Efficacy of UBITh® AD Immunotherapeutic Vaccine (UB-311) in Patients With Mild Alzheimer's Disease

The purpose of this Phase IIa study is to determine whether the AD Immunotherapeutic Vaccine (UB-311), targeting the amyloid beta peptide (N-terminal amino acids, 1-14), is safe and immunogenic in mild AD patients. In addition, the efficacy profiles will be evaluated as the secondary endpoint.

开始日期2015-10-01

申办/合作机构

United Neuroscience Ltd.

100 项与 UBITh AD immunotherapeutic vaccine(United Biomedical, Inc.) 相关的临床结果

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100 项与 UBITh AD immunotherapeutic vaccine(United Biomedical, Inc.) 相关的转化医学

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100 项与 UBITh AD immunotherapeutic vaccine(United Biomedical, Inc.) 相关的专利（医药）

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项与 UBITh AD immunotherapeutic vaccine(United Biomedical, Inc.) 相关的文献（医药）

2023-08-01·EBioMedicine

Safety, tolerability, immunogenicity, and efficacy of UB-311 in participants with mild Alzheimer's disease: a randomised, double-blind, placebo-controlled, phase 2a study

Article

作者: Hendrix, Suzanne B ; Chang, Chiung-Chih ; Dickson, Samuel P ; Wang, Pei-Ning ; Dodart, Jean-Cosme ; Yu, Hui Jing ; Verma, Ajay ; Huang, Chin-Chang ; Cummings, Jeffrey ; Wang, Chang Yi ; Liu, Hope ; Chiu, Ming-Jang

BACKGROUND:

Anti-amyloid vaccines may offer a convenient, affordable, and accessible means of preventing and treating Alzheimer's disease. UB-311 is an anti-amyloid-β active immunotherapeutic vaccine shown to be well-tolerated and to have a durable antibody response in a phase 1 trial. This phase 2a study assessed the safety, immunogenicity, and preliminary efficacy of UB-311 in participants with mild Alzheimer's disease.

METHODS:

A 78-week, randomised, double-blind, placebo-controlled, parallel-group, multicentre, phase 2a study was conducted in Taiwan. Participants were randomised in a 1:1:1 ratio to receive seven intramuscular injections of UB-311 (Q3M arm), or five doses of U311 with two doses of placebo (Q6M arm), or seven doses of placebo (placebo arm). The primary endpoints were safety, tolerability, and immunogenicity of UB-311. Safety was assessed in all participants who received at least one dose of investigational product. This study was registered at ClinicalTrials.gov (NCT02551809).

FINDINGS:

Between 7 December 2015 and 28 August 2018, 43 participants were randomised. UB-311 was safe, well-tolerated, and generated a robust immune response. The three treatment-emergent adverse events (TEAEs) with the highest incidence were injection-site pain (14 TEAEs in seven [16%] participants), amyloid-related imaging abnormality with microhaemorrhages and haemosiderin deposits (12 TEAEs in six [14%] participants), and diarrhoea (five TEAEs in five [12%] participants). A 97% antibody response rate was observed and maintained at 93% by the end of the study across both UB-311 arms.

INTERPRETATION:

These results support the continued development of UB-311.

FUNDING:

Vaxxinity, Inc. (Formerly United Neuroscience Ltd.).

2016-06-01·JOURNAL OF NEUROCHEMISTRY

A retrospective analysis of the Alzheimer's disease vaccine progress – The critical need for new development strategies

Review

作者: Marciani, Dante J.

Abstract:

The promising results obtained with aducanumab and solanezumab against Alzheimer's disease (AD) strengthen the vaccine approach to prevent AD, despite of the many clinical setbacks. It has been problematic to use conjugated peptides with Th1/Th2 adjuvants to induce immune responses against conformational epitopes formed by Aβ oligomers, which is critical to induce protective antibodies. Hence, vaccination should mimic natural immunity by using whole or if possible conjugated antigens, but biasing the response to Th2 with anti‐inflammatory adjuvants. Also, selection of the carrier and cross‐linking agents is important to prevent suppression of the immune response against the antigen. That certain compounds having phosphorylcholine or fucose induce a sole Th2 immunity would allow antigens with T‐cell epitopes without inflammatory autoimmune reactions to be used. Another immunization method is DNA vaccines combined with antigenic ones, which favors the clonal selection and expansion of high affinity antibodies needed for immune protection, but this also requires Th2 immunity. Since AD transgenic mouse models have limited value for immunogen selection as shown by the clinical studies, screening may require the use of validated antibodies and biophysical methods to identify the antigens that would be most likely recognized by the human immune system and thus capable to stimulate a protective antibody response.imageTo induce an anti‐Alzheimer's disease protective immunity and prevent possible damage triggered by antigens having B‐cell epitopes‐only, whole antigens might be used; while inducing Th2 immunity with sole anti‐inflammatory fucose‐based adjuvants. This approach would avert a damaging systemic inflammatory immunity and the suppression of immunoresponse against the antigen because of carrier and cross‐linkers; immune requirements that extend to DNA vaccines.

2009-01-01·Progress in brain research4区 · 医学

Developing novel immunogens for a safe and effective Alzheimer's disease vaccine

4区 · 医学

Review

作者: Lemere, Cynthia A

Alzheimer's disease (AD) is the most prevalent form of neurodegeneration; however, therapies to prevent or treat AD are inadequate. Amyloid-beta (Abeta) protein accrues in cortical senile plaques, one of the key neuropathological hallmarks of AD, and is elevated in brains of early onset AD patients in a small number of families that bear certain genetic mutations, further implicating its role in this devastating neurological disease. In addition, soluble Abeta oligomers have been shown to be detrimental to neuronal function. Therapeutic strategies aimed at lowering cerebral Abeta levels are currently under development. One strategy is to immunize AD patients with Abeta peptides so that they will generate antibodies that bind to Abeta protein and enhance its clearance. As of 1999, Abeta immunotherapy, either through active immunization with Abeta peptides or through passive transfer of Abeta-specific antibodies, has been shown to reduce cerebral Abeta levels and improve cognitive deficits in AD mouse models and lower plaque load in nonhuman primates. However, a Phase II clinical trial of active immunization using full-length human Abeta1-42 peptide and a strong Th1-biased adjuvant, QS-21, ended prematurely in 2002 because of the onset of meningoencephalitis in approximately 6% of the AD patients enrolled in the study. It is possible that T cell recognition of the human full-length Abeta peptide as a self-protein may have induced an adverse autoimmune response in these patients. Although only approximately 20% of immunized patients generated anti-Abeta titers, responders showed some general slowing of cognitive decline. Focal cortical regions devoid of Abeta plaques were observed in brain tissues of several immunized patients who have since come to autopsy. In order to avoid a deleterious immune response, passive Abeta immunotherapy is under investigation by administering monthly intravenous injections of humanized Abeta monoclonal antibodies to AD patients. However, a safe and effective active Abeta vaccine would be more cost-effective and more readily available to a larger AD population. We have developed several novel short Abeta immunogens that target the Abeta N-terminus containing a strong B cell epitope while avoiding the Abeta mid-region and C-terminus containing T cell epitopes. These immunogens include dendrimeric Abeta1-15 (16 copies of Abeta1-15 on a lysine antigen tree), 2xAbeta1-15 (a tandem repeat of two lysine-linked Abeta1-15 peptides), and 2xAbeta1-15 with the addition of a three amino acid RGD motif (R-2xAbeta1-15). Intranasal immunization with our short Abeta fragment immunogens and a mucosal adjuvant, mutant Escherichia coli heat-labile enterotoxin LT(R192G), resulted in reduced cerebral Abeta levels, plaque deposition, and gliosis, as well as increased plasma Abeta levels and improved cognition in a transgenic mouse model of AD. Preclinical trials in nonhuman primates, and human clinical trials using similar Abeta immunogens, are now underway. Abeta immunotherapy looks promising but must be made safer and more effective at generating antibody titers in the elderly. It is hoped that these novel immunogens will enhance Abeta antibody generation across a broad population and avoid the adverse events seen in the earlier clinical trial.

项与 UBITh AD immunotherapeutic vaccine(United Biomedical, Inc.) 相关的新闻（医药）

2025-05-05

·PRNewswire

Breakthrough Alzheimer's Vaccine Duvax Secures $3 Million NIH Grant to Launch U.S. Clinical Trials

IRVINE, Calif., May 5, 2025 /PRNewswire/ -- Nuravax Inc., a biotechnology company pioneering immunotherapy for neurodegenerative disorders, has been awarded a $3 million grant from the National Institutes of Health (NIH) to support Duvax, the first dual-target Alzheimer's vaccine, in its entry into human clinical trials. Nuravax, in partnership with the non-profit Institute for Molecular Medicine (IMM), secured the award on its very first NIH grant submission, earning top-tier scores. This rare distinction highlights the scientific strength and strategic importance of the Duvax vaccine. The grant, awarded through NIH's highly competitive SBIR Fast-Track program, will fund a critical milestone in the clinical validation of Duvax. An initial portion of the $3 million grant has been allocated to initiate the Phase 1 clinical trial evaluating the safety and immunogenicity of Duvax as a secondary prevention therapy, with the remaining funds expected later in 2025. "This SBIR grant is a powerful endorsement of our mission to clinically validate and advance Duvax as a first-in-class vaccine for Alzheimer's prevention," said Roman Kniazev, CEO of Nuravax. "While IMM laid the scientific foundation, our focus at Nuravax is on translating that innovation into real-world impact. This funding enables us to move Duvax into clinical trials in the U.S. and brings us one step closer to delivering it as preventive therapy for individuals at risk – before symptoms begin." Duvax is a first-in-class vaccine that targets both amyloid-beta and tau proteins, the two hallmark drivers of Alzheimer's disease, positioning it at the forefront of Alzheimer's research. Unlike conventional treatments, Duvax is designed for use during the preclinical stage, when the disease is silently progressing but before cognitive symptoms appear. "The Phase 1 trial, supported by this SBIR grant awarded to our development and commercialization partner, Nuravax, marks a critical step in translating years of foundational research at IMM into a potential clinical breakthrough," said Dr. Michael Agadjanyan, VP of IMM and Head of Immunology. "Based on strong preclinical data, we at IMM expect Duvax to elicit a robust immune response against both Aβ and tau pathologies, an approach that could fundamentally shift the paradigm of Alzheimer's treatment from symptomatic and disease-modifying treatment (DMT) to secondary preventive therapy for cognitively unimpaired people at risk of disease." The vaccine's use is guided by highly precise and specific blood tests that detect early pathological changes, enabling timely intervention. By clearing toxic forms of amyloid-beta and tau before irreversible damage occurs, Duvax aims to shift the treatment paradigm from symptom management to secondary preventive therapy. About Nuravax Nuravax is a clinical-stage biotech company developing and advancing immunotherapeutic vaccines for neurodegenerative diseases, including Alzheimer's, Parkinson's, TBI, and CTE. Focused on early intervention, Nuravax aims to alter disease progression before irreversible damage occurs. The company leads the clinical development, regulatory strategy, and manufacturing of Duvax, a dual-target vaccine licensed from the Institute for Molecular Medicine (IMM), a nonprofit dedicated to neurodegenerative disease research. About IMM The Institute for Molecular Medicine (IMM) is a non-profit research organization dedicated to understanding, preventing, and curing chronic human diseases, with a focus on neurodegeneration. IMM is advancing MultiTEP — a universal vaccine platform technology that enables the development of diverse vaccine formats, including DNA, RNA, and recombinant protein-based designs. Disclaimer: Research reported in this publication was supported by the National Institute On Aging of the NIH under Award Number R44AG091903. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. SOURCE Nuravax Inc WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

疫苗免疫疗法快速通道临床1期

2025-04-27

·小药说药

AD疫苗：阿尔茨海默病的预防新希望

-01-引言阿尔茨海默病（Alzheimer′s disease，AD）是发生于老年期和老年前期的神经系统退行性疾病，起病隐袭且病程呈进行性发展，临床表现以获得性认知功能损害为核心症状，涉及记忆、学习、定向、理解、判断、计算、语言和视空间等认知域，不同程度地影响日常生活能力及社会职业功能，最终进展为全面性痴呆。根据GBD数据，2019年全球AD及相关痴呆的患病人数达到5162万，总体患病率为 667.2/10万，年龄标化患病率为 682.5/10万。同年，我国 AD 及相关痴呆总人数为1314 万，大约占全球AD患者总人数的25.5%，我国AD及相关痴呆总体患病率为924.1/10万，年龄标化患病率为788.3/ 10万。目前我国国家药品监督管理局批准用于治疗 AD的一线药物包括胆碱酯酶抑制剂，如多奈哌齐、卡巴拉汀等，以及N‑甲基‑D‑门冬氨酸（NMDA）受体拮抗剂美金刚。2019年国家药品监督管理局有条件批准了甘露特钠胶囊上市注册申请，用于治疗轻度至中度AD。2024 年 1 月仑卡奈单抗（lecanemab）注射液获国家药品监督管理局批准上市，用于治疗由 AD引起的 MCI和轻度痴呆。然而，这些方法多半是对症治疗，近一半的患者对现有药物治疗的效果不满，其次是药物价格贵。因此，亟须针对这些问题和痛点进一步改善我国AD患者的治疗现状。主动免疫疗法，即疫苗接种，是针对淀粉样β（Aβ）的阿尔茨海默病（AD）研究最彻底的治疗方法之一。在20多年前， AN1792疫苗在临床进行了研究，虽然因为毒性问题没有继续开发，然而人们也从中看到了疫苗预防AD的潜力。AD的疫苗预防可能改变阿尔茨海默症目前的困境。-02-一、AD的发病机制目前，AD研究的主流观点认为，AD的发病机制是Aβ与Tau蛋白的协同作用结果：Aβ的毒性级联反应Aβ由淀粉样前体蛋白（APP）裂解产生，其可溶性寡聚体（AβOs）是神经毒性的“真凶”。它们攻击突触功能，触发炎症，并诱导Tau蛋白过度磷酸化，形成NFTs。研究表明，可溶性AβOs比斑块与认知衰退的相关性更强。Tau蛋白的雪崩效应Tau蛋白过度磷酸化后脱离微管，形成NFTs，破坏神经元运输系统。这种病理过程存在“交叉播种效应”：AβOs加速Tau病变扩散，而NFTs恶化神经元死亡。炎症与免疫失衡小胶质细胞和星形胶质细胞的慢性炎症反应进一步破坏脑内稳态，形成“病理恶性循环”。-03- 二、疫苗：AD预防的免疫堡垒传统药物治疗聚焦症状缓解，疫苗则直击疾病上游，提供“治未病”的可能。其核心策略包括：1. 精准打击Aβ毒性寡聚体AD疫苗通过诱导抗体中和AβOs，阻止其破坏突触并触发炎症。动物模型显示，靶向AβOs的疫苗可显著延缓认知衰退。2. Th2极化理想疫苗需诱导抗炎性Th2免疫反应，避免促炎性Th1反应加重脑损伤。佐剂选择是关键：传统铝佐剂（Alum）可能引发炎症副作用，而新型Th2偏向佐剂（如TLR9激动剂）可能解决上述问题。3. 被动免疫的局限性单克隆抗体（如Lecanemab、Donanemab和Aducanumab）虽可快速清除Aβ，但需频繁注射且成本高昂。主动免疫疫苗通过激发自身免疫记忆，提供长期保护，更适合预防性应用。-04-三、AD疫苗的开发现状AN-1792是第一个人类Aβ主动免疫疗法，由合成全长人类Aβ42和佐剂QS-21组成。AN-1792的1期临床研究包括372名轻度至中度AD患者。第1阶段试验的结果表明，该疫苗可诱导对Aβ42的抗体反应，并可清除大脑中的斑块。然而，在II期试验中，由于患者发展为脑膜炎，临床试验暂停。尽管AN-1792临床试验有副作用，但该研究的结果鼓励开发新的主动抗Aβ免疫治疗方法。 CAD106疫苗由诺华公司研发，通过诱导抗体产生来减少β淀粉样斑块。该疫苗由截短的β-淀粉样蛋白片段（Aβ1-6）组成，以避免T细胞活化。在第一阶段试验的52周内没有出现脑膜炎的迹象。然而由于缺乏疗效，目前已停止开发。ABvac40疫苗由Araclon Biotech开发，其结构针对Aβ40的C末端，包含与KLH偶联的Aβ33–40。ABvac40 2023年公布了II期临床结果，达到了主要终点，与安慰剂相比，ABvac40治疗可将疾病进展的速度减慢38%。ACI-24疫苗由AC Immune开发，包含Aβ1-15表位，不包括T细胞表位，以避免T细胞反应。ACI‐24的 II期临床试验由于低免疫原性撤回，正在继续优化；新分子ACI-24.060被武田以里程碑总价22亿美元引进。UB-311疫苗由United Biomedical开发，含有Aβ1-14表位，并与辅助T细胞肽表位融合，利用CpG作为佐剂。肽混合物将诱导B细胞反应，同时避免T细胞的炎症反应。2023年发表的2期研究结果显示，UB-311治疗达到了主要终点，该疗法具有良好安全性、耐受性，并产生稳健的免疫应答。-05-四、AD疫苗研发开发的挑战虽然AD疫苗展现出缓解AD进展的前景，但AD疫苗研发仍面临多重“拦路虎”：1. 免疫衰老（Immunosenescence）:老年人群免疫应答低下，疫苗需克服T细胞功能衰退和慢性炎症背景。2. 血脑屏障（BBB）阻碍98%的大分子抗体无法穿透BBB，新型的递送技术是破局方向。3. 患者异质性：AD亚型复杂，需基于生物标志物（如Aβ-PET、脑脊液pTau）细分人群，实现精准免疫。4. 临床试验设计困境：AD进程缓慢，需超长随访（10年以上）和替代终点（如Aβ清除率）加速验证。5. 安全性红线：避免诱发自身免疫性脑膜炎（如AN1792）或微出血，是疫苗设计的核心原则。-06-五、未来方向：多靶点联合与技术创新1. 靶向“Aβ-Tau轴”复合疫苗：同时激活针对AβOs和异常Tau的免疫应答，阻断病理级联。2. 新型递送系统：鼻内疫苗、DC细胞疫苗或外泌体载体可能增强脑内抗体渗透。3. 佐剂革命：开发纯Th2极化佐剂，平衡免疫激活与安全性。4. 人工智能助力设计：AI预测抗原表位和抗体结合构象，缩短疫苗开发周期。-07-结语AD是一种严重影响人类健康的多因素异质性神经退行性疾病，目前还没有能够治愈的药物，已获得批准的药物也只能减缓疾病的进展。因此，AD最好在发生严重认知障碍之前进行早期干预，AD预防有潜力可能实现延迟或预防AD痴呆的治疗目标。AD疫苗研发虽荆棘密布，但随着对病理机制的解码和技术迭代，未来十年或有革命性疫苗问世。“疫苗或许不能逆转时光，但能让我们优雅地老去。”愿未来AD将不再成为困扰我们的严重疾病。参考资料：1. The Importance of Vaccines in Preventing Impending Alzheimer's Epidemic. Rev Recent Clin Trials.2025 Apr 14.2. The informed road map to prevention of Alzheimer Disease: A call to arms. Mol Neurodegener.2021 Jul 21;16(1):49.公众号内回复“ADC”或扫描下方图片中的二维码免费下载《抗体偶联药物：从基础到临床》的PDF格式电子书！公众号已建立“小药说药专业交流群”微信行业交流群以及读者交流群，扫描下方小编二维码加入，入行业群请主动告知姓名、工作单位和职务。

免疫疗法临床结果疫苗临床2期

2024-10-08

·循因缉药

贺建奎老师去搞AD（阿尔茨海默病）疫苗了？

环球视野，深度视角各位亲爱的股东们，大家早上好中午好晚上好。我先叠个甲：本文不讨论贺建奎老师之前的“事业”对错，也不代表本人认可或不认可其工作，对其目前的项目进展了解仅限于互联网且不能确认信源的真实性。所以，本文将尽可能的抛开事实不谈（指贺的部分）。 #01 “又换方向了？” 2024年10月8日，据美国媒体STAT报道贺建奎已经获得来自美国加密货币企业家Ryan Shea的资助用以支持其关于人类胚胎的CRISPR基因编辑技术，用以降低未来罹患Alzheimer's disease（阿尔茨海默病）的风险。再次声明，该信息来自STAT并没有其他信源可以证实或证伪。只有某不知名社交软件同名账号提到过一嘴这个事，这账号是不是何老师的咱也不敢问。但是对我们而言最大的震撼是：贺老师又换赛道了？ 2023年1月7日，贺老师刚宣布要在2～3年攻克3-5种罕见病，而DMD将是首个目标。还有差不多1年的时间，总觉得这个时间做完临床有点厉害，不知道贺老师有什么革命性的技术说服监管机构。在其社交媒体某条信息下面，有人问出了类似的问题。那就是我记错了，也许是2025年启动临床。也是很厉害了，期待。不过，这个“genetic vaccine”是个啥？ #02 是个啥？我们首先排除DNA/RNA疫苗，毕竟贺老师是要用基因编辑技术排除“future risk”。众所周知且不一定对的是阿尔茨海默病的病因是由于脑蛋白质无法正常运作，这扰乱了脑细胞（神经元）的工作，进而引发一系列事件。这包括：斑块。β-淀粉样蛋白是一种较大蛋白质的片段。这些片段一旦聚集成团块，似乎会对神经元产生毒性作用，破坏大脑细胞之间的通讯。团块形成的较大沉积物被称作淀粉样斑块，其中还含有其他细胞碎片。缠结。Tau 蛋白在大脑细胞的内部支持和运输系统中发挥携带营养物质和其他必需物质的作用。在阿尔茨海默病患者体内，Tau 蛋白会改变形状，形成被称为神经原纤维缠结的结构。此缠结会破坏运输系统，对细胞造成损伤。（来自mayo）这显然跟“genetic vaccine”也没太大关系，那么剩下的可能性只有一个了。载脂蛋白 E（APOE）的一种基因分型-APOE e4 会增加患阿尔茨海默病的风险。 APOE e4 携带者大约占人口的 25% 到 30%。（上图来自华大基因）我国已经有针对APOE分型的试剂盒获批医疗器械证了，比如康录、达安等都有。不过，但并非每个携带这种基因分型的人都会患病。但是，你说是不是“future risk”吧？当然，我是比较阴暗，推断是因为就两个snp，比较好编.... （图片来自CRD，参考原文）这比起DMD那么大的基因(79个外显子），那么复杂的突变类型也确实比较容易进行基因编辑。当然，这都是个人非常幼稚且业余的推测，作为基因编辑大佬想出来的方案一定有着非常fancy的moa（mechanism of action），我们要做的就是等贺老师公布即可。那么，我们抛开“genetic”不谈，AD的vaccine有么？还真有。 #03 疫苗们据不完全统计，Vaxxinity、ACI、Axon、Araclon和Novartis均有候选药物进入临床。其中，Vaxxinity的UB-311已经进入III期临床，属于走的最快的一款产品。 UB-311是美国Vaxxinity公司研发的一款用于治疗阿尔兹海默症的全合成肽疫苗，由两种合成的Aβ1-14-靶向肽（B细胞表位）构成，每个肽均连接至不同的辅助T细胞肽表位。在临床试验中，不论是biomarker还是各种量表的表现，用药组均优于安慰剂组。 Vaxxinity于2021年11月纳斯达克上市， UB-311在2022年获得FDA快速通道认定。尽管，在临床I期和II期UB-311都表现不错，然而Vaxxinity股市表现拉跨。最终，Vaxxinity在2024年4月19日宣布从纳斯达克退市。一个可能的原因是，公司针对新冠的UB-612浪费了太多的公司资源，而其最终无法上市耗光了投资者的耐心。不过，公司虽然退市了，仍然还在运营，希望他能把UB-311带上市。哦，对了。 “UB-311是一种治疗性疫苗...显然不如贺老师的一劳永逸。” 另一个彩蛋是，Vaxxinity的创始人和CEO Mei Mei Hu是哈佛的法学博士... END 啊对对对对，扫描这货能联系到我至此，各位股东星标了么？点赞了么？转发了么？在看了么？谢谢！所有内容均不作为投资建议，信息均来自公开资料。近期文章： miRNA研究者获得2024年诺贝尔生理或医学奖 Cassava离得谱中谱，方为人上人 NGS/NIPT谁能斩获2024诺奖？ Relay Therapeutics的裁员接力赛终于按下了暂停键 Cologuard Plus正式获得FDA批准！肠癌早筛新标杆！相关资料：注1：https://www.statnews.com/2024/10/08/crispr-babies-scientist-he-jiankui-human-embryo-research-ryan-shea/注2：https://bydrug.pharmcube.com/news/detail/b2f0f1c14b1401958912766f79e0e58d注3：https://www.mayoclinic.org/zh-hans/diseases-conditions/alzheimers-disease/symptoms-causes/syc-20350447注4：https://www.fiercebiotech.com/biotech/vaxxinity-retreats-abusive-relationship-after-3-years-public-markets

疫苗诊断试剂

100 项与 UBITh AD immunotherapeutic vaccine(United Biomedical, Inc.) 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
阿尔茨海默症	临床2期	中国台湾	United Neuroscience Ltd.	2015-10-01

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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


NCT03531710 (CTgov)	临床2期	阿尔茨海默症	34	placebo+UB-311+V203-AD-EXT (E1) (M7E1)	鏇淵蓋蓋憲遞淵鏇製鹹 = 齋積範簾製願觸窪鹹淵觸選鹽遞選蓋淵夢願鹽 (選簾鹽膚艱鬱網醖選築, 鹽艱鹽積製鹽醖範遞鹽 ~ 襯鏇夢醖鏇鏇鏇積鏇齋) 更多	-	2020-12-17
				V203-AD-EXT (E3)+UB-311 (M7E3)	鏇淵蓋蓋憲遞淵鏇製鹹 = 簾鏇膚襯遞憲醖襯觸廠觸選鹽遞選蓋淵夢願鹽 (選簾鹽膚艱鬱網醖選築, 繭淵鏇餘觸鬱糧憲獵獵 ~ 鑰鑰觸鬱壓廠簾憲憲衊) 更多
NCT02551809 (CTgov)	临床2期	阿尔茨海默症	43	UB-311 (3 Priming Doses Followed by 4 Boosters)	憲蓋築鏇鬱蓋廠蓋鹹積 = 鑰築淵鹹築糧鏇選淵築構選窪壓積獵觸築觸獵 (範築築積顧壓鏇構範鹽, 醖廠鏇鹽網淵窪製醖餘 ~ 壓憲願製醖簾壓簾糧顧) 更多	-	2020-01-13
				Placebo+UB-311 (3 Priming Doses Followed by 2 Boosters)	憲蓋築鏇鬱蓋廠蓋鹹積 = 獵鬱糧衊積願簾範憲觸構選窪壓積獵觸築觸獵 (範築築積顧壓鏇構範鹽, 窪膚製廠鬱範襯膚衊獵 ~ 構鏇壓製餘糧願鑰艱繭) 更多