A Phase 2A Randomized Double-Blind Placebo-Controlled Trial to Evaluate the Efficacy and Safety of Varoglutamstat (PQ912) in Patients With Early Alzheimer's Disease With a Stage-Gate to Phase 2B (VIVA-MIND)

This is a Phase 2A multi-center, randomized, double blind, placebo-controlled, parallel group study of varoglutamstat, with a stage gate to Phase 2B.
In Phase 2A there will be adaptive dosing evaluation of three dose levels with exposure to varoglutamstat or placebo for a minimum of 24 weeks, with preliminary evaluation of both cognitive function and pharmacodynamic changes on EEG spectral analysis in approximately 180 participants.
In the event that the stage gate for Phase 2B is reached, then Phase 2B will assesses efficacy and longer-term safety in a larger study group, i.e., 414.

开始日期2021-11-15

申办/合作机构

Vivoryon Therapeutics NV

[+1]

NCT02389413

/ Completed临床2期

A Phase 2A Multicentre, Randomised, Double Blind, Placebo-Controlled, Parallel-Group Safety and Tolerability Study of PQ912 in Subjects With Early Alzheimer's Disease

The aim of this study is to evaluate the safety, tolerability and preliminary efficacy of PQ912 in subjects with Mild Cognitive Impairment (MCI) due to Alzheimers Disease (AD) or mild dementia due to AD.

开始日期2015-03-01

申办/合作机构

Vivoryon Therapeutics NV

[+1]

NCT02190708

/ Completed临床1期

A Phase I, Open Label Study to Assess the Effects of PQ912 on the Pharmacokinetics of Midazolam and Omeprazole in Healthy Male Subjects

Midazolam is a rapid-acting benzodiazepine, with a short half-life (approximately 1.9 hours) and is primarily metabolised by CYP3A.
Omeprazole is a selective proton pump inhibitor substrate used to reduce gastric acid secretion. Omeprazole is primarily metabolised by CYP2C19.
Midazolam and omeprazole are both used as probe drugs in clinical pharmacology studies to evaluate clinical CYP3A and CYP2C19 drug interactions, respectively. Furthermore the EMA and the FDA guidance on drug interactions recommend the use of these drugs for such evaluations.
The aim of this study is to assess the effect of PQ912 on the PK of midazolam and omeprazole. In vitro studies have demonstrated that PQ912 inhibits several CYP enzymes, including CYP3A4 and CYP2C19 and at the expected exposure levels in patients, has the potential to inhibit these enzymes in-vivo. This study is therefore planned to investigate the potential changes in the PK of midazolam and omeprazole due to the effect of PQ912 at steady-state. In clinical practice it is likely that co-administration of PQ912 with other drugs that are metabolised via the CYP3A and/or CYP2C19 enzymes will occur. This study will provide important information for the requirement of dose adjustments or contraindications in these circumstances.

开始日期2014-06-01

申办/合作机构

Vivoryon Therapeutics NV

[+1]

100 项与 Varoglutamstat 相关的临床结果

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100 项与 Varoglutamstat 相关的转化医学

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100 项与 Varoglutamstat 相关的专利（医药）

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项与 Varoglutamstat 相关的文献（医药）

2025-09-18·JOURNAL OF PHYSICAL CHEMISTRY B

Varoglutamstat Inhibits the Dimerization of the Aβ_25–35 Fragment in Aqueous Solution

Article

作者: Nguyen, Hoang Anh ; Vu, Van V. ; Ngo, Son Tung ; Nguyen, Trung Hai ; Derreumaux, Philippe

The self-aggregation of amyloid-beta (Aβ) peptides is strongly associated with Alzheimer's disease. In this study, the influence of the small varoglutamstat compound on the conformations of the FAβ_25-35 dimer was extensively characterized by using MD simulations. The influence of the ligand on the conformation of the FAβ_25-35 dimer was studied during the first 10.0 μs. However, its real influence was clarified when the trajectory was extended to 20.0 μs. This indicates that the investigation of a ligand inhibiting Aβ requires a longer MD simulation than previously thought. The ligand changes ensemble properties by reducing the formation of nonbonded intermolecular contacts and β-content. Although varoglutamstat has weak binding to the FAβ_25-35 dimer, the free energy landscape is impacted in shape, free energy barrier, and number of minima. Notably, it is found that the population of the amyloid-competent dimer structure is substantially reduced upon ligand addition. Furthermore, the change from β-hairpin conformation to antiparallel structure may occur through a transition state forming a random coil conformation.

2025-07-02·BRIEFINGS IN BIOINFORMATICS

A 3D pocket-aware lead optimization model with knowledge guidance and its application for discovery of new glutaminyl cyclase inhibitors

Article

作者: Rao, Jiahua ; Deng, Qirui ; Xie, Jiancong ; Zheng, Shuangjia ; Meng, Fanbo ; Li, Guo-Bo ; Chen, Yuting ; Lei, Jinping ; Xu, Mingyuan ; Yang, Yuedong ; Chen, Hongming ; Huang, Weifeng ; Zhang, Hao ; Qiao, Anjie ; Deng, Ji ; Wang, Zhen ; Xie, Junjie

Abstract:

Lead optimization, aimed at improving binding affinity or other properties of hit compounds, is a crucial task in drug discovery. Though deep learning-based 3D generative models showed promise in enhancing the efficiency of de novo drug design recently, less research and attention has garnered for structure-based lead optimization. Herein, we propose a 3D pocket-aware diffusion model named Diffleop, which explicitly incorporates the knowledge of protein-ligand binding affinity and information on covalent bonds to guide the denoising sampling process for lead optimization with enhanced binding affinity and rational properties. Specifically, the bond constraint is achieved through diffusion on fully connected molecular graphs, and the determination of atom positions, atom and bond types in each sampling step is guided by the gradient of the binding affinity that is predicted through fitting with an E(3)-equivariant expert network. The comprehensive evaluations indicated that Diffleop outperforms baseline models on lead optimization with higher affinity and more binding interactions, and can generate more drug-like molecules with more rational structures. Diffleop was further applied to optimize 5-methyl-1H-imidazole, our newly discovered lead compound targeting human glutaminyl cyclases (QCs). Three synthesized compounds exhibit substantially improved inhibitory activities against QCs, with the most effective one showing an IC50 value of 8 nM and 3.5-fold better than clinical candidate PQ912.

2024-10-18·JOURNAL OF ALZHEIMERS DISEASE

Varoglutamstat: Inhibiting Glutaminyl Cyclase as a Novel Target of Therapy in Early Alzheimer’s Disease

Article

作者: Messer, Karen ; Lopez, Oscar ; Revta, Carolyn ; Smith, Amanda ; Galasko, Douglas ; Schell-Mader, Sylvia ; Balasubramanian, Archana ; Weber, Frank ; Qiu, Yuqi ; Wassmann, Tanja ; Jacobs, Diane M. ; Sabbagh, Marwan ; Durant, January ; Léger, Gabriel ; Kuehn-Wache, Kerstin ; Salmon, David P. ; Turner, R. Scott ; DeMarco, Mari L. ; Feldman, Howard H. ; Lupo, Jody-Lynn

Background: Varoglutamstat is a first-in-class, small molecule being investigated as a treatment for early Alzheimer’s disease (AD). It is an inhibitor of glutaminyl cyclase (QC), the enzyme that post-translationally modifies amyloid-β (Aβ) peptides into a toxic form of pyroglutamate Aβ (pGlu-Aβ) and iso-QC which post-translationally modifies cytokine monocyte chemoattractant protein-1 (CCL2) into neuroinflammatory pGlu-CCL2. Early phase clinical trials identified dose margins for safety and tolerability of varoglutamstat and biomarker data supporting its potential for clinical efficacy in early AD. Objective: Present the scientific rationale of varoglutamstat in the treatment of early AD and the methodology of the VIVA-MIND (NCT03919162) trial, which uses a seamless phase 2A-2B design. Our review also includes other pharmacologic approaches to pGlu-Aβ. Methods: Phase 2A of the VIVA-MIND trial will determine the highest dose of varoglutamstat that is safe and well tolerated with sufficient plasma exposure and a calculated target occupancy. Continuous safety evaluation using a pre-defined safety stopping boundary will help determine the highest tolerated dose that will carry forward into phase 2B. An interim futility analysis of cognitive function and electroencephalogram changes will be conducted to inform the decision of whether to proceed with phase 2B. Phase 2B will assess the efficacy and longer-term safety of the optimal selected phase 2A dose through 72 weeks of treatment. Conclusions: Varoglutamstat provides a unique dual mechanism of action addressing multiple pathogenic contributors to the disease cascade. VIVA-MIND provides a novel and efficient trial design to establish its optimal dosing, safety, tolerability, and efficacy in early AD.

项与 Varoglutamstat 相关的新闻（医药）

2025-12-14

·百度百家

多肽合成，Prion Protein (106-126) (human)；Lys-Thr-Asn-Met-Lys-His-Met-Ala-Gly-Ala-Ala-Ala-Ala-Gly-Ala-Val-Val-Gly-Gly-Leu-Gly

一、作用机理 PrP106-126 是朊病毒蛋白（PrP）的关键病理片段，其核心作用机理围绕淀粉样纤维化和细胞毒性，是介导朊病毒病（如克 - 雅病）病理损伤的核心环节，具体如下：构象转化与纤维化聚合：该片段具有天然的构象不稳定性，在生理条件下可从可溶性 α- 螺旋结构向不可溶性 β- 折叠构象转化，进而通过疏水相互作用（片段中含多聚 Ala、Gly 等疏水性残基）自发聚集，形成淀粉样纤维聚集体 —— 这种纤维化过程具有 “模板效应”，可诱导正常 PrP（PrP^C）发生构象转变为致病性 PrP（PrP^Sc），形成病理级联反应。细胞毒性机制：直接损伤：纤维化聚集体可插入细胞膜，破坏脂质双层结构的完整性，导致细胞内钙离子稳态失衡、活性氧（ROS）大量产生，最终引发神经元等细胞凋亡；间接调控：通过激活细胞内应激通路（如未折叠蛋白反应 UPR、MAPK 通路），抑制细胞自噬对异常聚集体的清除，同时促进促炎因子（如 TNF-α、IL-6）释放，引发神经炎症，进一步加重组织损伤；信号通路紊乱：与细胞表面受体（如整合素、糖胺聚糖）结合，干扰正常细胞信号传导，抑制神经细胞存活通路（如 PI3K/Akt），激活凋亡相关基因（如 caspase-3）表达。病理扩散机制：形成的淀粉样纤维可作为 “种子”，在体内（如中枢神经系统）诱导更多正常 PrP 转化为 PrP^Sc，且聚集体具有抗蛋白酶降解特性，可在组织中持续沉积，推动疾病进展。二、药物研发方向 PrP106-126 的病理特性使其成为朊病毒病药物研发的核心靶点，同时其作为特异性工具肽可辅助药物筛选，主要研发方向如下：纤维化抑制剂研发：作用目标：阻断 PrP106-126 的构象转化或聚集过程；药物类型：小分子化合物（如黄酮类、多酚类、苯并噻唑类）、肽类抑制剂（如靶向片段的竞争性肽、α- 螺旋模拟肽）、抗体 / 纳米抗体；设计逻辑：通过结合 PrP106-126 的疏水区域或关键位点（如多聚 Ala/Gly 结构），稳定其可溶性 α- 螺旋构象，阻止 β- 折叠形成和纤维化聚集；或破坏已形成的淀粉样纤维，促进其解聚。细胞毒性拮抗剂研发：作用目标：抑制 PrP106-126 介导的细胞损伤通路；药物类型：抗氧化剂（如谷胱甘肽衍生物、维生素 E 类似物）、钙通道阻滞剂、抗炎药物（如抗炎细胞因子、小分子抗炎剂）；设计逻辑：通过清除 ROS、维持细胞内钙离子稳态，减轻氧化应激损伤；或抑制促炎因子释放，缓解神经炎症，阻断 “纤维化 - 炎症 - 细胞死亡” 的恶性循环。自噬调节剂研发：作用目标：增强细胞自噬对 PrP106-126 聚集体的清除能力；药物类型：自噬激活剂（如雷帕霉素衍生物、甜菜碱）、溶酶体功能增强剂；设计逻辑：通过激活自噬通路（如 mTOR 信号抑制），促进自噬体与溶酶体融合，加速异常聚集体的降解，减少其在细胞内的积累。肽类药物优化：基于 PrP106-126 的反向序列、截短序列或修饰序列（如引入 D - 氨基酸、环化修饰），设计具有竞争性结合能力的肽类药物，阻止天然片段与正常 PrP 或受体的相互作用；通过 PEG 化、脂质体包裹等修饰，提高肽类药物的体内稳定性、血脑屏障穿透性（朊病毒病主要累及中枢神经系统），降低免疫原性。诊断工具与药物联用：以 PrP106-126 为抗原开发特异性抗体或分子探针，用于疾病早期诊断，同时可作为靶向药物载体，实现 “诊断 - 治疗” 一体化；联合用药策略：将纤维化抑制剂与自噬激活剂、抗炎药物联用，多靶点阻断病理进程，提升治疗效果。三、研究进展近年来，围绕 PrP106-126 的基础研究与药物研发取得多项关键进展，核心方向集中在靶点验证、药物筛选与临床前研究：作用机理深化：明确了 PrP106-126 的纤维化关键位点：研究发现片段中 Ala113-Ala117 的多聚丙氨酸区域是 β- 折叠形成和聚集的核心，突变该区域（如替换为 Pro）可显著降低其纤维化能力和细胞毒性，为药物设计提供精准靶点；揭示了神经炎症的核心介导因子：证实 PrP106-126 可通过激活小胶质细胞表面的 Toll 样受体 4（TLR4），引发 NF-κB 通路激活和促炎因子释放，为抗炎药物研发提供理论依据。候选药物筛选与优化：小分子化合物：姜黄素衍生物、白藜芦醇类似物被证实可通过结合 PrP106-126 的疏水口袋，抑制其纤维化，在体外细胞实验（如 SH-SY5Y 神经细胞模型）中可降低细胞凋亡率达 50% 以上；苯并噻唑类化合物 AN-1284 通过稳定 PrP^C 的 α- 螺旋构象，在小鼠朊病毒病模型中延长生存期约 30%；肽类抑制剂：基于 PrP106-126 反向序列设计的肽段（如 Ala-Ala-Gly-Ala-Met-His-Lys-Met-Asn-Thr-Lys），可竞争性结合天然片段，阻止其聚集，且经 D - 氨基酸修饰后，体内半衰期延长至原序列的 8 倍；抗体药物：针对 PrP106-126 纤维化聚集体的单克隆抗体（如 D18），在体外可特异性识别并解聚淀粉样纤维，在动物模型中可通过血脑屏障（经转铁蛋白受体介导），显著减少脑组织中 PrP^Sc 沉积。治疗策略创新：基因治疗：通过 siRNA 或 CRISPR-Cas9 技术靶向沉默 PrP 基因表达，在细胞模型中可降低 PrP106-126 诱导的纤维化水平，但需解决中枢神经系统靶向递送难题；纳米药物递送系统：将纤维化抑制剂（如姜黄素）包裹于 PEG 修饰的脂质体或聚乳酸 - 羟基乙酸共聚物（PLGA）纳米粒中，可提升血脑屏障穿透效率（较游离药物提高 3-5 倍），在小鼠模型中显著减轻神经损伤。临床前与转化研究：目前尚无针对朊病毒病的上市药物，但多款候选药物已进入临床前后期研究：如小分子化合物 PQ912 在非人灵长类朊病毒病模型中，可降低脑组织 PrP^Sc 沉积量 70% 以上，且未观察到明显毒性；生物标志物开发：以 PrP106-126 为标准肽，建立了脑脊液中异常 PrP 片段的质谱检测方法，可用于疾病早期诊断和药物疗效评价。挑战与突破方向：血脑屏障穿透：通过受体介导的靶向递送（如转铁蛋白受体、胰岛素受体配体修饰）、鼻黏膜给药等方式，提升药物在中枢神经系统的浓度；耐药性问题：开发多靶点药物（如同时抑制纤维化和炎症），避免单一靶点药物引发的病理通路代偿激活；疾病早期干预：基于 PrP106-126 相关生物标志物，探索在疾病潜伏期进行药物干预的可行性，降低病理损伤程度。产品信息来源：楚肽生物相关其他产品：Ser-Phe-Pro-Trp-Met-Glu-Ser-Asp-Val-Thr Phe-Leu-Trp-Lys-Asp-Leu-Gln-Arg-Val-Arg-Gly-Asp-Leu-Gly-Ala-Ala-Leu-Asp-Ser-Trp-Ile-Thr Ser-Leu-Asp-Ser-Pro-Ala-Ala-Leu-Ala-Glu-Arg-Gly-Ala-Arg-Asn-Ala-Leu-Gly-Gly-His-Gln-Glu-Ala-Pro-Glu-Arg-Glu Cys-Tyr-Phe-Gln-Asn-Cys (Cys1,6 disulfide bridge) Lys-Thr-Asn-Met-Lys-His-Met-Ala-Gly-Ala-Ala-Ala-Ala-Gly-Ala-Val-Val-Gly-Gly-Leu-Gly Ala-Arg-Leu-Asp-Val-Ala-Ser-Glu-Phe-Arg-Lys-Lys-Trp-Asn-Lys-Trp-Ala-Leu-Ser-Arg-NH2 Ala-Arg-Leu-Asp-Thr-Ser-Ser-Gln-Phe-Arg-Lys-Lys-Trp-Asn-Lys-Trp-Ala-Leu-Ser-Arg-NH2 Arg-Phe-Ala-Arg-Lys-Gly-Ala-Leu-Arg-Gln-Lys-Asn-Val Arg-Phe-Ala-Arg-Lys-Gly-Ala-Leu-Arg-Gln-Lys-Asn-Val-His-Glu-Val-Lys-Asn Arg-Lys-Arg-Thr-Leu-Arg-Arg-Leu 所有产品仅用作实验室科学研究，不为任何个人用途提供产品和服务。

临床结果

2025-12-12

·药化杂谈

同济大学/药物所QPCT抑制剂是如何突破专利的

同济大学/药物所公开了一篇QPCT抑制剂专利WO2025247243A1，对临床前化合物SEN-177进行了专利突破。背景介绍（摘自专利WO2025247243A1）焦谷氨酰化是一种翻译后修饰，其中谷氨酰胺或谷氨酸氨基酸被转化为焦谷氨酸部分。目前已知人体中有两种基因编码的酶参与催化这个N端焦谷氨酰化反应，包括谷氨酰胺酰基环化酶/蛋白(QPCT)和谷氨酰胺酰基环化酶样蛋白(QPCTL)。研究表明 QPCTL,可以在多种细胞中特异性调控 CD47/SIRPα信号轴，且该调控作用依赖于 QPCTL酶活性。此外，在细胞中敲除 QPCTL或者使用 QPCTL化学抑制剂,可以有效抑制 CD47的N端焦谷氨酸化水平以及 CD47/SIRPa的结合，但是对细胞表面 CD47的表达无明显影响。通过抑制 QPCTL蛋白功能阻断 CD47/SIRPα 通路，有可能减少对正常红细胞 CD47功能的影响，从而避免 CD47抗体药物引起的严重副作用。因此，OPCTL是通过 CD47/SIRPa通路介导的肿瘤免疫治疗的潜在靶点。除 CD47 外，QPCT 和 QPCTL还可将其他蛋白质焦谷氨酸化。例如，已知参与阿尔茨海默病的β淀粉样蛋白会被 QPCT 焦谷氨酸化，而C- 基序趋化因子配体 2(CCL2)蛋白则被 QPCTL 焦谷氨酸化。此外，CX3CL1的N端也能被QPCT 和 QPCTL焦谷氨酸化。近期有研究发现，QPCTL也能对 BTN(butyrophilin)家族蛋白特别是BTN2A1、BTN3A1、BTN3A2和BTN3A3的N端发生焦谷氨酸化。因此，开发一种新的 QPCT 或 QPCTL抑制剂以为肿瘤、免疫性疾病、神经性疾病、肥胖或衰老提供新的治疗方法极具现实意义。目前进入临床的QPCT抑制剂为varoglutamstat（PQ-912），处于临床二期，适应症为阿尔兹海默症，QPCTL抑制剂为英矽智能的ISM-8207（临床一期），适应症为肿瘤。同济大学/药物所的QPCT抑制剂选择对SEN-177（临床前）进行的专利突破，突破策略选择将SEN-177的吡啶环的氮原子用氰基（常见策略）或各种酰胺进行取代。按照专利中披露的结构来看，估计在吡啶环处并环也可以，如下。中国科学院人才交流开发中心举办人工智能赋能药物研发全过程创新技术实践高级研修班（北京站） AI + 医疗，解锁临床 / 影像 / 慢病管理实操技能

临床2期临床1期引进/卖出

2025-12-12

·药化杂谈

英矽智能的QPCTL抑制剂是如何突破专利的

英矽智能的QPCTL抑制剂ISM-8207是唯一处于临床研发阶段的QPCTL抑制剂，目前处于临床一期，适应症为肿瘤。据报道该药是英矽智能与复星医药合作开发，利用英矽智能的Pharma.AI人工智能平台得到的。查询英矽智能相关专利仅发现了一篇CN118019737A，不出意外的话，ISM-8207就是出自该篇专利，是对VIVORYON公司的专利进行的专利突破，而VIVORYON化合物则是将PQ-912缩环得到的。英矽智能突破VIVORYON公司专利的主要突破点是在四元酰胺环上引入了取代基，代表性化合物如下。想了解AI在药物设计中的应用，可以点击这个链接。中国科学院人才交流开发中心举办人工智能赋能药物研发全过程创新技术实践高级研修班（北京站）

专利到期

100 项与 Varoglutamstat 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
轻度痴呆	临床2期	中国	江苏先声药业有限公司	2022-04-26
轻度痴呆	临床2期	中国	Haupt Pharma Wülfing GmbH	2022-04-26
轻度痴呆	临床2期	中国	Vivoryon Therapeutics NV	2022-04-26
轻度认知障碍	临床2期	丹麦	Vivoryon Therapeutics NV	2020-07-06
轻度认知障碍	临床2期	丹麦	Nordic Bioscience A/S	2020-07-06
轻度认知障碍	临床2期	德国	Nordic Bioscience A/S	2020-07-06
轻度认知障碍	临床2期	德国	Vivoryon Therapeutics NV	2020-07-06
轻度认知障碍	临床2期	荷兰	Vivoryon Therapeutics NV	2020-07-06
轻度认知障碍	临床2期	荷兰	Nordic Bioscience A/S	2020-07-06
轻度认知障碍	临床2期	波兰	Vivoryon Therapeutics NV	2020-07-06

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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


NCT03919162 (VIVA-MIND, CTgov)	临床2期	阿尔茨海默症	112	PQ912 (PQ912)	鹽鬱積鹽鏇鏇築窪淵簾 = 鹹製齋繭繭醖積願膚獵願選繭衊製衊願積衊願 (壓遞淵鹽簾積窪顧構艱, 蓋壓鏇鬱糧鹹淵願夢艱 ~ 醖衊鹽築繭獵齋繭鹹遞) 更多	-	2025-12-12
				Placebo (Placebo)	鹽鬱積鹽鏇鏇築窪淵簾 = 襯觸廠範醖積艱觸築夢願選繭衊製衊願積衊願 (壓遞淵鹽簾積窪顧構艱, 鬱艱鹽鹹選壓願網鏇窪 ~ 醖構網餘鹽獵獵鑰獵衊) 更多
NCT03919162 (VIVA-MIND, GlobeNewswire) 人工标引	临床2期	阿尔茨海默症	-	Varoglutamstat	鹹繭構糧壓構糧艱壓襯(鹹淵顧衊齋顧齋憲蓋鑰) = no clinically meaningful and no statistically significant differences between varoglutamstat 600mg BID and placebo 顧齋繭鑰廠壓構齋廠製 (選網獵遞積顧鬱餘夢襯 ) 更多	积极	2024-12-09
				placebo
NCT04498650 (VIVIAD, ASN2024)	临床2期	阿尔茨海默症 \| 轻度认知障碍	259	Varoglutamstat 300 mg	鏇簾鬱襯鏇製願觸齋糧(襯齋膚積餘積鏇餘選鏇) = 製鹹醖憲繭憲網鑰襯觸餘鏇淵蓋選鹹製襯窪廠 (顧鬱構網憲齋餘憲淵構 )	积极	2024-10-25
				Varoglutamstat 600 mg	艱製願膚積壓鹽艱壓築(構襯齋膚積糧鹽遞衊願) = 醖網齋鹽顧襯淵繭憲壓齋簾鑰窪獵窪築艱蓋積 (顧範繭鏇顧選築鏇餘顧 ) 更多
NCT04498650 (VIVIAD, GlobeNewswire \| ASN2024)	临床2期	阿尔茨海默症 \| 糖尿病肾病	32	Varoglutamstat	衊鬱鹽鏇蓋範艱壓選齋(憲範遞範襯構製遞構鑰) = 憲醖選醖廠衊艱鹹蓋鏇顧鬱壓鏇壓壓鏇窪簾衊 (餘鹽蓋網淵膚襯鹽觸網 )	积极	2024-10-25
				placebo	衊鬱鹽鏇蓋範艱壓選齋(憲範遞範襯構製遞構鑰) = 壓夢廠繭廠餘鏇遞齋範顧鬱壓鏇壓壓鏇窪簾衊 (餘鹽蓋網淵膚襯鹽觸網 )
NCT04498650 (VIVIAD, GlobeNewswire) 人工标引	临床2期	肾脏疾病 CCL2 Expression	-	Varoglutamstat 600mg BID	築夢選鏇獵鑰糧憲鹽廠(襯糧鹹顧顧醖選蓋淵艱) = 憲齋憲網鏇積願艱憲鏇鏇觸遞顧製糧顧鹹醖築 (鹹餘遞餘遞憲積齋遞衊 ) 更多	积极	2024-09-12
NCT04498650 (VIVIAD, Corporate Publications) 人工标引	临床2期	阿尔茨海默症	250	Varoglutamstat	窪顧繭鹹壓製築積觸憲(選遞簾製壓選襯糧醖範) = 築醖繭範範艱壓願艱壓顧網築鑰顧膚糧繭選範 (衊壓獵獵襯膚鑰衊壓鏇 ) 更多	积极	2022-07-31
NCT02389413 (Pubmed \| Alzheimers Res Ther) 人工标引	临床2期	阿尔茨海默症	120	PQ912	夢壓鹹糧鏇選蓋膚襯衊(獵齋餘廠餘構鬱糧襯憲) = There was no significant difference between treatments in the number of subjects with (serious) adverse events, although there were slightly more patients with a serious adverse event in the PQ912 group compared to placebo. 醖艱衊餘襯鬱齋餘願鹽 (築構遞構選構鹽淵遞簾 ) 更多	积极	2018-10-12
				Placebo