A Phase 1, Randomized, Double-Blind, Placebo- and Positive-Controlled, Parallel-Group Study to Evaluate the Effect of LMTM on the Response to an Oral Tyramine Challenge and to Determine the Multiple-Dose Pharmacokinetics of LMTM. - Tyramine challenge with LMTM

开始日期2022-03-15

申办/合作机构

TauRx Therapeutics Ltd.

NCT03446001 / Completed临床3期

Randomized, Double-Blind, Placebo-Controlled, Three-Arm, 12-Month, Safety and Efficacy Study of TRx0237 Monotherapy in Subjects With Alzheimer's Disease Followed by a 12-Month Open-Label Treatment

The purpose of this study is to determine the safety and efficacy of TRx0237 16 mg/day and 8 mg/day in the treatment of subjects with Alzheimer's Disease compared to placebo. In addition, an open-label, delayed-start phase is included to demonstrate a disease-modifying effect of TRx0237.

开始日期2018-01-10

申办/合作机构

TauRx Therapeutics Ltd.

EUCTR2014-002013-37-NL / Not yet recruiting临床3期

An Open-Label, Extension Study of the Effects of Leuco-methylthioninium bis(hydromethanesulfonate) in Subjects with Alzheimer’s Disease or Behavioral Variant Frontotemporal Dementia

开始日期2016-03-24

申办/合作机构

TauRx Therapeutics Ltd.

100 项与甲磺酸氢甲硫堇相关的临床结果

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100 项与甲磺酸氢甲硫堇相关的转化医学

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100 项与甲磺酸氢甲硫堇相关的专利（医药）

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项与甲磺酸氢甲硫堇相关的文献（医药）

2024-09-01·CELLULAR SIGNALLING

Rescue of synaptosomal glutamate release defects in tau transgenic mice by the tau aggregation inhibitor hydromethylthionine

Article

作者: Wischik, Claude M ; Kraev, Igor ; Armstrong, Paul ; Robinson, Lianne ; Palliyil, Soumya ; Santos, Renato X ; Stewart, Mike G ; Riedel, Gernot ; Horsley, David ; Harrington, Charles R ; Dreesen, Eline ; Cranston, Anna L

Glutamatergic neurotransmission, important for learning and memory, is disrupted in different ways in patients with Alzheimer's disease (AD) and frontotemporal dementia (FTD) tauopathies. We have previously reported that two tau transgenic mouse models, L1 and L66, produce different phenotypes resembling AD and FTD, respectively. The AD-like L1 model expresses the truncated core aggregation domain of the AD paired helical filament (PHF) form of tau (tau296-390) whereas the FTD-like L66 model expresses full-length tau carrying two mutations at P301S/G335D. We have used synaptosomes isolated from these mice to investigate K⁺-evoked glutamate release and, if abnormal, to determine responsiveness to hydromethylthionine, a tau aggregation inhibitor previously shown to reduce tau pathology in these models. We report that the transgenes in these two mouse lines cause opposite abnormalities in glutamate release. Over-expression of the core tau unit in L1 produces a significant reduction in glutamate release and a loss of Ca²⁺-dependency compared with wild-type control mice. Full-length mutant tau produces an increase in glutamate release that retains normal Ca²⁺-dependency. Chronic pre-treatment with hydromethylthionine normalises both reduced (L1) and excessive glutamate (L66) and restores normal Ca²⁺-dependency in L1 mice. This implies that both patterns of impairment are the result of tau aggregation, but that the direction and Ca²⁺-dependency of the abnormality is determined by expression of the disease-specific transgene. Our results lead to the conclusion that the tauopathies need not be considered a single entity in terms of the downstream effects of pathological aggregation of tau protein. In this case, directionally opposite abnormalities in glutamate release resulting from different types of tau aggregation in the two mouse models can be corrected by hydromethylthionine. This may help to explain the activity of hydromethylthionine on cognitive decline and brain atrophy in both AD and behavioural-variant FTD.

2024-07-22·JACS Au

Mechanism of Methylene Blue Inducing the Disulfide Bond Formation of Tubulin-Associated Unit Proteins

Article

作者: Seo, Dong-Hyun ; Kim, Eun-Hee ; Huh, Yang Hoon ; Cheong, Hae-Kap ; Lee, Min Jung ; Lee, Donghan ; Lim, Jong-Soo ; Ryu, Kyoung-Seok

Methylene blue (MB) has recently completed a Phase-3 clinical trial as leuco-methylthioninium (LMT) bis(hydromethanesulfonate) for treating Alzheimer's disease. Herein, we investigated the mechanism underlying the MB inhibition of tubulin-associated unit (tau) aggregation by focusing on tau monomers. We found that MB causes disulfide bond formation, resulting in strong nuclear magnetic resonance chemical shift perturbations in a large area of tau proteins. The oxidized form of MB, namely methylthioninium (MT⁺), specifically catalyzed the oxidation of cysteine residues in tau proteins to form disulfide bonds directly using O₂. This process is independent of the MT⁺-to-LMT redox cycle. Moreover, MT⁺ preferentially oxidized C291 and C322 in the lysine-rich R2 and R3 domains. Under in vivo brain physoxia conditions, LMT may convert to MT⁺, possibly interfering with tau fibrillation via disulfide bond formation.

2024-06-01·Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Tau Aggregation‐Dependent Lipid Peroxide Accumulation Driven by the hsa_circ_0001546/14‐3‐3/CAMK2D/Tau Complex Inhibits Epithelial Ovarian Cancer Peritoneal Metastasis

Article

作者: Xie, YaQing ; Wu, Yong ; Meng, Jiao ; Pan, Wei ; Cao, SiYu ; Li, YanLi ; Zhang, XiaoFei ; Fan, BiaoFeng ; Zhang, JiaLi ; Yang, HengHui ; Chai, BinShu ; Hu, ZhiXiang ; Shao, Yang ; Zhang, YunKui ; Ma, ZhongLiang ; Wang, ShaoJia ; Tian, WenJuan ; Meng, Wei

Abstract:

Intraperitoneal dissemination is the main method of epithelial ovarian cancer (EOC) metastasis, which is related to poor prognosis and a high recurrence rate. Circular RNAs (circRNAs) are a novel class of endogenous RNAs with covalently closed loop structures that are implicated in the regulation of tumor development. In this study, hsa_circ_0001546 is downregulated in EOC primary and metastatic tissues vs. control tissues and this phenotype has a favorable effect on EOC OS and DFS. hsa_circ_0001546 can directly bind with 14‐3‐3 proteins to act as a chaperone molecule and has a limited positive effect on 14‐3‐3 protein stability. This complex recruits CAMK2D to induce the Ser324 phosphorylation of Tau proteins, changing the phosphorylation status of Tau bound to 14‐3‐3 and ultimately forming the hsa_circ_0001546/14‐3‐3/CAMK2D/Tau complex. The existence of this complex stimulates the production of Tau aggregation, which then induces the accumulation of lipid peroxides (LPOs) and causes LPO‐dependent ferroptosis. In vivo, treatment with ferrostatin‐1 and TRx0237 rescued the inhibitory effect of hsa_circ_0001546 on EOC cell spreading. Therefore, based on this results, ferroptosis caused by Tau aggregation occurs in EOC cells, which is not only in Alzheimer's disease‐ or Parkinson's disease‐related cells and this kind of ferroptosis driven by the hsa_circ_0001546/14‐3‐3/CAMK2D/Tau complex is LPO‐dependent rather than GPX4‐dependent is hypothesized.

项与甲磺酸氢甲硫堇相关的新闻（医药）

2024-07-03

·药智网

礼来开启AD药物新纪元

一丝曙光击穿黑暗。 7月2日，礼来Aβ抗体Donanemab（商品名：Kisunla）获得FDA批准上市，用于治疗早期有症状的阿尔茨海默症（AD），定价695.65美元/支。阿尔茨海默症是全球公认的研发黑洞，近20年的时间里，AD新药领域的研究几乎全军覆没，上市的药物基本只能延缓而无法有效治愈。随着礼来Donanemab上市，AD药物新纪元正式开启。研发“死亡谷” AD发病机制复杂且临床试验审核程序非常严苛，AD新药研发有着业界公认99.6%的最高失败率，被称为药物研发“死亡谷”。阿尔茨海默病（AD）治疗主要以对症治疗为主，根据《中国阿尔茨海默病痴呆诊疗指南(2020年版)》建议，针对AD的临床一线治疗主要分为认知症状治疗、精神行为症状治疗和中医药治疗三种疗法。 1、认知症状的治疗目前用于治疗AD的临床一线治疗药物主要包括乙酰胆碱酯酶抑制剂和谷氨酸受体拮抗剂。（1）胆碱酯酶抑制剂（ChEI）：ChEIs对轻中度AD痴呆认知、功能、总体有效，用于重度AD痴呆仍可获益。多奈哌齐10 mg/d可产生最佳维持效果，认知获益突出，安全性好。卡巴拉丁9.5 mg/d贴剂可产生最佳维持效果，认知和总体获益与12 mg/d胶囊相当，安全性优于胶囊。加兰他敏24 mg/d可产生最佳维持效果，总体获益明显，安全性好。当一种ChEI初始药物缺乏满意的疗效或不耐受时，换用另一种ChEI可获得与初始药物相似的效果。（2）谷氨酸受体拮抗剂：美金刚20 mg/d对中重度AD痴呆的认知和总体有轻微疗效。美金刚联合胆碱酯酶抑制剂治疗中重度AD痴呆的认知、总体、行为有协同效应。 2、精神行为症状的治疗目前针对AD精神行为症状的治疗则主要非典型抗精神病药和5-羟色胺类药为主（1）非典型抗精神病药：非典型抗精神病药可缓解AD引起的精神和行为症状，但都有加重认知损害等风险。奥氮平缓解AD精神和行为症状较突出，利培酮次之，喹硫平再次之。（2）5-羟色胺类药：匹莫范色林对AD痴呆的精神症状有短期效益。 3、中医药治疗中医药治疗AD痴呆可根据临床分期，通过辨证施治进行个体化治疗。清宫寿桃丸对前驱期AD认知有益，银杏叶提取物EGb761对早中期AD痴呆认知、行为和功能有轻微疗效。序贯疗法加常规西药对AD痴呆认知和行为有协同效益。图1 中医药治疗AD的贯序疗法图片来源：《中国阿尔茨海默病痴呆诊疗指南(2020年版)》各靶点在研药物 1、Aβ靶点在研药物（1）Remternetug（LY3372993） Remternetug是礼来旗下一款IgG1单克隆抗体，靶向仅存在于脑淀粉样蛋白斑块中的淀粉样β肽第三个氨基酸的焦谷氨酸修饰。目前处于3期临床阶段（TRAILRUNNER ALZ 1），预计2025年3月完成研究，以评估其对早期症状性阿尔茨海默病（AD）患者的安全性和有效性。 2023年1月，Remternetug注射液获得中国药品审评中心（CDE）批准进入临床阶段，并于2023年4月被授予突破性疗法认定。根据2023年阿尔茨海默病和帕金森病国际会议上发布的1期临床试验结果，Remternetug可快速且稳定地减少AD患者的淀粉样斑块，但会引发淀粉样蛋白相关成像异常（ARIA）的常见副作用（图2）。图2 Remternetug的有效性和安全性数据图片来源：Safety and Amyloid Plaque Reduction Effects of Remternetug in Patients with Alzheimer’s Disease:Interim Analysis from a Phase 1 Study. （2）Valiltramiprosate（ALZ-801） ALZ-801是Alzheon公司研发的一种口服小分子抑制剂，通过阻断淀粉样蛋白寡聚体形成来阻止淀粉样蛋白斑块的产生。ALZ-801是III期临床失败的Tramiprosate的前体药物（pro-durg），它在2017年获得了美国FDA的快速通道资格。当前，ALZ-801正处于针对带有APOE4/4纯合子的早期阿尔茨海默病患者的3期临床研究，预计在2024年第3季度公布数据并申请新药上市许可。2022年9月，ALZ-801在2期生物标志物临床试验中取得积极结果，显示其能显著降低患者的血浆P-tau181蛋白水平，并具有潜在的神经保护作用。此外，ALZ-801在2000多名患者中未见血管源性脑水肿，表明其具有良好的安全性。（3）Galectin-3抑制剂（TB006） Galectin-3是一种可溶性的β-半乳糖苷结合蛋白，参与细胞凋亡、粘附、增殖、迁移等多个生理过程，并在多种神经退行性疾病中高表达。它与Aβ、P-tau等蛋白质结合，导致有毒低聚物形成，损害阿尔茨海默病（AD）患者的认知功能。TB006是一种靶Galectin-3的单克隆抗体，通过结合Galectin-3使其无法与Aβ、P-tau等蛋白质结合，从而减少斑块沉积，恢复神经元之间的交流。 TrueBinding公司于2022年11月宣布其靶向Galectin-3的TB006人源化单抗在1b/2a期临床试验中达主要终点，并在12月展示了结果，显示TB006具有良好的安全性和有效性，显著改善患者认知和功能，CDR-SB评分变化为-0.44分，相较对照组差异为63%。 2、Tau蛋白靶点在研药物（1）甲磺酸氢甲硫堇HMTM（TRx0237） TRx0237是TauRx Pharmaceuticals公司开发的一款Tau蛋白聚集抑制剂，主要靶向Tau蛋白、TDP-43蛋白和突触核蛋白的异常聚集及纤维缠结。该药目前正在海外针对因阿尔茨海默症引起的轻度认知障碍患者开展III期临床研究，III期临床试验LUCIDITY的结果显示，接受16mg/天TRx0237的受试者在12个月内神经丝轻链减少93%。 2022年4月，TRx0237的三期临床试验在中国获批，计划招募约400名受试者，预计于2025年Q2完成。这一研究旨在评估TRx0237的疗效和安全性，并补充国际上LUCIDITY研究的结果（图3）。图3 TRx0237临床试验进展情况图片来源：https://www.alzforum.org/therapeutics/hmtm （2）抗微管结合区Tau抗体E2814 抗微管结合区Tau抗体E2814是卫材与伦敦大学学院合作研究的成果，该抗体在临床前研究中已显示能有效抑制Tau蛋白在体外的聚集。显性遗传阿尔茨海默氏网络试验单位（DIAN-TU）已选择E2814作为其DIAN-TU Tau研究的抗Tau药物中的第一个探索性治疗。目前，E2814正在华盛顿大学圣路易斯分校进行II/III期临床试验。 3、神经炎症靶点在研药物（1）马赛替尼（Masitinib）马赛替尼是由法国AB Science公司研发的一种口服多靶点酪氨酸激酶抑制剂。它通过抑制特定蛋白激酶和受体CSF-1R来减少肥大细胞和小胶质细胞的活性，从而重塑神经元微环境，发挥神经保护作用。（2）Bezisterim（NE3107） NE3107是BioVie公司研发的一种小分子药物，是一种口服、可穿过血脑屏障的小分子化合物，具有抗炎、胰岛素增敏和ERK结合特性。2期临床试验结果显示，NE3107能改善阿尔茨海默病（AD）患者的认知和生物标志物水平，目前正进行3期临床试验（图4）。图4 NE3107分子结构和作用机制图片来源：太平洋证券 4、突触可塑性靶点在研药物（1）Blarcamesine（ANAVEX®2-73） ANAVEX®2-73是由Anavex Life Sciences公司研发的一种Sigma-1受体激动剂，有助于恢复神经细胞稳态和促进神经可塑性。在2022年12月，该公司公布了ANAVEX®2-73的2b/3期临床试验结果，显示该药物显著改善了早期阿尔茨海默病（AD）患者的认知能力，达到了主要和关键次要终点，该药目前已提交NDA申请，距离获批上市指日可待。图5 ANAVEX®2-73临床试验进展情况图片来源：https://www.anavex.com/ （2）AR1001 AR1001是由AriBio公司研发的一种靶向磷酸二酯酶-5的小分子抑制剂，具有神经保护作用，且对淀粉样斑块和Tau蛋白显示积极效果。在2期临床研究中，接受AR1001治疗52周的轻度阿尔茨海默病患者在10 mg组和30 mg组分别有15.1%和46.3%的评分改善。当前AriBio公司正在进行3期临床研究，以进一步评估其在早期阿尔茨海默病人群中的疗效和安全性。创新疗法未来可期近年来，阿尔茨海默症创新药物研发主要集中在其关键病理生物标志物—β淀粉样蛋白（Aβ）和Tau蛋白，最近三年，有两款针对Aβ的单克隆抗体药物—Aducanumab和Lecanemab已被美国FDA批准上市，用于治疗前驱期和轻度AD患者。这些创新药物在清除AD患者大脑中所积聚的β淀粉样蛋白方面，均表现出了显著的疗效。 1、Aducanumab疗效争议尽管Aducanumab在2021年初公开的临床试验数据显示其在减缓认知能力下降方面并不一致，且具有较高的不良反应发生率，FDA还是在2021年6月加速批准其用于治疗前驱期和轻度阿尔茨海默病（AD）患者。然而，由于疗效和安全性备受质疑，阿杜卡尼单抗未能在临床上广泛应用，销售额远低于预期，2021年和2022年仅分别达到300万美元和480万美元。 2、Lecanemab登陆国内市场 Lecanemab是Biogen和卫材联合开发的人源化单克隆抗体药物，于2023年1月获得美国FDA加速批准，并于2023年7月完全批准用于治疗阿尔茨海默病引起的轻度认知障碍和轻度痴呆。这是自2003年以来首个完全获得FDA批准的阿尔茨海默病新药。其靶向可溶性Aβ聚合体，具有显著的临床效果和较好的安全性。 2023年10月12日，该药物在海南省药品监督管理局审核通过，并于2024年1月9日获得国家药品监督管理局批准在中国上市，定价为2508元/瓶，2024年6月26日，Lecanemab在国内首次开方，这一进展标志着我国在AD药物精准治疗领域进入了一个新的阶段。参考资料 1.《中国阿尔茨海默病痴呆诊疗指南(2020年版)》 2.Safety and Amyloid Plaque Reduction Effects of Remternetug in Patients with Alzheimer’s Disease:Interim Analysis from a Phase 1 Study. 3.Two Randomized Phase 3 Studies of Aducanumab in Early Alzheimer’s Disease. 声明：本内容仅用作医药行业信息传播，为作者独立观点，不代表药智网立场。如需转载，请务必注明文章作者和来源。对本文有异议或投诉，请联系maxuelian@yaozh.com。责任编辑 | 德清君转载开白 | 马老师 18996384680（同微信）商务合作 | 王存星 19922864877（同微信）阅读原文，是昨天最受欢迎的文章哦

临床结果上市批准临床2期

2024-07-01

·PipelineReview

TauRx Submits UK Marketing Authorisation Application for HMTM as a Treatment for Alzheimer’s Disease

ABERDEEN, UK I July 01, 2024 I TauRx Pharmaceuticals Ltd, a global leader in tau-based research in Alzheimer’s disease (AD), has announced the submission of a UK Marketing Authorisation Application (MAA) for hydromethylthionine mesylate (HMTM) for treatment of mild cognitive impairment (MCI-AD) and mild to moderate stages of dementia due to Alzheimer’s disease. HMTM has been designated by the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) for the Innovative Licensing and Access Pathway (ILAP). If successful, the UK could be the first country in which an accessible, safe, oral treatment, which targets the hallmark tau pathology of the disease, becomes available to patients. The MAA is based on the totality of evidence available from the recently released 24-month Phase 3 LUCIDITY data and two earlier Phase 3 trials in mild to moderate AD. These studies have been consistent in showing benefit on measures of decline in cognition, ability to perform normal activities of daily living, and reduction in the rate of brain shrinkage. Tau aggregation is strongly correlated with the rate and severity of cognitive decline, brain atrophy, and the damage to neurons responsible for the characteristic neurodegeneration of the disease. HMTM acts by selectively inhibiting the aggregation of tau-protein in brain nerve cells. It also has a second mode of action which results in enhancement of brain functioning. Commenting on the submission, Professor Claude Wischik, Executive Chairman of TauRx, said: “This is a significant milestone for TauRx and is an important step in potentially bringing a new type of treatment and a new hope to patients and families who carry the burden of this terrible disease.” NOTES ABOUT HMTM Hydromethylthionine mesylate (HMTM) has been developed as a potential oral treatment for AD targeting tau aggregation. It also has a secondary tau-independent mode of action which increases acetylcholine levels in the hippocampus. The global Phase 3 clinical trial LUCIDITY has recently completed and the data were presented at the AD/PD™ 2024 Alzheimer’s & Parkinson’s Diseases Conference in Lisbon, Portugal, on 7 March. With over 3,000 subjects studied, HMTM has a strong safety profile and could be delivered with minimal patient and physician burden. Neurofilament Light Chain (NfL) is an established biomarker for neurodegeneration. LUCIDITY showed a significant reduction in the change of NfL, in the randomised double-blind portion of the study at 12 months. Clinical measures of cognition showed improvement over baseline levels that was sustained over 18 months in MCI, as diagnosed in the LUCIDITY trial. Patients who were in the control group were unable to catch up in terms of cognitive function despite transitioning to 16mg per day HMTM (target dose) in the open-label phase after 12 months. This emphasises the importance of early intervention with effective therapies in AD. ABOUT TAURx PHARMACEUTICALS LTD TauRx was founded in 2002 in Singapore, with primary research facilities and operations based in Aberdeen, UK. In collaboration with the University of Aberdeen, the company has dedicated the past two decades to developing treatments and diagnostics for Alzheimer’s and other neurodegenerative diseases due to pathological aggregation of tau and other proteins. AD is a leading cause of disability and death throughout the world and is one of the most important global public health issues. TauRx will contribute to addressing this urgent unmet need with data from the totality of evidence available from LUCIDITY and the earlier AD trials in pursuit of regulatory approvals starting in UK. TauRx’s hope is to make HMTM available for people living with Alzheimer’s as soon as possible. Future research is planned for other related neurodegenerative diseases. https://taurx.com/ SOURCE: TAURx Pharmaceuticals

临床3期临床结果

2024-07-01

·Pharmaceutical Technology

TauRx seeks UK MHRA approval for Alzheimer’s treatment

The application for HMTM to treat Alzheimer’s is based on data from Phase III LUCIDITY trial and two prior Phase III studies. Credit: CGN089 / Shutterstock. TauRx Pharmaceuticals has filed a marketing authorisation application (MAA) with the UK Medicines and Healthcare products Regulatory Agency, seeking approval for hydromethylthionine mesylate (HMTM) to treat Alzheimer’s disease (AD). HMTM is intended for treating mild cognitive impairment due to Alzheimer’s disease (MCI-AD) and mild to moderate dementia stages associated with AD. The UK regulator had previously designated the innovative licensing and access pathway for HMTM. The UK could become the first country to offer this oral treatment on approving HMTM. TauRx’s MAA for the asset is underpinned by comprehensive evidence from the 24-month Phase III LUCIDITY clinical trial and two previous Phase III studies. See Also: Pharma M&A: The top high value deals in 2023 Medical packaging companies in pharmaceutical contract manufacturing These trials consistently demonstrated HMTM’s benefits in slowing cognitive decline, maintaining daily living activities and reducing brain atrophy rates. Tau aggregation, a key factor in Alzheimer’s, correlates with cognitive decline severity and brain nerve cell damage. HMTM counters this by selectively inhibiting tau-protein aggregation. Designed as an oral AD treatment, HMTM targets tau aggregation and enhances brain function through a secondary, tau-independent action that raises acetylcholine levels in the hippocampus. The global Phase III LUCIDITY trial involving over 3,000 subjects has concluded and established the safety profile of HMTM. A notable finding from the LUCIDITY trial was the significant reduction in neurofilament light chain, a biomarker for neurodegeneration, at the 12-month mark of the study. Clinical assessments of cognition revealed sustained improvements from baseline over 18 months in MCI-diagnosed patients. TauRx executive chairman professor Claude Wischik stated: “This is a significant milestone for TauRx and is an important step in potentially bringing a new type of treatment and a new hope to patients and families who carry the burden of this terrible disease.”

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适应症	最高研发状态	国家/地区	公司	日期
阿尔茨海默病引起的痴呆症	申请上市	英国	TauRx Pharmaceuticals Ltd.	2024-07-01
轻度认知障碍	申请上市	英国	TauRx Pharmaceuticals Ltd.	2024-07-01
额颞痴呆	临床3期	美国	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	澳大利亚	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	加拿大	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	克罗地亚	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	德国	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	意大利	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	荷兰	TauRx Therapeutics Ltd.	2013-05-01
额颞痴呆	临床3期	波兰	TauRx Therapeutics Ltd.	2013-05-01

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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


LUCIDITY (BusinessWire) 人工标引	临床3期	阿尔茨海默症	3,000	HMTM 16 mg/day	夢衊積衊膚製獵蓋餘鬱(淵選餘繭網餘夢構範糧) = Within this subgroup, progression of symptoms to the dementia stage of the disease was significantly less than in the control group. 糧網糧獵餘憲鹽鑰網鏇 (網獵獵願淵衊憲糧觸廠 ) 更多	积极	2024-03-07
				control
NCT03446001 (LUCIDITY, PRNewswire) 人工标引	临床3期	阿尔茨海默症	598	HMTM	齋繭淵簾鬱衊餘蓋觸選(餘糧鹹鏇構蓋壓襯餘鑰) = The safety profile is good and consistent with previous HMTM studies 衊遞積網遞範鹽壓憲夢 (鑰鹽衊糧繭觸構壓齋襯 )	积极	2022-06-01
NCT02245568 (CTgov)	临床3期	阿尔茨海默症 \| 额颞痴呆	913	LM	蓋構鬱遞窪夢簾壓製積(顧顧範蓋遞鏇鏇蓋觸網) = 顧襯網憲淵醖糧觸遞淵襯膚選願鹽窪襯艱鬱築 (積遞膚淵糧淵淵積繭齋, 遞願遞鏇願廠遞膚範選 ~ 積鏇襯艱壓範鏇壓餘蓋) 更多	-	2020-06-02
NCT01626391 (CTgov)	临床2期	阿尔茨海默症	9	TRx0237 (TRx0237)	顧鹹獵積餘廠鹽憲範獵(鬱衊蓋艱遞鏇蓋醖簾糧) = 選憲鹹艱鏇遞壓憲糧鏇膚鬱膚網構積艱網淵窪 (襯膚鏇齋壓網壓網鏇鑰, 鏇鹽觸獵顧窪製壓顧鏇 ~ 願製網繭醖築獵壓蓋襯) 更多	-	2014-07-11
				Placebo (Placebo)	顧鹹獵積餘廠鹽憲範獵(鬱衊蓋艱遞鏇蓋醖簾糧) = 選廠鬱願淵願簾繭壓窪膚鬱膚網構積艱網淵窪 (襯膚鏇齋壓網壓網鏇鑰, 襯簾蓋繭壓夢鏇製鬱憲 ~ 廠鹽積鑰齋選獵鹹憲鹹) 更多