拉喹莫德(Laquinimod) - 药物靶点：BDNF_在研适应症：多发性硬化症_专利_临床

概要

基本信息

药物类型

小分子化药

别名

laquinimod、Laquinimod Sodium、Laquinimod sodium (USAN)

+ [4]

靶点

BDNF

作用方式

激动剂、调节剂

作用机制

BDNF激动剂(脑源性神经营养因子激动剂)、免疫调节剂

治疗领域

在研适应症

非在研适应症

原研机构

在研机构

非在研机构

Teva Branded Pharmaceutical Products R&D LLCTeva Generics GmbH

权益机构-

最高研发阶段批准上市

首次获批日期

俄罗斯 (2018-08-22),

多发性硬化症

最高研发阶段(中国)-

特殊审评孤儿药 (美国)

登录后查看时间轴

结构/序列

分子式C19H17ClN2NaO3

InChIKeyAHIFNCNCUYJCOR-UHFFFAOYSA-N

CAS号248282-07-7

关联

18

项与拉喹莫德相关的临床试验

NCT06161415

/ Recruiting临床1期IIT

Safety, Tolerability, and Distribution of Topical Laquinimod Eye Drops , an Innovative ImmunomodulatOr Targeting Aryl hydrocarboN Receptor (AhR): The LION Study

The LION Study is a prospective, single-center phase 1 clinical trial to evaluate the safety, tolerability, and distribution of Laquinimod administered as topical eye drops for two weeks in human participants.

开始日期2024-05-03

申办/合作机构

Stanford University

NCT05187403

/ Completed临床1期

A Placebo-Controlled, Double-masked Phase-1 Study in Healthy Subjects Investigating the Safety and Tolerability of Laquinimod Eye Drops

This is a Phase 1 randomized, double-masked, placebo-controlled study performed with healthy participants to assess the safety and tolerability of laquinimod eye-drops.

开始日期2021-12-09

申办/合作机构

Active Biotech AB

NL-OMON43112

/ CompletedN/A

A randomized, open-label, two-way crossover study to assess the relative bioavailability of Laquinimod 0.6 mg test tablet versus Laquinimod 0.6 mg reference capsule after single dose administration with a single sequence extension to assess the pharmacokinetics of Laquinimod and its metabolites after single and multiple oral 0.6 mg dose administration in healthy subjects. - Bioavailability study Laquinimod test tablets

开始日期2016-10-05

申办/合作机构

Teva Pharmaceutical Industries Ltd.

100 项与拉喹莫德相关的临床结果

登录后查看更多信息

100 项与拉喹莫德相关的转化医学

登录后查看更多信息

100 项与拉喹莫德相关的专利（医药）

登录后查看更多信息

212

项与拉喹莫德相关的文献（医药）

2025-06-01·NEUROREHABILITATION

What Is the Evidence on Immunomodulators and Immunosuppressants for Progressive Multiple Sclerosis? - A Cochrane Review Summary with Commentary.

Review

作者: Moretti, Antimo

BackgroundMultiple sclerosis (MS) is a chronic inflammatory demyelinating disease affecting the central nervous system and is a major cause of disability in adults, particularly in those affected by progressive MS. A variety of drugs with different effects, some carrying significant risks, are currently available, making evidence-based approach essential for clinicians treating MS patients.ObjectiveTo compare the efficacy and safety of immunomodulators and immunosuppressants for progressive multiple sclerosis (PMS).MethodsA systematic search was performed in CENTRAL, MEDLINE, Embase, and trials registers on 8 august 2022, including RCTs comparing immunomodulators and immunosuppressants versus placebo or another drug.ResultsThe network meta-analysis (NMA) included 23 RCTs (with 10,167 participants). Moderate certainty of evidence suggests that rituximab probably not reduce the risk of relapse at 2 years, while interferon beta-1b probably reduces the risk of relapses at 3 years (-18%) compared to placebo in PMS people. Regarding SAE, low-to-very-low certainty of evidence for no increased risk with disease-modifying therapies (DMTs) versus placebo is available, except for immunoglobulins that seem to have a 7-fold increased risk of serious adverse events (SAEs). Only low-to-very low certainty of evidence is available about disability progression and SAEs in PMS people treated with DMTs versus placebo. On the other side, the risk for treatment discontinuation due to AEs is increased with interferon beta-1a by 2.93-fold, and probably increased with interferon-beta-1b, glatiramer acetate, and fingolimod by 2.98-fold, 3.98-fold, and 2.29-fold, respectively. Also, rituximab, natalizumab, siponimod, and ocrelizumab probably do not increase the risk for treatment discontinuation due to AEs, while laquinimod may not increase the risk treatment discontinuation due to AEs.ConclusionsCompared with placebo, two-, and three-year treatment with rituximab or interferon beta-1b, respectively, probably slightly reduce relapses in PMS people. A slight increase of treatment discontinuation due to AEs has been reported for rituximab, interferon beta-1b, interferon beta-1a, immunoglobulins, glatiramer acetate, natalizumab, fingolimod, siponimod, and ocrelizumab. No reliable evidence is available for disability progression and SAEs with available DMTs compared to placebo.

2025-02-01·JOURNAL OF INTERNATIONAL MEDICAL RESEARCH

Efficacy and safety of laquinimod versus placebo in relapsing-remitting multiple sclerosis: a systematic review and meta-analysis of randomized controlled trials

Review

作者: Ikram, Jibran ; Hussain, Amna ; Monis, Arysha ; Khan, Safeena ; Khan, Muhammad Haris ; Tahir, Ammara ; Azeem, Touba ; Ali, Moosa ; Moeez, Abdul ; Ali, Aizaz ; Khattak, Fazia ; Mian, Aban Masaud ; Zeb Khan, Malik Waleed

Objective:

To investigate the safety and efficacy of laquinimod in treating relapsing-remitting multiple sclerosis (RRMS).

Methods:

An extensive electronic search was conducted across PubMed, Embase, Cochrane Database of Systematic Reviews, and ClinicalTrials.gov to identify suitable studies. Risk of bias was assessed using Cochrane’s Risk of Bias tool. Statistical analysis was performed using RevMan 5.4.1.

Results:

The meta-analysis of four randomized controlled trials including 3665 patients found that laquinimod significantly reduced the annualized relapse rate compared with placebo (mean difference = −0.08, 95% confidence interval [CI] = −0.12, −0.04, I2 = 0%). For disability progression confirmed at 3 months, laquinimod provided a significant advantage over placebo (hazard ratio [HR] = 0.75, 95% CI = 0.59, 0.96, I2 = 25%), whereas no benefit was achieved at 6 months (HR = 0.69, 95% CI = 0.45, 1.06, I2 = 66%). Laquinimod was also significantly better than placebo in maintaining a relapse-free status (risk ratio [RR] = 1.14 95% CI = 1.06, 1.22, I2 = 10%). Laquinimod had a comparable safety profile as placebo (RR = 1.06, 95% CI = 0.81, 1.39, I2 = 33%).

Conclusions:

These findings support the efficacy of laquinimod in managing RRMS but necessitate careful monitoring during treatment.

2025-01-01·ADVANCES IN THERAPY

Real-World Safety and Effectiveness of Dimethyl Fumarate in Patients with MS: Results from the ESTEEM Phase 4 and PROCLAIM Phase 3 Studies with a Focus on Older Patients

Article

作者: Foley, John ; Everage, Nicholas ; Giuliani, Fabrizio ; Smoot, Kyle ; Lyons, Jennifer ; Mokliatchouk, Oksana ; Bame, Eris ; Mao-Draayer, Yang ; Mendoza, Jason P ; Božin, Ivan ; Longbrake, Erin E ; Balashov, Konstantin ; Lewin, James B ; Bar-Or, Amit ; Robertson, Derrick

INTRODUCTION:

Real-world studies in the USA report that 41-56% of patients with multiple sclerosis (MS) are ≥ 50 years old, yet data on their response to disease-modifying therapies (DMTs) is limited. Dimethyl fumarate (DMF) is an oral DMT approved for treating relapsing MS. This analysis evaluated the safety, efficacy, and immunophenotype changes of DMF in patients ≥ 50 years compared with patients < 50 years.

METHODS:

ESTEEM, a 5-year, real-world, observational phase 4 study, assessed the safety and effectiveness of DMF, including treatment-emergent serious adverse events (SAEs) and adverse events (AEs) leading to treatment discontinuation. Absolute lymphocyte counts (ALCs) were recorded from a subset of patients. The PROCLAIM study, a phase 3b interventional study, reported safety outcomes and lymphocyte subset changes in patients with relapsing-remitting MS (RRMS) treated with DMF. The study evaluated safety outcomes by analyzing the incidence of SAEs and detailed changes in CD4⁺ and CD8⁺ T cell compartments over 96 weeks of DMF treatment.

RESULTS:

ESTEEM included 4020 patients aged < 50 years and 1069 aged ≥ 50 years. AEs leading to discontinuation were reported by 19.6% patients < 50 years and 29.6% of patients ≥ 50 years, with gastrointestinal disorders being the most common. SAEs were reported by 5.2% of patients < 50 years and 8.9% those ≥ 50 years. In PROCLAIM, SAEs were reported in 13% of patients < 50 years and 10% of those ≥ 50 years. Median ALC decreased by 35% in patients < 50 years and 50% in those ≥ 50 years in ESTEEM, with similar patterns observed in PROCLAIM.

CONCLUSIONS:

ESTEEM found no unexpected safety signals in older patients and annualized relapse rates (ARRs) were significantly reduced in both age groups. Both studies indicated that DMF is efficacious and has a favorable safety profile in patients with RRMS aged ≥ 50 years.

CLINICAL TRIAL REGISTRATION:

ESTEEM (NCT02047097), PROCLAIM (NCT02525874).

30

项与拉喹莫德相关的新闻（医药）

2026-04-20

·activebiotech.com

Active Biotech publishes results from the LION study on ocular absorption and distribution of laquinimod in the eye

“I am tremendously satisfied and gratified to learn that topical laquinimod, even at a low dose, can penetrate into the anterior chamber and, more importantly, the vitreous of human eyes. The potential applications of a topical formulation and delivery that reaches the posterior segment are quite significant and can lead to very important and novel therapeutic implications. Our talented team at Byers and Stanford is very excited with the outcomes of the study,” said Quan Dong Nguyen, MD, MSc, FAAO, FARVO, FASRS, Professor of Ophthalmology, Medicine and Pediatrics at the Byers Eye Institute and the Stanford University School of Medicine (Palo Alto, USA) and Principal Investigator of the LION Study. The article, titled Safety and Biodistribution of Topical Laquinimod, an Immunomodulator Targeting Aryl Hydrocarbon Receptor: The LION Study, was published in Ophthalmology Science with Dr. Dalia El Feky, a Visiting Scholar at the Byers Eye Institute, Stanford University as well as an ophthalmologist and uveitis specialist in the Faculty of Medicine, Tanta University in Egypt, as the lead author. There is an unmet need for a topical, non-steroidal therapy with a favourable safety profile for patients with non-anterior non-infectious uveitis. Previously, several steroidal and non-steroidal topical agents have failed to reliably demonstrate absorption to the posterior segment of the eye. LION was designed to study the ocular biodistribution of the topical hydrogel formulation of laquinimod and to evaluate its therapeutic potential for ocular inflammatory diseases involving the posterior segment of the eye. The article is the result of a collaboration between Active Biotech, clinician-researchers at the Byers Eye Institute at Stanford University and the Global Ophthalmic Research Center (GORC). The results showed that daily doses of either 0.6, 1.2 or 1.8 mg of laquinimod in the topical formulation resulted in dose related intraocular concentrations of laquinimod in the posterior as well as the anterior parts of the eye. Topical laquinimod was well tolerated, and no dose-limiting toxicities were reported. Such findings support investigating laquinimod’s therapeutic potential for inflammatory eye diseases affecting the posterior segment. Active Biotech’s focus for the laquinimod program is now directed towards identifying the best development partner for the continued clinical development of laquinimod in eye disorders. Link to article: https://www.ophthalmologyscience.org/article/S2666-9145(26)00124-7/fulltext

临床结果

2026-04-01

·activebiotech.com

Annual Report 2025 Active Biotech AB (publ)

The Annual Report will only be digitally distributed. “Building on progress in 2025, the coming year will focus on the tasquinimod clinical studies in myelofibrosis and intensified business development for laquinimod,” says Active Biotech CEO Helén Tuvesson.

2026-03-23

·百度百家

BDNF/脑源性神经营养因子：从神经可塑性调控到神经精神疾病治疗核心靶点

脑源性神经营养因子（brain-derived neurotrophic factor，BDNF）是神经营养因子家族中研究最为广泛的核心成员，在中枢神经系统发育、神经元存活及突触可塑性调控中发挥不可替代的作用。BDNF通过TrkB受体激活PI3K/Akt、MAPK/ERK等下游信号通路，调控神经元存活、轴突生长及认知功能。其表达异常与阿尔茨海默病、帕金森病、抑郁症、精神分裂症等多种神经精神疾病密切相关，同时在疼痛调控、药物依赖及神经损伤修复中也具有重要功能。本文系统梳理BDNF的基因结构、蛋白加工、信号通路、疾病关联及靶向治疗进展，为相关研究与临床转化提供参考框架。 1. BDNF的生物学特性与信号通路 2. BDNF相关疾病 3. BDNF靶向药物最新研究进展 4. BDNF研究工具推荐：重组蛋白、抗体与ELISA试剂盒选型指南 1. BDNF的生物学特性与信号通路 1.1 BDNF基因结构与蛋白加工 BDNF基因具有复杂的转录调控结构，包含多个启动子及外显子。不同启动子驱动的转录可产生多种mRNA亚型，这些转录本在编码区基本一致，但在5′非翻译区存在差异，从而赋予其不同的表达调控特性 [1]。神经元活动可通过Ca²⁺信号及cAMP反应元件结合蛋白（CREB）等转录因子调控BDNF表达，但这种调控在不同脑区之间存在明显差异 [2]。除了神经活动调控外，多种激素及转录因子同样参与BDNF表达调节。例如，雌二醇、糖皮质激素以及myocyte enhancer factor-2（MEF2）均可通过作用于BDNF启动子区域影响其转录水平 [3]。此外，DNA甲基化及microRNA等表观遗传机制也被证明能够调节BDNF表达 [4,5]。在蛋白水平，BDNF首先以前体形式pro-BDNF合成，随后经蛋白酶加工生成成熟BDNF。两者在功能上存在明显差异：pro-BDNF通常通过p75NTR受体介导突触削弱或细胞凋亡，而成熟BDNF则通过TrkB受体促进神经元存活及突触增强 [7]。因此，pro-BDNF与成熟BDNF之间的动态平衡被认为是调控神经可塑性的关键机制。此外，BDNF基因Val66Met（rs6265）多态性可影响BDNF的细胞内运输和分泌效率，并与多种神经系统疾病风险相关 [6]。结构生物学研究进一步表明，BDNF蛋白关键残基突变可能改变其构象稳定性及受体结合能力，从而影响信号传导效率 [8]。 1.2 BDNF-TrkB信号通路 BDNF的主要生物学功能通过高亲和力受体TrkB（tropomyosin receptor kinase B）介导。BDNF与TrkB结合后可诱导受体二聚化并发生酪氨酸残基自磷酸化，从而激活多个下游信号通路，包括PI3K/Akt、MAPK/ERK以及PLC-γ通路等 [9,10]。这些信号网络共同调控神经元存活、轴突生长和突触可塑性。 1.2.1 MAPK/ERK通路 MAPK/ERK通路是BDNF-TrkB信号最经典的下游通路之一。TrkB受体磷酸化后可通过Shc和Grb2等接头蛋白激活Ras-Raf-MEK-ERK级联反应。活化的ERK进入细胞核后可磷酸化多种转录因子，如CREB，从而调控神经元分化和突触相关基因表达。该通路在树突生长、突触形成以及长期记忆形成中发挥重要作用，是BDNF调控学习和记忆的关键分子基础。 1.2.2 PI3K-Akt通路 PI3K-Akt信号通路主要参与细胞存活及抗凋亡调控。TrkB激活后可招募PI3K并促进Akt磷酸化。Akt进一步磷酸化Bad和GSK-3β等蛋白，从而抑制细胞凋亡并增强神经元存活能力 [10]。在多种神经退行性疾病模型中，PI3K-Akt通路的激活通常与神经保护效应相关，因此被认为是BDNF介导神经保护的重要机制之一。 1.2.3 PLC-γ通路 PLC-γ通路主要参与细胞内钙信号调控。TrkB激活后可磷酸化PLC-γ，使其催化PIP2水解产生IP3和DAG。IP3可促进内质网Ca²⁺释放，而DAG则激活蛋白激酶C（PKC）。这些信号共同调控神经递质释放及突触可塑性。 PLC-γ信号在长时程增强（long-term potentiation，LTP）等突触可塑性过程中具有重要作用。 1.2.4 p75NTR信号通路除TrkB外，BDNF前体pro-BDNF还可通过低亲和力受体p75NTR发挥作用。p75NTR通常与神经元凋亡、轴突修剪以及突触削弱相关。该受体可通过JNK和NF-κB等信号通路调控细胞命运。因此，pro-BDNF/p75NTR 与 mBDNF/TrkB 两种信号轴之间的平衡被认为是决定神经元存活与突触可塑性的关键因素。 2. BDNF相关疾病 2.1 神经退行性疾病在阿尔茨海默病和帕金森病等神经退行性疾病中，BDNF表达普遍下降，这与神经元丢失及突触功能障碍密切相关。BDNF减少会削弱TrkB信号通路，从而降低神经元生存信号并加速神经退行过程。在阿尔茨海默病模型中，BDNF表达降低与海马突触可塑性受损和认知功能下降密切相关。恢复BDNF信号可在一定程度上改善突触功能并减轻认知损伤。 2.2 精神疾病 BDNF在抑郁症、焦虑症及精神分裂症等精神疾病中同样发挥重要作用。研究表明，抑郁症患者血清BDNF水平通常降低，而抗抑郁治疗可部分恢复其表达。 BDNF通过调节海马神经发生及突触可塑性参与情绪调控，因此其表达异常可能导致情绪调节功能紊乱。 2.3 神经损伤在脑卒中、脊髓损伤及创伤性脑损伤等情况下，BDNF表达会发生动态变化。BDNF可通过促进轴突再生、突触重建以及神经网络重塑参与神经功能恢复。实验研究表明，提高BDNF水平能够促进神经再生并改善神经功能恢复。 2.4 疼痛与药物依赖 BDNF在慢性疼痛和阿片类药物耐受形成中具有重要作用。在脊髓水平，BDNF可增强突触传递并调节疼痛信号传导。在吗啡耐受模型中，脊髓BDNF表达显著升高，而干预BDNF信号能够部分缓解耐受现象 [1]。这些研究提示BDNF可能是疼痛调控及药物依赖研究的重要分子靶点。 2.5 神经发育相关疾病 BDNF在神经发育过程中参与神经元迁移、轴突导向以及突触形成。因此，其表达异常可能影响神经网络形成并导致神经发育障碍。近年来研究发现，BDNF与自闭症谱系障碍及注意缺陷多动障碍等疾病存在一定关联，特别是pro-BDNF向成熟BDNF转化异常可能影响突触可塑性并参与发育异常 [7]。 3. BDNF靶向药物最新研究进展 BDNF是促进神经元存活与可塑性的关键分子，其靶向药物研发已覆盖多种神经精神疾病。目前拉喹莫德已获批用于多发性硬化症，多项临床研究正探索BDNF调节剂在抑郁症、躁郁症等精神障碍中的疗效。临床前阶段项目则广泛布局阿尔茨海默病、帕金森病、青光眼及中枢神经系统损伤，涉及小分子化药、基因治疗及中药等多种技术路径，整体呈现多元化发展态势。部分在研管线整理如下表：药物类型适应症研发阶段研发机构拉喹莫德小分子调节剂多发性硬化症已上市 Teva Pharmaceuticals TrkB激动剂小分子化合物抑郁症/阿尔茨海默病临床2期多家药企 BDNF基因疗法基因治疗帕金森病/青光眼临床1期生物技术公司 7,8-二羟基黄酮小分子TrkB激动剂阿尔茨海默病临床前多个研究机构中药活性成分（黄芩苷、人参皂苷Rb1等）天然产物抑郁症/神经损伤临床前国内科研院所 BDNF纳米递送系统纳米制剂中枢神经系统损伤临床前高校合作项目（数据截止到2026年3月11日，来源于synapse） 4. BDNF研究工具推荐：重组蛋白、抗体与ELISA试剂盒选型指南 BDNF作为中枢神经系统中分布最广、研究最深入的神经营养因子，是连接神经可塑性、认知功能与多种神经精神疾病病理机制的核心分子，其信号通路调控已成为治疗阿尔茨海默病、抑郁症等难治性疾病的战略性靶点。华美生物提供BDNF重组蛋白、抗体及ELISA试剂盒产品，助力您进行相关机制研究及靶向药物开发。 ● BDNF 重组蛋白 Recombinant Human Neurotrophic factor BDNF precursor form (BDNF) CSB-EP002655HU(A4) Recombinant Rat Brain-derived neurotrophic factor (Bdnf), partial CSB-RP166394r Recombinant Dog Brain-derived neurotrophic factor (BDNF) CSB-EP002655DO ● BDNF 抗体 BDNF Recombinant Monoclonal Antibody; CSB-RA567297A0HU BDNF Recombinant Monoclonal Antibody; CSB-RA989910A0HU ● BDNF ELISA 试剂盒 Human Brain derived neurotrophic factor,BDNF ELISA Kit CSB-E04501h Mouse Brain derived neurotrophic factor,BDNF ELISA Kit CSB-E04505m Rat Brain derived neurotrophic facor,BDNF ELISA Kit CSB-E04504r Monkey Brain-derived neurotrophic factor(BDNF) ELISA kit CSB-EL002655RH 参考文献： [1] Zahra Khoshdel, Somayeh Ahmadpour Jirandeh, Mohammad Ali Takhshid, Farideh Jalali Mashayekhi, Shahla Shojaei, Ali Akbar Owji.(2019). The BDNF Protein and its Cognate mRNAs in the Rat Spinal Cord during Amylin-induced Reversal of Morphine Tolerance. [2] Eli-Eelika Esvald, Jürgen Tuvikene, Andra Moistus, Käthy Rannaste, Susann Kõomägi, Tõnis Timmusk.(2022). Differential Regulation of the BDNF Gene in Cortical and Hippocampal Neurons. [3] R Chow, J M Wessels, W G Foster.(2020). Brain-derived neurotrophic factor (BDNF) expression and function in the mammalian reproductive Tract. [4] Te Zhao, Lian-Hua Piao, Dan-Ping Li, Shi-Han Xu, Shu-Yi Wang, Hai-Bo Yuan, Chun-Xiao Zhang.(2023). BDNF gene hydroxymethylation in hippocampus related to neuroinflammation-induced depression-like behaviors in mice. [5] Gilmara Gomes De Assis, Eugenia Murawska-Ciałowicz.(2024). BDNF Modulation by microRNAs: An Update on the. [6] Iwona Przybylska, Jarosław Marusiak, Beata Toczyłowska, Adam Stępień, Bogdan Brodacki, Józef Langfort, Małgorzata Chalimoniuk.(2024). Association between the Val66Met (rs6265) polymorphism of the brain-derived neurotrophic factor (BDNF) gene, BDNF protein level in the blood and the risk of developing early‑onset Parkinson's disease. [7] Feng Yang, He You, Toshiyuki Mizui, Yasuyuki Ishikawa, Keizo Takao, Tsuyoshi Miyakawa, Xiaofei Li, Ting Bai, Kun Xia, Lingling Zhang, Dizhou Pang, Yiran Xu, Changlian Zhu, Masami Kojima, Bai Lu.(2024). Inhibiting proBDNF to mature BDNF conversion leads to ASD-like phenotypes in vivo. [8] V M Datta Darshan, Natarajan Arumugam, Abdulrahman I Almansour, Venketesh Sivaramakrishnan, Subbarao Kanchi.(2024). In silico energetic and molecular dynamic simulations studies demonstrate potential effect of the point mutations with implications for protein engineering in BDNF. [9] Peiyuan Huang, Aofei Liu, Yutong Song, Jen M Hope, Bianxiao Cui, Liting Duan.(2020). Optical Activation of TrkB Signaling. [10] Si-Rui Sun, Jia-Ning Zhao, Peng-Wei Bi, Hui-Ying Zhang, Guang-Xiang Li, Jiao-Zhao Yan, Yun-Feng Li, Yong-Yu Yin, Hao Cheng.(2025). Pharmacologically activating BDNF/TrkB signaling exerted rapid-acting antidepressant-like effects through improving synaptic plasticity and neuroinflammation.

信使RNA临床研究

100 项与拉喹莫德相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D08938	拉喹莫德	N07XX10	DB06685

研发状态

批准上市

10 条最早获批的记录,

登录

后查看更多信息

适应症	国家/地区	公司	日期
多发性硬化症	俄罗斯	Active Biotech AB	2018-08-22

未上市

10 条进展最快的记录,

登录

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
复发性多发性硬化	临床3期	美国	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	奥地利	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	保加利亚	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	加拿大	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	捷克	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	爱沙尼亚	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	法国	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	德国	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	匈牙利	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10
复发性多发性硬化	临床3期	以色列	Teva Branded Pharmaceutical Products R&D LLC	2009-11-10

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT01085084 (CTgov)	临床2期	系统性红斑狼疮	82	Placebo (Placebo)	憲獵製艱艱餘衊夢積獵 = 積築窪廠鹽憲願齋簾鬱鏇鹹鹽繭窪選簾範築廠 (構廠簾鹽築鏇廠築壓窪, 齋願糧淵願積艱顧醖遞 ~ 廠網網壓襯齋顧遞遞選) 更多	-	2022-07-07
				Placebo+Laquinimod (Laquinimod 0.5 mg)	憲獵製艱艱餘衊夢積獵 = 獵廠遞顧鹹鹹繭鑰構蓋鏇鹹鹽繭窪選簾範築廠 (構廠簾鹽築鏇廠築壓窪, 範艱窪鹽淵鬱範願選餘 ~ 鑰淵衊襯顧製襯鬱窪醖) 更多
NCT00605215 (BRAVO, CTgov)	临床3期	复发-缓解型多发性硬化	1,331	Placebo (Placebo)	廠廠築壓憲鹽廠鬱築淵(構夢淵鬱願鬱鹽鬱簾蓋) = 顧網顧觸鑰繭窪製網廠夢簾鏇襯積鹽鏇艱窪艱 (遞觸觸顧鹽顧選膚齋淵, 膚鹹繭窪鬱構壓壓蓋壓 ~ 壓鬱衊衊簾鏇鑰簾蓋膚) 更多	-	2022-04-21
				Laquinimod (Laquinimod)	廠廠築壓憲鹽廠鬱築淵(構夢淵鬱願鬱鹽鬱簾蓋) = 繭淵鏇鏇鏇鏇遞膚衊積夢簾鏇襯積鹽鏇艱窪艱 (遞觸觸顧鹽顧選膚齋淵, 鏇憲觸遞壓廠鹹顧製醖 ~ 繭廠壓壓繭淵簾衊構構) 更多
NCT01085097 (CTgov)	临床2期	狼疮性肾炎	46	Placebo+Methylprednisolone+Prednisone+Prednisolone+mycophenolate mofetil (Placebo)	簾襯鹹齋窪艱鹽築鬱艱 = 積築窪齋鏇繭壓簾壓膚壓顧鑰積積積鬱鏇簾製 (願艱選夢簾襯窪範廠構, 艱餘鑰選製蓋製選膚簾 ~ 淵淵範選鏇顧獵淵製膚) 更多	-	2022-03-09
				Placebo+Methylprednisolone+Prednisone+Prednisolone+mycophenolate mofetil+Laquinimod (Laquinimod 0.5 mg)	簾襯鹹齋窪艱鹽築鬱艱 = 鬱憲簾夢齋鬱壓簾淵膚壓顧鑰積積積鬱鏇簾製 (願艱選夢簾襯窪範廠構, 顧範襯顧願願鑰淵醖積 ~ 顧構鹽糧鏇糧觸願糧鹹) 更多
NCT00509145 (ALLEGRO, CTgov)	临床3期	复发-缓解型多发性硬化	1,106	Laquinimod (Laquinimod)	鹹遞簾觸積簾鏇遞衊夢(鹹窪艱餘遞築積糧鑰積) = 築築鹽鏇淵鑰選艱齋構遞膚鹽窪鹽壓選鬱蓋鹹 (艱獵觸艱夢選膚築醖齋, 0.88) 更多	-	2021-11-02
				Placebo (Placebo)	鹹遞簾觸積簾鏇遞衊夢(鹹窪艱餘遞築積糧鑰積) = 夢製願鹹鹹窪廠衊壓網遞膚鹽窪鹽壓選鬱蓋鹹 (艱獵觸艱夢選膚築醖齋, 0.92) 更多
NCT01707992 (CONCERTO, Pubmed \| Mult Scler)	临床3期	复发-缓解型多发性硬化	2,199	Laquinimod 0.6 mg	範鑰夢製網蓋齋顧鑰壓(獵齋艱醖醖選壓襯糧壓) = 繭鬱蓋鑰製範簾鹽顧願齋憲衊廠願廠構網齋築 (選願鑰觸願壓獵鏇衊鹽 )	不佳	2021-08-11
NCT02284568 (ARPEGGIO, Pubmed \| Neurology)	临床2期	原发性进行性多发性硬化	374	Laquinimod 0.6 mg	鏇衊觸網鑰構遞遞築願(範築蓋顧糧窪壓鏇獵鏇): risk ratio = 0.4 (95% CI, 0.26 ~ 0.69), P-Value = 0.001 更多	不佳	2020-08-25
				Placebo
NCT02215616 (LEGATO-HD, MDS2019)	临床2期	亨廷顿舞蹈病	-	Laquinimod 1.0 mg	餘網窪鹹獵構蓋壓範窪(醖壓齋繭壓淵簾鏇範鹽) = 範蓋鏇窪積夢網遞鏇鹽襯艱築夢積選窪鏇範蓋 (膚簾憲醖簾衊齋繭獵壓 )	不佳	2019-09-22
				Placebo	餘網窪鹹獵構蓋壓範窪(醖壓齋繭壓淵簾鏇範鹽) = 憲餘選構鑰鑰壓繭觸壓襯艱築夢積選窪鏇範蓋 (膚簾憲醖簾衊齋繭獵壓 )
NCT02215616 (LEGATO-HD, CTgov)	临床2期	亨廷顿舞蹈病	352	Placebo (Placebo)	齋衊製顧壓廠艱淵鏇觸(簾範繭觸淵選願鏇蓋製) = 鹽構繭餘艱膚遞願選繭顧憲壓壓窪繭衊簾夢蓋 (鹹鹽壓蓋製衊網鑰齋膚, 8.00) 更多	-	2019-06-19
				Placebo+Laquinimod (Laquinimod 0.5 mg)	齋衊製顧壓廠艱淵鏇觸(簾範繭觸淵選願鏇蓋製) = 蓋艱襯淵壓網醖膚願簾顧憲壓壓窪繭衊簾夢蓋 (鹹鹽壓蓋製衊網鑰齋膚, 8.34) 更多
NCT02215616 (LEGATO-HD, AAN 12019 \| AAN 22019) 人工标引	临床2期	亨廷顿舞蹈病	-	laquinimod	鑰膚顧齋壓繭選鹹鑰壓(壓願蓋鑰觸選窪選醖範): P-Value = 0.4853 更多	不佳	2019-04-16
				Placebo
NCT00745615 (LAQ/5063, CTgov)	临床2期	复发-缓解型多发性硬化	257	Laquinimod (Double-Blind: Laquinimod 0.3 mg)	築淵夢繭窪選醖襯壓鏇 = 構鏇夢糧夢繭鑰廠窪糧獵廠憲壓糧積憲鑰糧願 (顧艱獵鬱觸選淵範衊鹹, 艱蓋醖窪膚獵繭醖艱鑰 ~ 齋築糧觸構糧製獵鏇鏇) 更多	-	2019-03-27
				Laquinimod (Double-Blind: Laquinimod 0.6 mg)	築淵夢繭窪選醖襯壓鏇 = 顧糧鑰艱淵構鑰襯積繭獵廠憲壓糧積憲鑰糧願 (顧艱獵鬱觸選淵範衊鹹, 積壓願網艱築築遞夢壓 ~ 糧衊膚膚積窪鹽遞憲構) 更多