Mavoglurant(Mavoglurant) - 药物靶点：mGluR5_在研适应症：物质滥用，戒酒，酒精使用障碍_专利_临床

概要

基本信息

药物类型

小分子化药

别名

AFQ-056、STP 7、STP7

靶点

mGluR5

作用机制

mGluR5 负变构调节剂(代谢型谷氨酸受体-5 负变构调节剂)

治疗领域

其他疾病肿瘤神经系统疾病

在研适应症

物质滥用戒酒酒精使用障碍+ [5]

非在研适应症

药物性运动障碍运动失调脆性X综合征+ [7]

原研机构

Novartis Pharma AG

在研机构

Stalicla SA初创企业

National Institute on Alcohol Abuse & Alcoholism

Novartis AG

+ [1]

非在研机构

Novartis Pharmaceuticals Corp.

Novartis Pharmaceuticals Canada, Inc.

最高研发阶段临床3期

首次获批日期-

最高研发阶段(中国)-

特殊审评孤儿药 (欧盟)

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结构

分子式C19H23NO3

InChIKeyZFPZEYHRWGMJCV-ZHALLVOQSA-N

CAS号543906-09-8

关联

31

项与 Mavoglurant 相关的临床试验

NCT06136195 / Recruiting临床2期IIT

Influence of Mavoglurant on Alcohol Craving and Drinking in Heavy Drinkers

The purpose of this research study is to find out about the effects of a drug called mavoglurant on alcohol consumption.

开始日期2024-07-01

申办/合作机构

Yale University

[+1]

NCT05203965 / Recruiting早期临床1期IIT

Functional Neuroimaging of Alcoholism Vulnerability: Probing Glutamate and Reward, Using the mGluR5 Inhibitor Mavoglurant

The purpose of this study is to evaluate the role of Mavoglurant in clarifying the neurobiology of alcoholism risk. This is a one-site, randomized, within subjects, counterbalanced double-blind study of a single dose (200mg) of Mavoglurant and placebo.

开始日期2022-05-17

申办/合作机构

Yale University

NCT04771143 / Withdrawn临床1期

A Randomized, Participant- and Investigator-blinded, Placebo-controlled, Parallel Group Study to Assess Safety, Tolerability, and Potential Interactions of Oral AFQ056 Given Concurrently With Cocaine

This is a study to assess safety, tolerability and interactions of AFQ056 and cocaine in patients with cocaine use disorder.

开始日期2021-07-21

申办/合作机构

Novartis Pharmaceuticals Canada, Inc.

[+1]

100 项与 Mavoglurant 相关的临床结果

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100 项与 Mavoglurant 相关的转化医学

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100 项与 Mavoglurant 相关的专利（医药）

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61

项与 Mavoglurant 相关的文献（医药）

2024-03-01·The Journal of clinical investigation

Effects of AFQ056 on language learning in fragile X syndrome

Article

作者: Cudkowicz, Merit ; Hagerman, Randi ; Veenstra-VanderWeele, Jeremy ; Harkey, Brittney ; Klingner, Elizabeth ; Berry-Kravis, Elizabeth ; Coffey, Christopher S ; Pearson, Brenda ; Abbeduto, Leonard ; Huff, Trevis ; Costigan, Michele ; Tassone, Flora ; Long, Jeff ; Erickson, Craig A ; Kaufmann, Walter E ; Fedler, Janel ; Staley, Kevin ; Ecklund, Dixie ; Klements, David ; Ethridge, Lauren ; Moshinsky, Michael ; Friedmann, Katherine ; Hoffmann, Anne ; McDuffie, Andrea ; Hessl, David ; Bullard, Lauren

BACKGROUNDFXLEARN, the first-ever large multisite trial of effects of disease-targeted pharmacotherapy on learning, was designed to explore a paradigm for measuring effects of mechanism-targeted treatment in fragile X syndrome (FXS). In FXLEARN, the effects of metabotropic glutamate receptor type 5 (mGluR5) negative allosteric modulator (NAM) AFQ056 on language learning were evaluated in 3- to 6-year-old children with FXS, expected to have more learning plasticity than adults, for whom prior trials of mGluR5 NAMs have failed.METHODSAfter a 4-month single-blind placebo lead-in, participants were randomized 1:1 to AFQ056 or placebo, with 2 months of dose optimization to the maximum tolerated dose, then 6 months of treatment during which a language-learning intervention was implemented for both groups. The primary outcome was a centrally scored videotaped communication measure, the Weighted Communication Scale (WCS). Secondary outcomes were objective performance-based and parent-reported cognitive and language measures.RESULTSFXLEARN enrolled 110 participants, randomized 99, and had 91 who completed the placebo-controlled period. Although both groups made language progress and there were no safety issues, the change in WCS score during the placebo-controlled period was not significantly different between the AFQ056 and placebo-treated groups, nor were there any significant between-group differences in change in any secondary measures.CONCLUSIONDespite the large body of evidence supporting use of mGluR5 NAMs in animal models of FXS, this study suggests that this mechanism of action does not translate into benefit for the human FXS population and that better strategies are needed to determine which mechanisms will translate from preclinical models to humans in genetic neurodevelopmental disorders.TRIAL REGISTRATIONClincalTrials.gov NCT02920892.FUNDING SOURCESNeuroNEXT network NIH grants U01NS096767, U24NS107200, U24NS107209, U01NS077323, U24NS107183, U24NS107168, U24NS107128, U24NS107199, U24NS107198, U24NS107166, U10NS077368, U01NS077366, U24NS107205, U01NS077179, and U01NS077352; NIH grant P50HD103526; and Novartis IIT grant AFQ056X2201T for provision of AFQ056.

2024-01-04·Brain : a journal of neurology

Inhibiting metabotropic glutamate receptor 5 after stroke restores brain function and connectivity

Article

作者: Kim, Byungchan ; Olsson, Roger ; Hakon, Jakob ; Ruscher, Karsten ; Moyanova, Slavianka ; Di Menna, Luisa ; Bauer, Adam Q ; Mastroiacovo, Federica ; Sjölund, Carin ; Wieloch, Tadeusz ; Quattromani, Miriana J ; Englund, Elisabet ; Nicoletti, Ferdinando ; Talhada, Daniela

Abstract:

Stroke results in local neural disconnection and brain-wide neuronal network dysfunction leading to neurological deficits. Beyond the hyper-acute phase of ischaemic stroke, there is no clinically-approved pharmacological treatment that alleviates sensorimotor impairments. Functional recovery after stroke involves the formation of new or alternative neuronal circuits including existing neural connections. The type-5 metabotropic glutamate receptor (mGluR5) has been shown to modulate brain plasticity and function and is a therapeutic target in neurological diseases outside of stroke. We investigated whether mGluR5 influences functional recovery and network reorganization rodent models of focal ischaemia.Using multiple behavioural tests, we observed that treatment with negative allosteric modulators (NAMs) of mGluR5 (MTEP, fenobam and AFQ056) for 12 days, starting 2 or 10 days after stroke, restored lost sensorimotor functions, without diminishing infarct size. Recovery was evident within hours after initiation of treatment and progressed over the subsequent 12 days. Recovery was prevented by activation of mGluR5 with the positive allosteric modulator VU0360172 and accelerated in mGluR5 knock-out mice compared with wild-type mice. After stroke, multisensory stimulation by enriched environments enhanced recovery, a result prevented by VU0360172, implying a role of mGluR5 in enriched environment-mediated recovery. Additionally, MTEP treatment in conjunction with enriched environment housing provided an additive recovery enhancement compared to either MTEP or enriched environment alone. Using optical intrinsic signal imaging, we observed brain-wide disruptions in resting-state functional connectivity after stroke that were prevented by mGluR5 inhibition in distinct areas of contralesional sensorimotor and bilateral visual cortices. The levels of mGluR5 protein in mice and in tissue samples of stroke patients were unchanged after stroke.We conclude that neuronal circuitry subserving sensorimotor function after stroke is depressed by a mGluR5-dependent maladaptive plasticity mechanism that can be restored by mGluR5 inhibition. Post-acute stroke treatment with mGluR5 NAMs combined with rehabilitative training may represent a novel post-acute stroke therapy.

2024-01-01·SAGE Open Medicine

Negative effect of treatment with mGluR5 negative allosteric modulator AFQ056 on blood biomarkers in young individuals with Fragile X syndrome

Article

作者: Gropman, Andrea ; Veenstra-VanderWeele, Jeremy ; Protic, Dragana ; Coffey, Christopher ; Hagerman, Randi ; Zafarullah, Marwa ; Cudkowicz, Merit ; Berry-Kravis, Elizabeth ; Tartaglia, Nicole ; Tassone, Flora ; Ashwood, Paul ; Durbin-Johnson, Blythe ; Erickson, Craig A ; Mendoza, Guadalupe ; Abbeduto, Leonard ; Lehwald, Lenora ; Breeze, Elizabeth ; Morris, Stephanie ; Maxwell-Horn, Angela ; Bennett, Amanda Palladino ; Prock, Lisa ; Filipink, Robin ; Talboy, Amy

Background::

Fragile X syndrome, with an approximate incidence rate of 1 in 4000 males to 1 in 8000 females, is the most prevalent genetic cause of heritable intellectual disability and the most common monogenic cause of autism spectrum disorder. The full mutation of the Fragile X Messenger Ribonucleoprotein-1 gene, characterized by an expansion of CGG trinucleotide repeats (>200 CGG repeats), leads to fragile X syndrome. Currently, there are no targeted treatments available for fragile X syndrome. In a recent large multi-site trial, FXLEARN, the effects of the mGluR5 negative allosteric modulator, AFQ056 (mavoglurant), were investigated, but did not show a significant impact of AFQ056 on language development in children with fragile X syndrome aged 3–6 years.

Objectives::

The current analyses from biospecimens collected in the FXLEARN study aimed to determine whether AFQ056 affects the level of potential biomarkers associated with Akt/mTOR and matrix metalloproteinase 9 signaling in young individuals with fragile X syndrome. Previous research has indicated that these biomarkers play crucial roles in the pathophysiology of fragile X syndrome.

Design::

A double-blind placebo-controlled parallel-group flexible-dose forced titration design.

Methods::

Blood samples for biomarkers were collected during the FXLEARN at baseline and subsequent visits (1- and 8-month visits). Biomarker analyses included fragile X messenger ribonucleoprotein-1 genotyping by Southern blot and PCR approaches, fragile X messenger ribonucleoprotein-1 mRNA levels determined by PCR, matrix metalloproteinase 9 levels’ detection using a magnetic bead panel, and targets of the Akt/mTOR signaling pathway with their phosphorylation levels detected.

Results::

This research revealed that administering AFQ056 does not affect the expression levels of the investigated blood biomarkers in young children with fragile X syndrome.

Conclusion::

Our findings of the lack of association between clinical improvement and biomarkers’ levels in the treatment group are in line with the lack of benefit observed in the FXLEARN study. These findings indicate that AFQ056 does not provide benefits as assessed by primary or secondary endpoints.

Registration::

ClincalTrials.gov NCT02920892.

12

项与 Mavoglurant 相关的新闻（医药）

2024-09-19

·GlobeNewswire-Health Care

Dr. Paulo Fontoura, MD, PhD, joins STALICLA as Chief Scientific and Clinical Development Advisor

Press Release Dr. Paulo Fontoura, MD, PhD, joins STALICLA as Chief Scientific and Clinical Development Advisor Geneva, Switzerland – September 19, 2024 – STALICLA SA, a Swiss neuro precision biotech company dedicated to developing precision medicine-based treatments for neurodevelopmental disorders, announced today that Dr. Paulo Fontoura will be joining their drug development team as Chief Scientific and Clinical Development Advisor. Dr. Fontoura will work to support STALICLA’s mission to transform the treatment landscape for neurodevelopmental disorders. Lynn Durham, CEO of STALICLA, said: “We are delighted and humbled to welcome Paulo to the STALICLA team. With his unparalleled insight and unique understanding of CNS drug development and neurodevelopmental disorders, he is strengthening STALICLA’s position as a pioneer in precision neuropsychiatry. Paulo’s expertise will be instrumental in helping us achieve our next milestones, notably our entry into two Phase 2 clinical trials in subgroups of patients with autism spectrum disorder (ASD), each with expected readouts in the coming 24 months.” Dr. Paulo Fontoura is a pioneer in innovative clinical development strategies. During his 16-year tenure at Roche, he served as the Global Head of Neuroscience Clinical Development; he was instrumental in the launch of several groundbreaking medications targeting neurological conditions, including Multiple Sclerosis (MS), Spinal Muscular Atrophy (SMA), and Neuromyelitis Optica Spectrum Disorder (NMOSD), as well as pioneering work on Alzheimer's, Parkinson's, Huntington's disease, and several psychiatric and neurodevelopmental disorders. Specifically, he and his team spearheaded the clinical development of new therapies for Fragile X, Down's and Angelman's syndromes, and the first pharmacological treatment for core symptoms of ASD which reached Phase 3 clinical trials in both adults and children. Additionally, his team co-led the Autism Innovative Medicine Studies (AIMS) including EU-AIMS and AIMS-2-TRIALS public private partnership. Dr. Fontoura has also had an illustrious academic career. He held multiple faculty positions at the New University of Lisbon and Stanford University, where he earned his MD and a PhD in Neuroimmunology and trained as a clinical neurologist. In recognition of his exceptional achievements in the field of neuroscience, he was elected as a Fellow of the American Academy of Neurology in 2022. He currently serves as a visiting professor at the New University of Lisbon and lectures at the European Center of Pharmaceutical Medicine in Basel. Paulo Fontoura MD, PhD, Chief Scientific and Clinical Development Advisor, said: “I am thrilled to join the STALICLA team and help them develop therapies for people with neurodevelopmental disorders. Their approach promises to bring real breakthroughs in this area of great medical need.” About STALICLA: STALICLA SA is a Swiss clinical-stage biopharmaceutical company, revolutionizing the treatment of neurodevelopmental disorders. The company has developed a clinically validated neuro precision development platform, successfully delivering stratified patient subgroups and advancing tailored treatment options. Its lead NDD asset, STP1, and a second NDD asset are set to enter Phase 2 trials with expected readouts within 24 months. STP7 (Mavoglurant), is also being advanced for Phase 3 trials, fully funded by the US government. For more information, please visit: www.stalicla.com. Contacts: STALICLA SALynn Durham Founder & Chief Executive Officerlynn.durham@stalicla.com Media & InvestorsChris MaggosCohesion Bureauchris.maggos@cohesionbureau.com+41 79 367 6254 Attachment 20240918 Paulo Fontoura PR_final

临床2期临床3期高管变更

2024-06-28

·GlobeNewswire-Health Care

STALICLA publishes pioneering phase 1b data on precision treatment for autism spectrum disorder in Biomedicines

STALICLA’s precision psychiatry study highlights strong EEG-based target engagement of STP1 treatment in defined subgroup of patients with autism and numerical improvement in core symptoms June 27, 2024 – STALICLA SA, a Swiss neuro precision biotech company dedicated to developing precision medicine-based treatments for neuropsychiatric and neurodevelopmental disorders, today announced the publication of a landmark phase 1b study with STP1, a novel combination therapy tailored for the treatment of a clinically and biologically defined subgroup of patients with autism spectrum disorder (ASD), named ASD Phenotype 1 (ASD-Phen1). The results of the study were published in the peer-reviewed journal Biomedicines, in an article titled “Safety, Tolerability, and EEG-Based Target Engagement of STP1 (PDE3,4 Inhibitor and NKCC1 Antagonist) in a Randomized Clinical Trial in a Subgroup of Patients with ASD”. Lynn Durham, CEO of STALICLA, highlighted: “This study marks a significant milestone in the advancement of precision medicine for ASD. It is a first-of-its-kind stratification-based approach for clinical development in neurodevelopmental disorders, demonstrating the potential of precision medicine in ASD.” The randomized, double-blind, placebo-controlled phase 1b clinical trial evaluated the safety and tolerability of STP1, a combination of ibudilast and bumetanide, in ASD-Phen1 patients. The clinical trial (registered at clinicaltrials.gov NCT04644003), involved two 14-day treatment phases of ASD-Phen1 patients receiving STP1 or placebo. The results showed that STP1 was well-tolerated with no significant adverse effects reported. Significant and dose-related reductions in gamma power were observed in the whole brains of patients taking STP1, particularly in regions associated with executive function and memory. Additionally, STP1 increased alpha 2 power in frontal and occipital regions, while improving habituation and neural synchronization to auditory chirps. Dr. Craig A. Erickson, Associate Professor, UC Department of Psychiatry and Behavioral Neuroscience, Cincinnati Children’s Hospital Medical Center, and the principal investigator of the study, remarked: “The electrophysiological signals from this study are remarkable and represent the strongest early trial target engagement signals our lab has seen in the autism field.” Dr. Laura Pérez-Cano, Head of Discovery at STALICLA and co-author of the study, added: “These findings not only highlight the potential of STP1 as a therapeutic option for ASD-Phen1 patients but also underscore the importance of combining biologically-based patient stratification with quantifiable outcome measures such as EEG that can then be correlated with behavioral measures.” By focusing on a biologically defined subgroup of ASD patients, STALICLA is moving closer to making personalized treatment options a reality for patients with ASD. This approach has the potential to revolutionize the treatment of ASD and other neuropsychiatric conditions. STALICLA is a global, clinical-stage biotechnology company focused on advancing precision medicine for brain disorders. The company has developed a unique neuro precision development platform, DEPI, supported by clinical validation in a first indication: Autism Spectrum Disorder. Its lead neurodevelopmental disorder asset, STP1, is entering Phase 2 trials. Its lead neuropsychiatry asset, STP7 (Mavoglurant), fully funded by the US government, will soon be Phase 3 ready for Cocaine Use Disorder. ‎ The content above comes from the network. if any infringement, please contact us to modify.

临床结果

2024-05-08

·GlobeNewswire-Health Care

STALICLA initiates U.S. Phase 3 enabling DDI study of STP7 (Mavoglurant) to treat cocaine use disorder

May 2, 2024 – STALICLA SA, a late-stage biotechnology company specializing in precision medicine for brain disorders, announces the First Patient First Visit (FPFV) for the company's drug-drug interaction (DDI) study of STP7 (Mavoglurant), an mGluR5 negative allosteric modulator, licensed to STALICLA by Novartis. The DDI study is the last regulatory requirement in a comprehensive Phase 2 program and completion is expected to trigger initiation of a Phase 3 study in the U.S. in 2025. Lynn Durham, CEO and Founder of STALICLA said, “This DDI study unlocks the opportunity under our Cooperative Research and Development Agreement with the U.S. NIH National Institute of Drug Abuse (NIDA) to begin Phase 3 trials for STP7 in 2025 to address the high unmet medical need of cocaine abuse globally. Results from successfully completed Phase 2 studies for cocaine use disorder (CUD) showed highly convincing and unprecedented efficacy results including increase in abstinence from cocaine use and reduction in co-morbid dependencies such as alcohol abuse with STP7 (Mavoglurant). In addition, STALICLA is investigating alternative therapeutic indications for STP7 (Mavoglurant) to benefit patients with other CNS conditions.” STP7 (Mavoglurant) is the most clinically advanced negative allosteric modulator of the glutamate receptor 5 (mGluR5 NAM). As well as its role in addiction pathophysiology, mGluR5 has been implicated in mood disorders and neurodevelopmental disorders such as Fragile X and autism spectrum disorder. Comprehensive clinical studies by Novartis of STP7 (Mavoglurant) to date have included over 1800 adults for up to 2 years, demonstrating good safety and tolerability and significant reduction in cocaine use and positioning STP7 (Mavoglurant) as a strong candidate therapy for substance use and other CNS disorders. STALICLA SA is a Swiss clinical-stage biopharmaceutical company, pioneering precision treatment in neurodevelopmental and neuropsychiatric disorders. Its AI-driven precision neuro medicine platform has allowed to identify two precision small molecule drug candidates for autism spectrum disorder, STP1 and STP2, both planned to enter Phase 2 trials in 2024. Following the in-licensing of Mavoglurant from Novartis in 2023, STALICLA has also established an advanced mGluR5 NAM platform offering multi-faceted late-stage clinical development opportunities broadening STALICLA’s scope to address wider CNS disease unmet needs. For more information, please visit: www.stalicla.com. The content above comes from the network. if any infringement, please contact us to modify.

临床3期临床结果

100 项与 Mavoglurant 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	Mavoglurant	-	DB13004

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
物质滥用	临床3期	美国	National Institute on Drug Abuse	2023-03-08
物质滥用	临床3期	美国	Stalicla SA初创企业	2023-03-08
脆性X综合征	临床3期	美国	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	澳大利亚	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	比利时	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	丹麦	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	法国	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	德国	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	以色列	Novartis Pharmaceuticals Corp.	2011-11-01
脆性X综合征	临床3期	意大利	Novartis Pharmaceuticals Corp.	2011-11-01

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临床结果

适应症

分期

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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


NCT03327792 (CTgov)	临床1期	致幻	34	Mavoglurant (200 mg Mavoglurant)	齋夢繭鑰憲衊鬱蓋積蓋(廠蓋鏇齋壓觸網鹽網鬱) = 積夢鬱艱憲鏇襯衊遞鹽積鹹淵膚鹽壓膚構鹽窪 (鑰築築顧鬱蓋壓艱鹽遞, 艱膚簾選廠積願襯艱糧 ~ 膚窪壓鹽糧構廠簾廠醖) 更多	-	2024-08-06
				Placebo (Placebo)	齋夢繭鑰憲衊鬱蓋積蓋(廠蓋鏇齋壓觸網鹽網鬱) = 夢廠壓衊範餘獵構築窪積鹹淵膚鹽壓膚構鹽窪 (鑰築築顧鬱蓋壓艱鹽遞, 鹽壓簾衊築獵廠憲糧選 ~ 鏇觸築鹹齋蓋艱糧鹹鏇) 更多
NCT02920892 (FX-LEARN, CTgov)	临床2期	脆性X综合征	110	placebo+AFQ056 (Placebo Comparator: Double-Blind Placebo With Language Intervention)	獵顧構醖獵鑰齋鏇窪膚(窪醖襯齋遞憲觸鏇遞獵) = 繭淵築鏇衊膚餘襯築簾壓範蓋鹹築鏇淵鏇鬱鹽 (鹽衊範網鏇簾製蓋網壓, 襯廠蓋獵蓋築膚願網構 ~ 廠網築壓壓顧網觸願壓) 更多	-	2023-10-10
				AFQ056 (Experimental: Double-Blind AFQ056 With Language Intervention)	獵顧構醖獵鑰齋鏇窪膚(窪醖襯齋遞憲觸鏇遞獵) = 願網襯構鹹顧顧選膚窪壓範蓋鹹築鏇淵鏇鬱鹽 (鹽衊範網鏇簾製蓋網壓, 網襯築窪網膚鹽淵淵製 ~ 獵鹽鏇願構鹹糧鹹壓簾) 更多
NCT03242928 (CTgov)	临床2期	可卡因相关疾病 \| 全身性肉碱缺乏症	68	AFQ056 (AFQ056)	鏇製鏇齋膚衊網餘餘齋(蓋選窪範顧窪選顧構鹹) = 願觸選簾選積淵鏇願鬱觸醖鏇衊壓鏇齋繭鏇壓 (顧膚觸鏇鬱獵願構製衊, 淵構襯遞艱網餘願獵淵 ~ 襯壓襯網網壓顧艱構艱) 更多	-	2021-02-04
				Placebo (Placebo)	鏇製鏇齋膚衊網餘餘齋(蓋選窪範顧窪選顧構鹹) = 積網夢壓衊簾繭糧廠壓觸醖鏇衊壓鏇齋繭鏇壓 (顧膚觸鏇鬱獵願構製衊, 艱鏇襯範繭獵鹽糧壓觸 ~ 鏇醖願蓋餘鬱窪憲鬱願) 更多
WPC	N/A	-	485	Mavoglurant (AFQ056)	簾廠鑰醖膚艱鹽艱淵鹹(鑰憲蓋醖壓窪鹹醖鑰網) = 網製憲鑰淵蓋淵遞構觸醖窪廠簾鬱憲簾獵築鹹 (蓋觸範憲醖遞衊襯廠鹽, -0.65 ~ 0.11) 更多	不佳	2019-06-03
				Placebo	簾廠鑰醖膚艱鹽艱淵鹹(鑰憲蓋醖壓窪鹹醖鑰網) = 壓鏇鬱壓築衊築範鑰醖醖窪廠簾鬱憲簾獵築鹹 (蓋觸範憲醖遞衊襯廠鹽, -0.09 ~ 0.66) 更多
NCT01348087 (Pubmed \| Sci Rep) 人工标引	临床2期	脆性X综合征	267	mavoglurant	觸膚窪醖遞鏇淵蓋製淵(遞廠選簾築繭築製製獵) = 夢窪選簾鏇膚壓憲壓繭顧壓願醖壓願觸網膚鹽 (壓糧膚窪醖憲鏇餘夢齋 ) 更多	不佳	2018-11-19
NCT01813019 (Pubmed \| Adv Ther) 人工标引	临床2期	强迫症	50	mavoglurant	醖鏇齋艱鹹簾網衊醖餘(鬱糧選構顧廠顧繭衊選) = 齋鏇膚鏇餘鹽襯鑰鏇壓壓積積鏇簾獵鏇範鏇獵 (廠廠顧範憲觸艱構夢繭 ) 更多	不佳	2017-02-01
				Placebo	醖鏇齋艱鹹簾網衊醖餘(鬱糧選構顧廠顧繭衊選) = 鑰鹹醖網蓋糧顧艱鑰簾壓積積鏇簾獵鏇範鏇獵 (廠廠顧範憲觸艱構夢繭 ) 更多
NCT01813019 (CTgov)	临床2期	强迫症	50	Placebo (Placebo)	製膚窪壓窪鹽襯糧鏇艱(築窪鹹構艱廠衊鏇築鏇) = 憲觸艱窪鹹醖廠鏇願醖製鏇鏇鹽齋廠鹽憲廠壓 (範觸襯膚鬱衊襯構鹽選, 構網積積繭願壓製獵簾 ~ 艱築餘簾顧遞憲廠齋夢) 更多	-	2016-07-21
				AFQ056 (AFQ056)	製膚窪壓窪鹽襯糧鏇艱(築窪鹹構艱廠衊鏇築鏇) = 鬱遞願顧鬱衊製齋構蓋製鏇鏇鹽齋廠鹽憲廠壓 (範觸襯膚鬱衊襯構鹽選, 選衊膚構糧簾廠鹹鏇鏇 ~ 鑰窪築糧糧顧衊顧衊網) 更多
NCT01385592 (Pubmed) 人工标引	临床2期	药物性运动障碍 \| 帕金森病	-	Mavoglurant	鑰鹽夢糧獵鬱顧觸顧壓(願選遞顧觸觸壓醖繭選) = did not reach statistical significance 鹹鏇糧願鑰襯膚窪範襯 (網網鬱製鹽憲壓糧鏇艱 )	不佳	2016-07-01
				Placebo
NCT01253629 (Pubmed \| Sci Transl Med) 人工标引	临床2期	脆性X综合征	314	Mavoglurant	淵鹽憲顧築壓蓋觸糧鹹(壓醖鬱選襯選簾襯遞襯) = Neither of the studies achieved 繭鏇構簾遞夢簾簾網蓋 (窪網壓廠網窪遞窪窪膚 )	不佳	2016-01-13
				Placebo
NCT01357239 (CTgov)	临床2期	脆性X综合征	139	Placebo	廠餘網窪衊廠鹹選窪構(積構夢壓顧遞觸壓遞淵) = 襯窪製蓋繭蓋鏇襯鹹鏇遞醖網遞淵膚鏇鏇獵廠 (繭鏇範獵鹹獵選艱簾鹹, 鬱蓋廠獵鬱鏇積齋鬱鑰 ~ 膚積糧鏇顧窪淵醖艱範) 更多	-	2015-05-12