Refanezumab(Refanezumab) - 药物靶点：MAG_专利_临床

概要

基本信息

药物类型

单克隆抗体

别名

Anti-MAG monoclonal antibody

+ [1]

靶点

MAG

作用方式

抑制剂

作用机制

MAG抑制剂(髓磷脂相关糖蛋白抑制剂)

治疗领域

神经系统疾病心血管疾病

在研适应症-

非在研适应症

短暂性脑缺血发作缺血性卒中脑卒中

原研机构

GSK Plc

在研机构-

非在研机构

GSK Plc

权益机构-

最高研发阶段终止临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构/序列

Sequence Code 319372583H

来源: *****

Sequence Code 17117615L

来源: *****

关联

6

项与 Refanezumab 相关的临床试验

NCT01808261

/ Terminated临床2期

Study MAG104615, a Proof of Concept Study for GSK249320 Versus Placebo in Stroke Patients

Study MAG104615, a Proof of Concept Study for GSK249320 versus placebo in Stroke Patients.

开始日期2013-05-18

申办/合作机构

GSK Plc

EUCTR2012-004494-23-DE

/ Not yet recruitingN/A

Study MAG104615, a Proof of Concept Study for GSK249320 versus placebo in Stroke Patients

开始日期2013-04-09

申办/合作机构

GlaxoSmithKline Research & Development Ltd.

EUCTR2010-024087-17-BE

/ Not yet recruiting临床2期

Study MAG104615, a Proof of Concept Study for GSK249320versus placebo in Stroke Patients - POC in patients with ischaemic stroke

开始日期2011-11-09

申办/合作机构

GlaxoSmithKline Research & Development Ltd.

100 项与 Refanezumab 相关的临床结果

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100 项与 Refanezumab 相关的转化医学

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100 项与 Refanezumab 相关的专利（医药）

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15

项与 Refanezumab 相关的文献（医药）

2017-12-01·Neurological Sciences4区 · 医学

Chronic demyelinating neuropathy with anti-myelin-associated glycoprotein antibody without any detectable M-protein

4区 · 医学

Article

作者: Tobisawa, Shinsuke ; Isozaki, Eiji ; Shimizu, Toshio ; Sakamoto, Yuki

Previous case reports and studies have shown that anti-myelin-associated glycoprotein (MAG) antibody can be detected in patients with polyneuropathy without any detectable M-protein. Nevertheless, the frequency of and related factors have not yet been adequately investigated. The objectives of this study are to examine the prevalence of anti-MAG antibody in patients with demyelinating neuropathy without M-protein and to determine their clinical characteristics. From January, 2004, to September, 2016, consecutive patients with chronic demyelinating neuropathy were recruited. Anti-MAG antibody presence was tested at the first evaluation. We determined the prevalence of anti-MAG antibody without M-protein among included patients and evaluated the clinical characteristics. A total of 44 patients were included in the present study (12 women; median age at first visit 60 years [interquartile range 47-67 years]; median duration between onset and first visit 9 months [3-26 months]). M-protein was found in eight patients (18%) at the first evaluation. Anti-MAG antibody was present in 2 of remaining 36 (5.6 [95% confidence interval 0-13.0] %) patients without M-protein. Patients with anti-MAG antibody exhibited slowly progressive and distal dominant neuropathy with elevated serum IgM levels and refractory to immunotherapy. There were no differences in clinical features between patients having anti-MAG antibody without M-protein, and those with M-protein. One patient with the anti-MAG antibody showed a delayed appearance of M-protein during a 4-year follow-up after diagnosis. The prevalence of the anti-MAG antibody in chronic demyelinating neuropathy without any detectable M-protein was 5.6%. Anti-MAG antibody may be detectable earlier than M-protein.

2017-03-01·Stroke1区 · 医学

Proof-of-Concept Randomized Trial of the Monoclonal Antibody GSK249320 Versus Placebo in Stroke Patients

1区 · 医学

Article

作者: Simeoni, Monica ; Thompson, Thomas R. ; Russell, Colleen K. ; Enney, Lori A. ; Cramer, Steven C.

Background and Purpose—One class of poststroke restorative therapy focuses on promoting axon outgrowth by blocking myelin-based inhibitory proteins such as myelin-associated glycoprotein. The purpose of the current study was to extend preclinical and clinical findings of GSK249320, a humanized monoclonal antibody to myelin-associated glycoprotein with disabled Fc region, to explore effects on motor outcomes poststroke.Methods—In this phase IIb double-blind, randomized, placebo-controlled study, patients at 30 centers with ischemic stroke 24 to 72 hours prior and gait deficits were randomized to 2 IV infusions of GSK249320 or placebo. Primary outcome measure was change in gait velocity from baseline to day 90.Results—A total of 134 subjects were randomized between May 2013 and July 2014. The 2 groups were overall well matched at baseline. The study was stopped at the prespecified interim analysis because the treatment difference met the predefined futility criteria cutoff; change in gait velocity to day 90 was 0.55±0.46 (mean±SD) in the GSK249320 group and 0.56±0.50 for placebo. Secondary end points including upper extremity function were concordant. The 2 IV infusions of GSK249320 were well tolerated. No neutralizing antibodies to GSK249320 were detected.Conclusions—GSK249320, within 72 hours of stroke, demonstrated no improvement on gait velocity compared with placebo. Possible reasons include challenges translating findings into humans and no direct evidence that the therapy reached the biological target. The antibody was well tolerated and showed low immunogenicity, findings potentially useful to future studies aiming to use a monoclonal antibody to modify activity in specific biological pathways to improve recovery from stroke.Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01808261.

2015-06-01·Stroke1区 · 医学

Effects of Postinfarct Myelin-Associated Glycoprotein Antibody Treatment on Motor Recovery and Motor Map Plasticity in Squirrel Monkeys

1区 · 医学

Article

作者: Cramer, Steven C. ; Nudo, Randolph J. ; Frost, Shawn B. ; Zoubina, Elena ; Plautz, Erik J. ; Barbay, Scott

Background and Purpose—New insights into the brain’s ability to reorganize after injury are beginning to suggest novel restorative therapy targets. Potential therapies include pharmacological agents designed to promote axonal growth. The purpose of this study was to test the efficacy of one such drug, GSK249320, a monoclonal antibody that blocks the axon outgrowth inhibition molecule, myelin-associated glycoprotein, to facilitate recovery of motor skills in a nonhuman primate model of ischemic cortical damage.Methods—Using a between-groups repeated-measures design, squirrel monkeys were randomized to 1 of 2 groups: an experimental group received intravenous GSK249320 beginning 24 hours after an ischemic infarct in motor cortex with repeated dosages given at 1-week intervals for 6 weeks and a control group received only the vehicle at matched time periods. The primary end point was a motor performance index based on a distal forelimb reach-and-retrieval task. Neurophysiological mapping techniques were used to determine changes in spared motor representations.Results—All monkeys recovered to baseline motor performance levels by postinfarct day 16. Functional recovery in the experimental group was significantly facilitated on the primary end point, albeit using slower movements. At 7 weeks post infarct, motor maps in the spared ventral premotor cortex in the experimental group decreased in area compared with the control group.Conclusions—GSK249320, initiated 24 hours after a focal cortical ischemic infarct, facilitated functional recovery. Together with the neurophysiological data, these results suggest that GSK249320 has a substantial biological effect on spared cortical tissue. However, its mechanisms of action may be widespread and not strictly limited to peri-infarct cortex and nearby premotor areas.

100 项与 Refanezumab 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	Refanezumab	-	DB14908

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
缺血性卒中	临床2期	德国	GSK Plc	2013-05-18
缺血性卒中	临床2期	加拿大	GSK Plc	2013-05-18
缺血性卒中	临床2期	美国	GSK Plc	2013-05-18
缺血性卒中	临床2期	英国	GSK Plc	2013-05-18
短暂性脑缺血发作	临床2期	加拿大	GSK Plc	2009-07-08
短暂性脑缺血发作	临床2期	美国	GSK Plc	2009-07-08
短暂性脑缺血发作	临床2期	德国	GSK Plc	2009-07-08
脑卒中	临床2期	美国	GSK Plc	2009-07-08
脑卒中	临床2期	德国	GSK Plc	2009-07-08
脑卒中	临床2期	加拿大	GSK Plc	2009-07-08

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临床结果

适应症

分期

评价

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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


NCT00833989 (MAG111539, CTgov)	临床2期	脑卒中 \| 短暂性脑缺血发作	42	PLACEBO	醖鬱鹽積顧獵齋窪齋願(選積鹽蓋網鑰遞衊構鑰) = 鹽遞廠壓願艱膚範構餘顧鏇獵淵遞鹹願繭膚鑰 (餘夢顧選廠鏇憲積夢觸, 鏇鹽觸構憲築觸膚獵顧 ~ 鏇鑰窪艱蓋獵獵鬱衊鏇) 更多	-	2017-10-16
NCT01808261 (104615, CTgov)	临床2期	缺血性卒中	134	Placebo	鹹憲壓醖鏇齋夢構選願(積艱顧繭鑰獵淵窪淵襯) = 簾衊製範構製夢廠夢遞鑰願繭憲鏇蓋築顧遞蓋 (壓糧鬱淵憲選憲範衊壓, 窪艱構顧鏇觸鹽鹽壓鏇 ~ 憲網鏇醖鹽築遞醖構鬱) 更多	-	2017-10-03
AAN2013	N/A	脑卒中 myelin-associated glycoprotein (MAG) \| S100β	42	GSK249320 1 mg/kg	襯簾積蓋壓襯網鑰淵醖(夢膚艱簾鑰遞廠夢糧糧) = 窪顧獵鏇積築糧壓簾網糧鹽選廠夢顧蓋齋構夢 (膚壓鬱顧積觸蓋積積齋 ) 更多	积极	2013-02-12
AAN2013	N/A	脑卒中 myelin-associated glycoprotein (MAG) \| S100β	42	GSK249320 5 mg/kg	襯簾積蓋壓襯網鑰淵醖(夢膚艱簾鑰遞廠夢糧糧) = 鬱廠窪膚襯鏇鹽鏇獵製糧鹽選廠夢顧蓋齋構夢 (膚壓鬱顧積觸蓋積積齋 ) 更多	积极	2013-02-12