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

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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90

项与 Refanezumab 相关的文献（医药）

2025-01-01·Neurology Neuroimmunology & Neuroinflammation

The Role of Complement Activation in IgM M-Protein–Associated Neuropathies

Article

作者: Vrancken, Alexander F.J.E. ; van der Pol, W. Ludo ; Dijkxhoorn, Kim ; Budding, Kevin ; van de Mortel, Johannes P.M. ; Minnema, Monique C. ; Notermans, Nicolette C.

BACKGROUND AND OBJECTIVESPolyneuropathy associated with an immunoglobulin M (IgM) monoclonal gammopathy is characterized by slowly progressive, predominantly distal sensorimotor deficits, sensory ataxia, and electrophysiologic features of demyelination. IgM antibodies against myelin-associated glycoprotein (MAG) are present in serum from most patients. Nerve damage most likely results from the concerted action of binding of anti-MAG antibodies to nerves, followed by complement activation. The interaction of anti-MAG antibodies with complement activation and their relation to clinical characteristics have not been studied in detail. We studied the correlation among anti-MAG antibody titers, complement activation, and IgM-associated polyneuropathy disease severity.METHODSWe used serum samples from 101 patients with IgM-associated polyneuropathy to assess IgM anti-MAG titers by ELISA and antibody-mediated complement deposition using both an ELISA-based system and a cell-based system of primate peripheral nerve slides. We studied correlations of complement activation with anti-MAG ELISA titers and clinical characteristics.RESULTSIgM anti-MAG titers varied from negative to strongly positive. Complement deposition in the ELISA-based system correlated significantly with anti-MAG antibody titer (Spearman rho 0.80; p < 0.0001) despite large variability between serum samples with comparable anti-MAG titers. This variability was even larger in the cell-based assay, which also showed complement deposition in IgM anti-MAG negative patients, indicating the presence of autoantibodies directed against epitopes other than MAG in a subset of patients with IgM-associated polyneuropathy. Clinical characteristics did not correlate with anti-MAG titers or complement activation.DISCUSSIONAnti-MAG antibody titers correlate with the level of complement activation in both ELISA and cell-based systems. However, clinical characteristics of IgM-associated polyneuropathy do not or only weakly correlate with titers or the level of complement deposition. The lack of clear correlations between complement activation and clinical characteristics does, at this stage, not support the use of complement inhibitors in the treatment of IgM-associated polyneuropathy.

2024-01-01·British Journal of Haematology

Clinical and clonal characteristics of monoclonal immunoglobulin M‐associated type I cryoglobulinaemia

Article

作者: Gupta, Rajeev ; Vos, Josephine M I ; Patel, Aisha ; Kwakernaak, Arjan J ; D'Sa, Shirley ; Japzon, Nicole ; Kyriakou, Charalampia ; Wechalekar, Ashutosh D ; Khwaja, Jahanzaib ; Rismani, Ali ; Salter, Simon ; Pluimers, Tessa E

SummaryMonoclonal immunoglobulin M‐associated type I cryoglobulinaemia is poorly characterised. We screened 534 patients with monoclonal IgM disorders over a 9‐year period and identified 134 patients with IgM type I cryoglobulins. Of these, 76% had Waldenström macroglobulinaemia (WM), 5% had other non‐Hodgkin lymphoma (NHL) and 19% had IgM monoclonal gammopathy of undetermined significance (MGUS). Clinically relevant IgM‐associated disorders (including cold agglutinin disease [CAD], anti‐MAG antibodies, amyloidosis and Schnitzler syndrome) coexisted in 31%, more frequently in MGUS versus WM/NHL (72% vs. 22%/29%, p < 0.001). The majority of those with cryoglobulins and coexistent CAD/syndrome had the molecular characteristics of a CAD clone (wild‐type MYD88 in 80%). A half of all patients had active manifestations at cryoglobulin detection: vasomotor (22%), cutaneous (16%), peripheral neuropathy (22%) and hyperviscosity (9%). 16/134 required treatment for cryoglobulin‐related symptoms alone at a median of 38 days (range: 6–239) from cryoglobulin detection. At a median follow‐up of 3 years (range: 0–10), 3‐year cryoglobulinaemia‐treatment‐free survival was 77% (95% CI: 68%–84%). Age was the only predictor of overall survival. Predictors of cryoglobulinaemia‐related treatment/death were hyperviscosity (HR: 73.01; 95% CI: 15.62–341.36, p < 0.0001) and cutaneous involvement (HR: 2.95; 95% CI: 1.13–7.71, p = 0.028). Type I IgM cryoglobulinaemia is more prevalent than previously described in IgM gammopathy and should be actively sought.

2023-02-01·European Journal of Neurology2区 · 医学

A diagnostic score for anti‐myelin‐associated‐glycoprotein neuropathy or chronic inflammatory demyelinating polyradiculoneuropathy in patients with anti‐myelin‐associated‐glycoprotein antibody

2区 · 医学

Article

作者: Bianchi, Elisa ; Marfia, Girola A. ; Cocito, Dario ; Doneddu, Pietro E. ; Giannotta, Claudia ; Briani, Chiara ; Cosentino, Giuseppe ; Ruiz, Marta ; Nobile‐Orazio, Eduardo ; Benedetti, Luana ; Filosto, Massimiliano ; Liberatore, Giuseppe ; Manganelli, Fiore

AbstractBackground and purposeA diagnostic score was developed to discriminate anti‐myelin‐associated‐glycoprotein (MAG) neuropathy from chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and applied it to patients with atypical anti‐MAG neuropathy.MethodsThe clinical and electrophysiological features of patients with a diagnosis of typical anti‐MAG neuropathy were compared to those of patients with a diagnosis of CIDP. The association of each feature with the diagnosis was assessed in the two groups. Features showing a significant association with the diagnosis were included in a multivariable logistic regression model and adjusted odds ratios were estimated for each feature. A score ranging from 1 to 3 was applied to each feature based on the magnitude of the estimated odds ratios. The score was then applied to patients with a clinical diagnosis of CIDP who also had high anti‐MAG antibody titers (CIDP‐MAG).ResultsThirty‐one anti‐MAG neuropathy patients, 45 typical CIDP patients and 16 CIDP‐MAG patients were included. Scores in anti‐MAG antibody patients ranged from 1 to 5 and in CIDP patients from −7 to −1. Using the score, 4/16 CIDP‐MAG patients were diagnosed to have anti‐MAG neuropathy and 12/16 patients to have CIDP. Response to intravenous immunoglobulin in the CIDP‐MAG patients classified as CIDP was similar to that of definite CIDP patients and higher than that of anti‐MAG neuropathy patients.ConclusionsOur score allowed an accurate discrimination to be made, amongst patients with anti‐MAG antibodies, of those affected by CIDP and the patients with anti‐MAG neuropathy. This score may help proper treatment to be chosen for patients with anti‐MAG antibodies with a CIDP‐like presentation.

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	英国	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	加拿大	GSK Plc	2013-05-18
短暂性脑缺血发作	临床2期	德国	GSK Plc	2009-07-08
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
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
脑卒中	临床2期	美国	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	窪餘餘齋蓋築蓋遞醖蓋(鏇鹹鹹鑰艱膚鹽選鹹積) = 醖餘製範顧鹹壓繭網鑰範獵憲醖顧壓醖夢選齋 (鑰製築餘獵夢膚廠蓋製, 鑰獵窪鏇鹹夢範鹽鬱願 ~ 齋製齋鑰獵衊鏇觸蓋襯) 更多	-	2017-10-16
NCT01808261 (104615, CTgov)	临床2期	缺血性卒中	134	Placebo	鏇鑰鹹壓鑰築襯艱願齋(鏇鬱繭選鏇襯網壓獵鑰) = 積製衊壓醖繭醖鏇醖觸觸獵鬱範鬱鑰膚鏇網構 (鏇襯積鏇窪繭夢襯觸艱, 鹽醖範鏇簾網蓋繭夢網 ~ 網鹹築願蓋鏇鹹繭餘衊) 更多	-	2017-10-03
AAN2013	N/A	脑卒中 myelin-associated glycoprotein (MAG) \| S100β	42	GSK249320 1 mg/kg	淵鏇構鬱壓範壓艱淵獵(遞鹹齋顧範艱壓選壓顧) = 顧醖壓鏇選衊憲廠鏇網襯鹽顧觸獵範鑰膚廠鏇 (鬱網艱鬱遞構製齋觸衊 ) 更多	积极	2013-02-12
AAN2013	N/A	脑卒中 myelin-associated glycoprotein (MAG) \| S100β	42	GSK249320 5 mg/kg	淵鏇構鬱壓範壓艱淵獵(遞鹹齋顧範艱壓選壓顧) = 齋憲鏇選遞憲獵衊衊淵襯鹽顧觸獵範鑰膚廠鏇 (鬱網艱鬱遞構製齋觸衊 ) 更多	积极	2013-02-12