更新于：2024-11-01

CD133 x GPVI

更新于：2024-11-01

基本信息

关联

项与 CD133 x GPVI 相关的药物

COR-3

靶点

CD133 x GPVI

作用机制

CD133调节剂 [+1]

在研机构-

原研机构

Corimmun GmbH

在研适应症-

非在研适应症

急性冠状动脉综合征 [+1]

最高研发阶段终止

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CD133 x GPVI 相关的临床结果

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100 项与 CD133 x GPVI 相关的转化医学

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0 项与 CD133 x GPVI 相关的专利（医药）

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项与 CD133 x GPVI 相关的文献（医药）

2012-06-01·Journal of Thrombosis and Haemostasis2区 · 医学

The recombinant bifunctional protein αCD133–GPVI promotes repair of the infarcted myocardium in mice

2区 · 医学

Article

作者: Heidrun Degen ; G. Münch ; M. Ungerer ; M. Elvers ; M. Gawaz ; Tanja Schönberger ; B. Schmid-Horch ; Yvonne Baumer ; A. Perk ; Carmen Ochmann ; Christoph Leder ; Melanie Ziegler ; B. Schlosshauer

BACKGROUNDBone-marrow-derived progenitor cells are important in myocardial repair mechanisms following prolonged ischemia. Cell-based therapy of diseased myocardium is limited by a low level of tissue engraftment.OBJECTIVESThe aim of this study was the development of the bifunctional protein αCD133-glycoprotein (GP)VI as an effective treatment for supporting vascular and myocardial repair mechanisms.RESULTSWe have generated and characterized a bifunctional molecule (αCD133-GPVI) that binds both to the subendothelium of the injured microvasculature and to CD133(+) progenitor cells with high affinity. αCD133-GPVI enhances progenitor cell adhesion to extracellular matrix proteins and differentiation into mature endothelial cells. In vivo studies showed that αCD133-GPVI favors adhesion of circulating progenitor cells to the injured vessel wall (intravital microscopy). Also, treatment of mice undergoing experimental myocardial infarction with αCD133-GPVI-labeled progenitor cells reduces infarction size and preserves myocardial function.CONCLUSIONSThe bifunctional trapping protein αCD133-GPVI represents a novel and promising therapeutic option for limiting heart failure of the ischemic myocardium.

2010-07-01·Journal of Molecular Medicine2区 · 医学

Capture of endothelial progenitor cells by a bispecific protein/monoclonal antibody molecule induces reendothelialization of vascular lesions

2区 · 医学

Article

作者: Hannah Schnell ; Alexandra Gauß ; Hans-Jörg Bühring ; Konstantinos Stellos ; Marc van Zandvoort ; Gundram Jung ; Stefanie Dimmeler ; Andreas E. May ; Michael Schumm ; Karin Klingel ; Sabine Conrad ; Peter Lang ; Martin Schaller ; Thomas Skutella ; Harald F. Langer ; Jürgen W. von der Ruhr ; Tanja Schoenberger ; Ramona Hafner ; Karin Daub ; Meinrad Gawaz

Tissue injury is inevitably accompanied by disruption of the endothelium and exposure of the subendothelial matrix. To generate a guidance molecule directing progenitor cells to sites of vascular lesions, we designed a bifunctional protein. The protein consists of the soluble platelet collagen receptor glycoprotein VI and an antibody to CD133 (hereafter called GPVI-CD133). In vitro and in vivo, this construct substantially mediates endothelial progenitor cell (EPC) homing to vascular lesions. Exposure of EPCs to GPVI-CD133 did not impair their capability to differentiate toward mature endothelial cells as verified by the formation of colony-forming units, the upregulation of endothelial markers CD31 and CD146 analyzed by flow cytometry or von Willebrand factor and endoglin assessed by immunofluorescence microscopy, as well as the presence of Weibel-Palade bodies using transmission electron microscopy. In vivo, GPVI-CD133 augments reendothelialization of vascular lesions. Thus, this bifunctional protein could be a potential new therapeutic option for cardiovascular diseases.

European Heart Journal1区 · 医学

Expression of stromal-cell-derived factor-1 on circulating platelets is increased in patients with acute coronary syndrome and correlates with the number of CD34+ progenitor cells

1区 · 医学

Article

作者: Annika Schad ; Tobias Geisler ; Harald Langer ; Iris Müller ; Dimitrios Stakos ; Stephan Lindemann ; Boris Bigalke ; Andreas Kögel ; Patrick Htun ; Meinrad Gawaz ; Konstantinos Stellos ; Florian Pfaff ; Peter Seizer

AIMSPrevious experimental studies have suggested that platelet stromal-cell-derived factor-1 (SDF-1) regulates mobilization and recruitment of haematopoietic progenitor cells supporting revascularization in mice. However, there are no clinical data available regarding platelet-bound SDF-1 in patients with acute coronary syndrome (ACS). The objective of this study was to evaluate the platelet-surface expression of SDF-1 in patients with ACS.METHODS AND RESULTSPatients with ACS (n = 418) showed a significantly enhanced SDF-1 expression on admission compared with those with stable angina pectoris (SAP, n = 486) [SAP (mean fluorescence intensity (MFI) +/- SD): 13.48 +/- 5.27; ACS: 18.45 +/- 12.85; P < 0.001) independent of cardiovascular risk factors and medication. Enhanced platelet-bound SDF-1 expression was found in patients with reduced left ventricular ejection fraction (LVEF <55%) in comparison to patients with normal LVEF (P = 0.005). Platelet-bound SDF-1 expression positively correlated with the degree of platelet activation [CD62P: r = 0.325; glycoprotein VI (GPVI): r = 0.277; PAC-1: r = 0.501; P < 0.001 for all] and showed a significant, but slight association with plasma levels of SDF-1 (r = 0.084; P = 0.045). In a subgroup of patients with coronary artery disease, platelet-bound SDF-1, but not other platelet activation markers, significantly correlated with the number of circulating CD34(+) progenitor cells (r = 0.252; P = 0.002) or CD34(+)/CD133(+) endothelial progenitor cells (r = 0.352; P = 0.008).CONCLUSIONPlatelet-bound SDF-1 may play an important role in peripheral homing of circulating progenitor cells thus in tissue regeneration.