Revacept, a Novel Inhibitor of Platelet Adhesion in Patients With Stable Coronary Artery Disease Undergoing Elective Percutaneous Coronary Interventions: a Phase II, Multicentre, Randomised, Double-blind and Placebo-controlled Study

The main objective is to evaluate the efficacy and safety of treatment with 2 doses (80 and 160 mg) of Revacept versus placebo in patients with stable coronary artery disease undergoing PCI.

开始日期2017-11-20

申办/合作机构

Deutsches Herzzentrum Berlin

[+4]

NCT01645306 / Completed临床2期

Revacept, an Inhibitor of Platelet Adhesion in Symptomatic Carotid Stenosis: A Phase II, Multicentre; Randomised, Dose-finding, Double-blind and Placebo Controlled Superiority Study With Parallel Groups

Patients suffering from symptomatic carotid artery stenosis, transient ischemic attacks (TIAs), amaurosis fugax or stroke receive either Revacept (single dose) plus antiplatelet monotherapy or monotherapy alone.
Patients receive a single dose of trial medication by intravenous infusion for 20 minutes. Patients are followed up one and three days after treatment, at 3 months and by a telephone interview at 12 months.

开始日期2013-03-08

申办/合作机构

advanceCOR GmbH

NCT01042964 / Completed临床1期

An Open-Label, Dose-Escalating Safety and Pharmacokinetic Study of an Acute Intravenous Administration of PR-15, an Inhibitor of Platelet Adhesion, in Six Different Strengths in Healthy Male Volunteers

Primary objective:
To evaluate safety and tolerability, adverse events (AEs), vital signs, ECG, bleeding time, evaluation of antibody titer and safety laboratory tests
Secondary objectives:
To evaluate the pharmacokinetics and pharmacodynamics (platelet aggregation)of six ascending single intravenous doses of PR-15 in healthy volunteers

开始日期2006-03-01

申办/合作机构

advanceCOR GmbH

[+1]

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2024-11-01·Arteriosclerosis, Thrombosis, and Vascular Biology

GP VI–Mediated Platelet Activation and Procoagulant Activity Aggravate Inflammation and Aortic Wall Remodeling in Abdominal Aortic Aneurysm

Article

作者: Grandoch, Maria ; Münch, Götz ; Krott, Kim J. ; Chatterjee, Madhumita ; Elvers, Margitta ; Bosbach, Agnes ; Goebel, Silvia ; Krüger, Evelyn ; Krüger, Irena ; Feige, Tobias ; Schelzig, Hubert ; Ortscheid, Julia ; Mulorz, Joscha ; Salehzadeh, Niloofar ; Wagenhäuser, Markus U. ; Ibing, Wiebke

BACKGROUND:Platelets play an important role in cardiovascular and cerebrovascular diseases. Abdominal aortic aneurysm (AAA) is a highly lethal, atherosclerosis-related disease with characteristic features of progressive dilatation of the abdominal aorta and degradation of the vessel wall, accompanied by chronic inflammation. Platelet activation and procoagulant activity play a decisive role in the AAA pathology as they might trigger AAA development in both mice and humans.METHODS:The present study investigated the impact of the major platelet collagen receptor GP (platelet glycoprotein) VI in pathophysiological processes underlying AAA initiation and progression. For experimental AAA induction in mice, PPE (porcine pancreatic elastase) and the external PPE model were used.RESULTS:Genetic deletion of GP VI offered protection of mice against aortic diameter expansion in experimental AAA. Mechanistically, GP VI deficiency resulted in decreased inflammation with reduced infiltration of neutrophils and platelets into the aortic wall. Furthermore, remodeling of the aortic wall was improved in the absence of GP VI, as indicated by reduced MMP (matrix metalloproteinase)-2/9 and OPN (osteopontin) plasma levels and an enhanced α-SMA (α-smooth muscle actin) content within the aortic wall, accompanied by reduced cell apoptosis. Consequently, an elevation in intima/media thickness and elastin content was observed in GP VI–deficient PPE mice, resulting in a significantly reduced aortic diameter expansion and reduced aneurysm incidence. In patients with AAA, enhanced plasma levels of soluble GP VI and fibrin, as well as fibrin accumulation within the intraluminal thrombus might serve as new biomarkers to detect AAA early. Moreover, we hypothesize that GP VI might play a role in procoagulant activity and thrombus stabilization via binding to fibrin.CONCLUSIONS:In conclusion, our results emphasize the potential need for a GP VI–targeted antiplatelet therapy to reduce AAA initiation and progression, as well as to protect patients with AAA from aortic rupture.

2024-05-27·Endocrinology

Mapping Thyroid Changes in Size and Position During Enlargement in Adult Mice With Hyperthyroidism

Article

作者: Cho, Yi-Li ; Wenhart, Clara ; Reimann, Andreas ; Li, Zhongmin ; Muench, Goetz ; Goebel, Silvia

AbstractThe thyroid in Graves’ disease undergoes a considerable divergence in size and position from the normal anatomy. However, knowledge of the pathological anatomy related to the change, which is required before planned surgical or local intervention, or diagnosis, is neglected. To investigate Graves’ disease, we established a model of mice that successfully mimicked all the signs presented in the clinic. Under a long-term immunization (35 weeks), the animals displayed large heterogeneity in thyroid size, such as the cases of natural occurrence. These thyroids in the model were sized into various phases and registered. A blend of the registered thyroids and the thyroid and tracheal cartilage landmarks led to the production of site-dependent incidence graphs of thyroid in the front view and on the section for each phase. The merger of the incidence graphs of all the phases resulted in thyroid phase-dependent topography. The depicted graphs illustrate the fine localization of the thyroid in various sizes and their dynamic changes during enlargement, which may facilitate currently used fine-needle aspiration biopsy and ultrasonography-guided biopsy techniques. Familiarity with this knowledge might avoid misclassifying an abnormality as normal, or vice versa, and be helpful for imaging diagnosis and local surgery therapy in Graves’ disease.

2024-04-01·Thrombosis and Haemostasis

Plasma Soluble Glycoprotein VI, Platelet Function, Bleeding, and Ischemic Events in Patients Undergoing Elective Percutaneous Coronary Intervention

Article

作者: Massberg, Steffen ; Ndrepepa, Gjin ; Holdenrieder, Stefan ; Mayer, Katharina ; Bernlochner, Isabell ; Laugwitz, Karl-Ludwig ; Bongiovanni, Dario ; Adler, Kristin ; Hein-Rothweiler, Ralph ; Gawaz, Meinrad ; Lahu, Shqipdona ; Kastrati, Adnan ; Schüpke, Stefanie ; Münch, Götz ; Schunkert, Heribert

Background and Aims Glycoprotein VI (GPVI) is the major platelet-specific collagen receptor. GPVI shedding with generation of soluble GPVI (sGPVI) is an endogenous feedback mechanism preventing platelet overstimulation. sGPVI has not been investigated in patients with chronic coronary syndrome (CCS) undergoing percutaneous coronary intervention (PCI), especially regarding its potential value as a predictor of ischemic and bleeding risk. Methods Baseline plasma sGPVI levels were available in 318 patients with CCS undergoing PCI. Platelet function was assessed by measuring both adenosine diphosphate (ADP) and collagen-induced platelet aggregation. Co-primary endpoints were a composite of death or myocardial injury at 48 hours after PCI, and Bleeding Academic Research Consortium (BARC) type 1 to 5 bleeding at 30 days. Results There was no significant correlation between sGPVI and platelet function at baseline or at 48 hours after PCI and loading with antiplatelet drugs. Baseline plasma sGPVI levels were not associated with the ischemic risk: the incidence of the ischemic endpoint was 25.0% in the lower, 22.9% in the middle, and 26.7% in the upper sGPVI tertile (p = 0.82). There was a significant nonlinear relationship between sGPVI and the risk of bleeding: the incidence of the bleeding endpoint was 11.8% in the lower, 12.6% in the middle, and 26.4% in the upper sGPVI tertile (p = 0.006). Conclusion In patients with CCS undergoing PCI, plasma levels of sGPVI did not correlate with ADP- or collagen-induced platelet aggregation. Patients with higher baseline levels of sGPVI may carry an increased risk of bleeding at 30 days after PCI but no excess risk of ischemic events.

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药物(靶点)	适应症	全球最高研发状态

COR-5 ( GPVI )	脑卒中更多	临床前
COR-3 ( CD133 x GPVI )	急性冠状动脉综合征更多	终止
COR-2 ( CD68 )	动脉粥样硬化更多	终止
GPVI-CD39	冠状动脉疾病更多	无进展
Dimeric glycoprotein VIFc(Corimmun) ( GPVI )	脑卒中更多	无进展