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Last Updated: March 29, 2024

CLINICAL TRIALS PROFILE FOR ANTI-INHIBITOR COAGULANT COMPLEX


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All Clinical Trials for anti-inhibitor coagulant complex

Trial ID Title Status Sponsor Phase Start Date Summary
NCT00457951 ↗ A Study Designed to Evaluate ODSH in Subjects With Exacerbations of COPD Terminated Cantex Pharmaceuticals Phase 2 2007-04-01 The purpose of this study is to determine whether ODSH, when added to conventional treatment, is more effective in treating COPD exacerbations than conventional therapy alone.
NCT00457951 ↗ A Study Designed to Evaluate ODSH in Subjects With Exacerbations of COPD Terminated Chimerix Phase 2 2007-04-01 The purpose of this study is to determine whether ODSH, when added to conventional treatment, is more effective in treating COPD exacerbations than conventional therapy alone.
NCT00901563 ↗ Gap Junction Potentiation of Endothelial Function With Rotigaptide Completed Chief Scientist Office of the Scottish Government N/A 2009-03-01 Hypothesis - Rotigaptide will improve endothelial function in the context of endothelial dysfunction. The lining of blood vessels (endothelium) can react to hormones in the blood stream causing the blood vessel muscle to relax (vasodilatation) and allow more blood to flow. The nitric oxide and prostacyclin pathways are well documented in this process. However, evidence points to the existence of a third powerful relaxant called endothelium derived hyperpolarising factor (EDHF) but its identity and mechanism of action have proved elusive. As well as causing blood vessels to relax and more blood to flow, EDHF may be involved in the endothelium signaling, triggering release of a specialised clot dissolving factor called tissue plasminogen activator (t PA). t PA is important to ensure small clots, which are constantly being formed in the circulation, are rapidly dissolved and do not grow large enough to cause heart attacks and strokes. Evidence points towards the requirement for 'gap junctions' in the mediation of EDHF responses. Gap junctions are specialised pores which allow small molecules and charge to pass between cells. They are found between endothelial cells and the underlying muscle of the blood vessel. A drug called Rotigaptide has been developed to cause gap junctions to open. It has been safely administered in healthy volunteers and is now in a Phase II drug trial. By opening gap junctions the investigators hypothesise that it could increase EDHF mediated activity and vasodilatation. It represents a useful tool with which to examine the role of gap junctions in EDHF activity in vivo. Previously the investigators have demonstrated that rotigaptide does not contribute to endothelial function in healthy volunteers. The investigators now wish to examine the effect of rotigaptide in conditions of endothelial dysfunction. By limiting the blood flow to the arm for 20mins the ability of the blood vessel to vasodilate is impaired. By administering an intra-arterial rotigaptide infusion the investigators want to assess any functional preservation.
NCT00901563 ↗ Gap Junction Potentiation of Endothelial Function With Rotigaptide Completed NHS Lothian N/A 2009-03-01 Hypothesis - Rotigaptide will improve endothelial function in the context of endothelial dysfunction. The lining of blood vessels (endothelium) can react to hormones in the blood stream causing the blood vessel muscle to relax (vasodilatation) and allow more blood to flow. The nitric oxide and prostacyclin pathways are well documented in this process. However, evidence points to the existence of a third powerful relaxant called endothelium derived hyperpolarising factor (EDHF) but its identity and mechanism of action have proved elusive. As well as causing blood vessels to relax and more blood to flow, EDHF may be involved in the endothelium signaling, triggering release of a specialised clot dissolving factor called tissue plasminogen activator (t PA). t PA is important to ensure small clots, which are constantly being formed in the circulation, are rapidly dissolved and do not grow large enough to cause heart attacks and strokes. Evidence points towards the requirement for 'gap junctions' in the mediation of EDHF responses. Gap junctions are specialised pores which allow small molecules and charge to pass between cells. They are found between endothelial cells and the underlying muscle of the blood vessel. A drug called Rotigaptide has been developed to cause gap junctions to open. It has been safely administered in healthy volunteers and is now in a Phase II drug trial. By opening gap junctions the investigators hypothesise that it could increase EDHF mediated activity and vasodilatation. It represents a useful tool with which to examine the role of gap junctions in EDHF activity in vivo. Previously the investigators have demonstrated that rotigaptide does not contribute to endothelial function in healthy volunteers. The investigators now wish to examine the effect of rotigaptide in conditions of endothelial dysfunction. By limiting the blood flow to the arm for 20mins the ability of the blood vessel to vasodilate is impaired. By administering an intra-arterial rotigaptide infusion the investigators want to assess any functional preservation.
NCT00901563 ↗ Gap Junction Potentiation of Endothelial Function With Rotigaptide Completed University of Edinburgh N/A 2009-03-01 Hypothesis - Rotigaptide will improve endothelial function in the context of endothelial dysfunction. The lining of blood vessels (endothelium) can react to hormones in the blood stream causing the blood vessel muscle to relax (vasodilatation) and allow more blood to flow. The nitric oxide and prostacyclin pathways are well documented in this process. However, evidence points to the existence of a third powerful relaxant called endothelium derived hyperpolarising factor (EDHF) but its identity and mechanism of action have proved elusive. As well as causing blood vessels to relax and more blood to flow, EDHF may be involved in the endothelium signaling, triggering release of a specialised clot dissolving factor called tissue plasminogen activator (t PA). t PA is important to ensure small clots, which are constantly being formed in the circulation, are rapidly dissolved and do not grow large enough to cause heart attacks and strokes. Evidence points towards the requirement for 'gap junctions' in the mediation of EDHF responses. Gap junctions are specialised pores which allow small molecules and charge to pass between cells. They are found between endothelial cells and the underlying muscle of the blood vessel. A drug called Rotigaptide has been developed to cause gap junctions to open. It has been safely administered in healthy volunteers and is now in a Phase II drug trial. By opening gap junctions the investigators hypothesise that it could increase EDHF mediated activity and vasodilatation. It represents a useful tool with which to examine the role of gap junctions in EDHF activity in vivo. Previously the investigators have demonstrated that rotigaptide does not contribute to endothelial function in healthy volunteers. The investigators now wish to examine the effect of rotigaptide in conditions of endothelial dysfunction. By limiting the blood flow to the arm for 20mins the ability of the blood vessel to vasodilate is impaired. By administering an intra-arterial rotigaptide infusion the investigators want to assess any functional preservation.
>Trial ID >Title >Status >Phase >Start Date >Summary

Clinical Trial Conditions for anti-inhibitor coagulant complex

Condition Name

Condition Name for anti-inhibitor coagulant complex
Intervention Trials
CNS Primary Tumor, NOS (Malignant Glioma) 1
Vascular Disease 1
Coronary Artery Disease 1
Diabetes Mellitus 1
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Condition MeSH

Condition MeSH for anti-inhibitor coagulant complex
Intervention Trials
Pneumonia 1
Diabetes Mellitus 1
Coronary Disease 1
COVID-19 1
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Clinical Trial Locations for anti-inhibitor coagulant complex

Trials by Country

Trials by Country for anti-inhibitor coagulant complex
Location Trials
United States 22
Canada 6
Poland 1
United Kingdom 1
Germany 1
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Trials by US State

Trials by US State for anti-inhibitor coagulant complex
Location Trials
Maryland 2
Pennsylvania 2
Georgia 2
California 2
Texas 2
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Clinical Trial Progress for anti-inhibitor coagulant complex

Clinical Trial Phase

Clinical Trial Phase for anti-inhibitor coagulant complex
Clinical Trial Phase Trials
Phase 4 2
Phase 3 1
Phase 2 2
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Clinical Trial Status

Clinical Trial Status for anti-inhibitor coagulant complex
Clinical Trial Phase Trials
Recruiting 3
Terminated 2
Unknown status 2
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Clinical Trial Sponsors for anti-inhibitor coagulant complex

Sponsor Name

Sponsor Name for anti-inhibitor coagulant complex
Sponsor Trials
Chief Scientist Office of the Scottish Government 1
IRCCS San Raffaele 1
NHS Lothian 1
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Sponsor Type

Sponsor Type for anti-inhibitor coagulant complex
Sponsor Trials
Other 10
Industry 4
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