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. |
| NCT01095822 ↗ | Effects of Valsartan and Aliskiren on Hemostatic Indices in Hypertensive Diabetics | Unknown status | Novartis | Phase 4 | 2010-03-01 | People with both hypertension and diabetes have a higher chance of developing heart and arterial problems that could be reduced with anti-coagulant therapy. Valsartan (Diovan), an FDA approved angiotensin-II receptor antagonist (blocker) clinically indicated for the treatment of essential hypertension is known to inhibit platelet activity in both an in vitro and ex vivo setting. Aliskiren (Tekturna) is a recently FDA-approved potent direct renin inhibitor which is also an effective anti-hypertensive agent in patients with mild-to-moderate hypertension and which, in vitro, modulates antithrombin III in plasma. Therefore, in addition to being clinically approved anti-hypertensive medications, combining these two agents will potentially target both primary hemostasis (platelets) and anticoagulant (antithrombin-III is a cornerstone substrate for heparin) properties to exert their anti-thrombotic efficacy simultaneously. This combination strategy may not only improve hypertension management, but also improve vascular outcomes in high-risk diabetic population via favorable effects on anti-thrombotic activity. Importantly, there have been no significant additional safety concerns of using the combination of aliskiren and valsartan. The investigators hypothesis is that valsartan 160 mg/daily in combination with aliskiren 150-300 mg/daily for 4 weeks will favorably affect blood levels of platelet/coagulation/fibrinolytic biomarkers (ie, diminish platelet activity, and enhance antithrombin III potency) when compared with monotherapy with aliskiren 150mg/daily in hypertensive patients with type 2 diabetes mellitus. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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