CLINICAL TRIALS PROFILE FOR UROKINASE
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All Clinical Trials for Urokinase
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00001713 ↗ | Treatment for Blood Clots in the Veins of the Legs | Completed | National Institutes of Health Clinical Center (CC) | Phase 1 | 1998-02-01 | Acute deep venous thrombosis (ADVT) of the lower extremity is a common disorder. Traditional treatment with anticoagulation therapy is effective in reducing the associated risk of pulmonary embolism, but is ineffective in restoring patency of the venous system of the lower extremity. While systemic thrombolytic therapy has been shown to be more effective than anticoagulation, catheter directed local thrombolytic therapy is the most effective treatment in restoring venous patency. Current treatment regimens are based on use of urokinase, infused continuously through catheters imbedded into the thrombus. These treatment regimens require doses on the order of 10,000,000 units of urokinase, resulting in significant bleeding complications and prohibitive costs. Experience at NIH with pulse-spray treatment of axillary subclavian venous thrombosis with rtPA indicates that this is a highly effective and safe alternative thrombolytic regimen. The proposed protocol is designed to evaluate the efficiency, safety, and doses of rtPA associated with pulse spray directed rtPA treatment of the more extensive venous thrombosis encountered in the lower extremity. |
| NCT00083525 ↗ | Urokinase-Plasminogen Activator (uPA) Inhibitor WX-UK1 in Combination With Capecitabine in Advanced Malignancies | Completed | United States Department of Defense | Phase 1 | 2004-05-01 | The purpose of this study is to determine the safety, tolerability, maximum tolerated dose (MTD), pharmacokinetics, and pharmacodynamics of the combination of WX-UK1 and capecitabine in patients with advanced malignancies. |
| NCT00083525 ↗ | Urokinase-Plasminogen Activator (uPA) Inhibitor WX-UK1 in Combination With Capecitabine in Advanced Malignancies | Completed | Heidelberg Pharma AG | Phase 1 | 2004-05-01 | The purpose of this study is to determine the safety, tolerability, maximum tolerated dose (MTD), pharmacokinetics, and pharmacodynamics of the combination of WX-UK1 and capecitabine in patients with advanced malignancies. |
| NCT00083525 ↗ | Urokinase-Plasminogen Activator (uPA) Inhibitor WX-UK1 in Combination With Capecitabine in Advanced Malignancies | Completed | Wilex | Phase 1 | 2004-05-01 | The purpose of this study is to determine the safety, tolerability, maximum tolerated dose (MTD), pharmacokinetics, and pharmacodynamics of the combination of WX-UK1 and capecitabine in patients with advanced malignancies. |
| NCT00144950 ↗ | Urokinase Versus Primary Video-Assisted Thorascopic Surgery for Empyema | Completed | Institute of Child Health | Phase 1 | 1969-12-31 | This study will compare VATS versus chest drain insertion and urokinase in the treatment of childhood empema by a randomised prospective study. |
| NCT00354900 ↗ | Phase I Study of Aprotinin in Advanced Breast Cancer | Terminated | Dartmouth-Hitchcock Medical Center | Phase 1 | 2006-07-01 | There is an intimate relationship between processes which promote growth, invasion, and metastasis of cancers, and processes which regulate blood clotting. The enzymes uPA and PAI-1 are key regulators of the remodeling of recently formed blood clots, and there is substantial information linking greater levels of uPA and PAI-1 in breast cancers with a greater likelihood of breast cancer recurrence and death. As uPA and PAI-1 are excellent markers for a cancer's aggressive clinical behavior, uPA and PAI-1 may be potential targets for anticancer therapy. Aprotinin is an inhibitor of uPA activation, and has been approved by the FDA to reduce blood loss in patients undergoing cardiopulmonary bypass surgery. Studies in animals and limited studies in patients have shown that Aprotinin slows the growth of tumors. Our hypothesis is that uPA is chronically activated in malignancies, and that inhibition of uPA by Aprotinin would slow the rate of progression of breast cancer. |
| NCT00431379 ↗ | Treatment of Acute Respiratory Distress Syndrome With Tenecteplase: A Dose Escalation Pilot Study | Withdrawn | Genentech, Inc. | Phase 1 | 2007-02-01 | The pathogenesis of ARDS appears to be from damage to the alveolar-capillary barrier, which is composed of the microvascular endothelium and the alveolar epithelium. This damage may occur from direct or indirect lung injury. The mechanism of injury to the alveolar capillary barrier appears to be through neutrophil-mediated injury, pro-inflammatory cytokines, ventilator-induced lung injury with alveolar over distention and abnormalities of the coagulation system. This results in blood clot formation in the microcirculation of the lung. Thrombolytics can dissolve blood clots and result in increased blood flow to the organs. This treatment may benefit ARDS patients, thus the purpose of this study. Hardaway, et al.studied the effects of thrombolytics on ARDS in pigs. The experimental group showed improved oxygenation and survival as compared to controls. There was no bleeding complications noted with this therapy. Dr. Hardaway followed this animal study with a phase I clinical trial involving 20 patients with ARDS. The patients were treated with IV streptokinase or urokinase. Nineteen of the 20 patients showed an increase in PA02 after thrombolytic therapy. There were no significant bleeding complications in patients that were critically ill on ventilators. We propose an additional phase I pilot study to evaluate the effectiveness and safety of Tenecteplase for the treatment of ARDS. Unlike the other fibrinolytics studied in this disease state, Tenecteplase, is more fibrin specific and has increased resistance to plasminogen activator inhibitor (PAI-I) at greater levels than other available fibrinolytics. We have chosen an experimental dose escalation trial design of tenecteplase that has demonstrated initial safety trends in a Phase I acute ischemic stroke trial. The initial dose is 0.1 mg/kg IV and will increase to 0.2 mg/kg, 0.3 mg/kg, with a final cohort of patients receiving 0.4 mg/kg. Drug administration will be a single dose bolus in each cohort. Advancement of dose will occur if safety is not in question in the previous cohort. We hope this will provide an acceptable benefit risk ratio as the mortality of ARDS is approximately 30 - 60%. All patients will be closely monitored for any change in clotting parameters and signs of bleeding. Tenecteplase will be administered via a peripheral IV as described in the package insert. |
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