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| Sponsored by: |
ParinGenix |
|---|---|
| Information provided by: | ParinGenix |
| ClinicalTrials.gov Identifier: | NCT00457951 |
Purpose
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.
| Condition | Intervention | Phase |
|---|---|---|
|
Chronic Obstructive Pulmonary Disease |
Drug: Normal Saline infusion Drug: ODSH |
Phase II |
| Study Type: | Interventional |
| Study Design: | Treatment, Randomized, Double Blind (Subject, Investigator), Placebo Control, Parallel Assignment, Safety/Efficacy Study |
| Official Title: | An Open-Label Phase Followed by a Randomized, Double-Blind, Placebo-Controlled Phase in a Study Designed to Evaluate Intravenous 2-O, 3-O Desulfated Heparin (ODSH) in Subjects With Exacerbations of Chronic Obstructive Pulmonary Disease |
| Estimated Enrollment: | 294 |
| Study Start Date: | April 2007 |
| Estimated Study Completion Date: | March 2009 |
| Estimated Primary Completion Date: | January 2009 (Final data collection date for primary outcome measure) |
| Arms | Assigned Interventions |
|---|---|
|
1: Experimental
ODSH infusion
|
Drug: ODSH
Bolus infusion followed by a 4 day continuous infusion of ODSH
|
|
2: Placebo Comparator
Normal Saline infusion
|
Drug: Normal Saline infusion
Bolus infusion followed by a 4 day continuous infusion of placebo
|
The management of acute exacerbations of COPD today is qualitatively the same as it was 40 years ago: bronchodilators, corticosteroids, and antibiotics. Because of the prominent pathophysiological role of neutrophils in exacerbations of COPD, neutrophils and their toxic oxidants and proteases represent therapeutic targets which are currently unchallenged in the treatment of this aspect of the disease. Ideally, to disrupt neutrophilic airway inflammation, one would both block neutrophilic influx from the vascular space into the airway, as well as neutralize or inactivate prominent neutrophilic toxins such as the proteases HLE and cathepsin G.
Heparin is a sulfated mucopolysaccharide that slows blood clot formation by inhibiting the reactions that lead to formation of fibrin clots. Physicians use heparin to prevent blood clot formation during open-heart surgery, bypass surgery and dialysis. Heparin also prevents previously formed clots from becoming larger and causing more serious problems. Heparin has other biological properties, most notably anti-inflammatory activity. At doses required to be therapeutically beneficial as an anti-inflammatory, heparin can cause severe, potentially life-threatening hemorrhage. ParinGenix has chemically modified heparin to retain the anti-inflammatory activity while reducing anti-coagulant properties.
Heparin has long been known to be a potent inhibitor, both in vitro and in vivo, of the cationic neutrophil proteases HLE and cathepsin G. However, heparin also has numerous other important anti-inflammatory effects. P-selectin is the primary endothelial attachment molecule mediating neutrophil rolling along the vessel wall. At concentrations close to those achieved in plasma near the high range of therapeutic anticoagulation, heparin inhibits P-selectin and P-selectin mediated interaction of leukocytes with endothelium. Heparin also blocks the leukocyte integrin Mac-1 (CD11b/CD18) and Mac-1-dependent leukocyte adherence to endothelial ICAM. These combined effects on rolling, integrin-dependent attachment and perhaps other aspects of cellular passage through the basement membrane prevent neutrophil accumulation in areas of inflammation. As an example, when given in much higher concentrations than those appropriate for therapeutic anticoagulation, heparin efficiently blocks neutrophilic influx into ischemic reperfused myocardium and brain reducing the size of both myocardial infarction and ischemic stroke. Thus, heparin and heparin analogues may have the potential to also reduce inflammatory influx of neutrophils into the airway during exacerbations of COPD.
All subjects will receive standard of care treatment, including corticosteroids, beta-2 agonists, and antibiotics as well as ODSH or placebo.
Eligibility| Ages Eligible for Study: | 40 Years and older |
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | No |
Inclusion Criteria:
Exclusion Criteria:
Certain diseases such as:
Certain medications such as:
Contacts and Locations| Contact: Beth Williams | (603) 894-7055 | Beth.Williams@parexel.com |
| Contact: Sandra Foschia | 1-514-624-0566 | sandra.foschia@parexel.com |
Show 38 Study Locations| Principal Investigator: | Marc Decramer, MD | Université Hopistal Gasthuisberg |
| Study Director: | Pedro Quintana, MD | ParinGenix |
| Principal Investigator: | Tobias Welte, MD | Hannover Medical School |
| Study Director: | Teresa Arledge, DVM | ParinGenix |
More Information
| Responsible Party: | ParinGenix ( Teresa Arledge/ Chief Development Officer ) |
| Study ID Numbers: | PGX-ODSH-2006 |
| Study First Received: | April 6, 2007 |
| Last Updated: | December 1, 2008 |
| ClinicalTrials.gov Identifier: | NCT00457951 |
| Health Authority: | United States: Food and Drug Administration; Canada: Health Canada; Germany: Federal Institute for Drugs and Medical Devices; Switzerland: Federal Office of Public Health; Belgium: Directorate general for the protection of Public health: Medicines |
|
Chronic Obstructive Pulmonary Disease COPD Heparin ODSH Exacerbations of COPD |
|
Lung Diseases, Obstructive Respiratory Tract Diseases Lung Diseases Respiration Disorders |
Heparin Calcium heparin Pulmonary Disease, Chronic Obstructive |
