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A Study Designed to Evaluate ODSH in Subjects With Exacerbations of COPD (COPD)

This study has been terminated.
(Interim analysis: safety without efficacy ODSH in patients with acute COPD.)
Sponsor:
Information provided by (Responsible Party):
Cantex Pharmaceuticals
ClinicalTrials.gov Identifier:
NCT00457951
First received: April 6, 2007
Last updated: October 25, 2016
Last verified: October 2016
April 6, 2007
October 25, 2016
April 2007
August 2009   (Final data collection date for primary outcome measure)
Incidence of Treatment Failure [ Time Frame: Time to hospital discharge and 21 days post-treatment, up to 31 days ]
The primary outcome of the study is "Treatment Failure" as defined by Failure to discharge from hospital based on GOLD (Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease) criteria or relapse after DC from hospital.
FEV1
Complete list of historical versions of study NCT00457951 on ClinicalTrials.gov Archive Site
Not Provided
  • Borg CR10 Scale®
  • pulmonary function test measures
  • quality of life scale
  • therapy intensification
  • pharmacodynamic measures of inflammation
  • coagulation parameters
  • length of hospitalization
  • length of ICU stay
  • 6MWT
  • readmission for COPD
  • pharmacokinetic parameters.
Not Provided
Not Provided
 
A Study Designed to Evaluate ODSH in Subjects With Exacerbations of COPD
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
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.

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.

Interventional
Phase 2
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Double (Participant, Investigator)
Primary Purpose: Treatment
Chronic Obstructive Pulmonary Disease
  • Drug: Open-Label
    ODSH administered open-label
    Other Name: PGX-100
  • Drug: Placebo Comparator: Placebo-Control Arm 0.9% Sodium Chloride
    Placebo-Control Arm: Bolus infusion followed by a 96 hour continuous infusion of 0.9%Sodium Chloride
    Other Name: 0.9% Sodium Chloride Solution Placebo-Control Arm
  • Drug: ODSH
    Randomized, Blinded, ODSH Arm
    Other Name: PGX-100
  • Experimental: Open Label
    Initial six subjects treated with ODSH open-label to confirm safety in subjects with an acute exacerbation of COPD; six additional patients will be enrolled following safety review.
    Intervention: Drug: Open-Label
  • Placebo Comparator: 0.9% Sodium Chloride
    Placebo Comparator: Placebo-Control Arm 0.9% Sodium Chloride Solution bolus; dose of 0.375mg/kg/hr over 96 hours.
    Intervention: Drug: Placebo Comparator: Placebo-Control Arm 0.9% Sodium Chloride
  • Active Comparator: Randomized, Blinded, ODSH Arm
    Subjects will receive standard of care treatment. ODSH is administered in bolus doses estimated to inhibit inflammatory mediators randomized 1:1 to ODSH 8mg/kg or placebo. The continuous infusion dose will be 0.375 mg/kg/hr over 96 hours.
    Intervention: Drug: ODSH
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Terminated
158
October 2009
August 2009   (Final data collection date for primary outcome measure)

Inclusion Criteria:

  1. Male and female patients (40 years of age or older) with an established diagnosis of COPD based upon medical history who are being admitted to the hospital to treat an exacerbation of COPD;
  2. Normal prothrombin time and activated partial thromboplastin time; Platelet count; hemoglobin and hematocrit

Exclusion Criteria:

  1. Certain diseases such as:

    • asthma;
    • left heart failure or pulmonary embolism;
    • lung cancer;
    • pneumonia
    • liver or kidney disease
    • blood clotting disorder
    • Positive HIV or hepatitis tests
    • GI bleeding, physical trauma with bleeding, any disease with bleeding within 60 days of study entry
  2. Certain medications such as:

    • Plavix®
    • Warfarin
    • Heparin therapy
    • Certain antibiotics
  3. Exacerbations that are too severe (requiring intubation and mechanical ventilation)
  4. Women of child-bearing potential, pregnancy or breast-feeding
  5. Unable or unwilling to provide informed consent and follow study procedures.
Sexes Eligible for Study: All
40 Years and older   (Adult, Senior)
No
Contact information is only displayed when the study is recruiting subjects
Belgium,   Canada,   Germany,   Poland,   United States
 
 
NCT00457951
PGX-ODSH-2006
Yes
Not Provided
Not Provided
Cantex Pharmaceuticals
Cantex Pharmaceuticals
Not Provided
Principal Investigator: Marc Decramer, MD Université Hopistal Gasthuisberg
Study Director: Pedro Quintana, MD Cantex Pharmaceuticals
Principal Investigator: Tobias Welte, MD Hannover Medical School
Cantex Pharmaceuticals
October 2016

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP