Ignite Creation Date:
2024-05-05 @ 11:42 AM
Last Modification Date:
2024-10-26 @ 9:12 AM
Study NCT ID:
NCT00116012
Status:
COMPLETED
Last Update Posted:
2006-11-29
First Post:
2005-06-26
Brief Title:
Anticoagulation With rNAPc2 to Eliminate MACETIMI 32
Sponsor:
ARCA Biopharma Inc
Organization:
ARCA Biopharma Inc
Study Overview
Official Title:
A Randomized Double-Blind Placebo-Controlled Study to Assess the Safety of Factor VIIaTissue Factor Inhibitor Recombinant Nematode Anticoagulant Protein c2 rNAPc2 in Subjects With Non-ST-Elevation Acute Coronary Syndromes - ANTHEM Anticoagulation With rNAPc2 to Help Eliminate MACETIMI 32 Amendment 3 - A Single Arm Open-Label Study of rNAPc2 With Reduced Doses of Unfractionated Heparin
Status:
COMPLETED
Status Verified Date:
2006-11
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The primary focus of this study is to explore the safety of a range of doses of rNAPc2 in subjects who are managed in hospitals that most typically practice an early invasive strategy catheterization during the index admission After completion of the ascending dose-ranging part of the trial and review of these data by the Data and Safety Monitoring Board DSMB the maximum tolerated dose of rNAPc2 will be studied in single-arm open-label panels approximately 25 subjects each of rNAPc2 with descending doses of unfractionated heparin UFH
Detailed Description:
Acute coronary syndromes ACS which include unstable angina and non-ST-elevation non-STE myocardial infarction represent a serious clinical condition affecting over 1000000 people in the US alone The combined rate of death and myocardial infarction MI in ACS patients is 8-15 after one month in spite of the best current therapy including use of low-molecular weight heparins glycoprotein IIbIIIa GPIIbIIIa inhibitors and an early invasive strategy Given the high prevalence of the disorder further improvements in the outcomes in these patients are very desirable
It is currently believed that the principle cause of the clinical symptoms characterizing ACS results from the transient thrombotic occlusion of one or more coronary vessels Coronary thrombosis is initiated by the exposure of the protein tissue factor TF which can be found in the sub-endothelial layer of the blood vessel and is a major component of atherosclerotic gruel The exposure of TF following vascular damage or rupture of a coronary atherosclerotic plaque results in the rapid formation of the enzymatic complex composed of TF and the serine protease factor VIIa fVIIaTF The fVIIaTF complex initiates an amplified cascade of proteolytic activation steps resulting in the formation of the serine protease thrombin The highly amplified generation of thrombin localized to the site of vascular damage or plaque rupture coupled with the high-shear rheological environment of the coronary vessel results in the activation and subsequent aggregation of platelets and the formation of an insoluble matrix of fibrin resulting in a platelet-rich thrombus
The critical role of the fVIIaTF complex in the initiation of coronary thrombosis suggests that it may be an ideal target for inhibitors that will result in an attenuation of thrombin generation and subsequent thrombus formation Recombinant nematode anticoagulant protein c2 rNAPc2 is a novel and potent inhibitor of fVIIaTF that may improve current therapeutic strategies in reducing the extent of coronary thrombosis and subsequent clinical events in patients diagnosed with ACS
It is currently believed that the principle cause of the clinical symptoms characterizing ACS results from the transient thrombotic occlusion of one or more coronary vessels Coronary thrombosis is initiated by the exposure of the protein tissue factor TF which can be found in the sub-endothelial layer of the blood vessel and is a major component of atherosclerotic gruel The exposure of TF following vascular damage or rupture of a coronary atherosclerotic plaque results in the rapid formation of the enzymatic complex composed of TF and the serine protease factor VIIa fVIIaTF The fVIIaTF complex initiates an amplified cascade of proteolytic activation steps resulting in the formation of the serine protease thrombin The highly amplified generation of thrombin localized to the site of vascular damage or plaque rupture coupled with the high-shear rheological environment of the coronary vessel results in the activation and subsequent aggregation of platelets and the formation of an insoluble matrix of fibrin resulting in a platelet-rich thrombus
The critical role of the fVIIaTF complex in the initiation of coronary thrombosis suggests that it may be an ideal target for inhibitors that will result in an attenuation of thrombin generation and subsequent thrombus formation Recombinant nematode anticoagulant protein c2 rNAPc2 is a novel and potent inhibitor of fVIIaTF that may improve current therapeutic strategies in reducing the extent of coronary thrombosis and subsequent clinical events in patients diagnosed with ACS
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| ANTHEM | None | None | None |