Ignite Creation Date:
2024-05-05 @ 12:06 PM
Last Modification Date:
2024-10-26 @ 9:20 AM
Study NCT ID:
NCT00248066
Status:
COMPLETED
Last Update Posted:
2007-02-08
First Post:
2005-11-01
Brief Title:
Safety and Efficacy of RESTEN-MP When Used in Conjunction With a Bare Metal Stent in Coronary Arteries
Sponsor:
Sarepta Therapeutics Inc
Organization:
Sarepta Therapeutics Inc
Study Overview
Official Title:
APPRAISAL Trial A Phase IIa Study to Evaluate the Safety and Preliminary Efficacy of RESTEN-MP When Used in Conjunction With a Bare Metal Stent in de Novo Native Coronary Artery Lesions
Status:
COMPLETED
Status Verified Date:
2007-02
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The process of re-narrowing of a coronary artery following a revascularization procedure such as angioplasty begins at the time of the procedure Restenosis has long been considered a major problem for effective long-term interventional success This often results in repeated procedures to deal with recurrent stenosis or restenosis of the original targeted vessel
There is a substantial body of literature suggesting that local MYC protein production in the injured coronary artery is a major stimulus and potential cause of restenosis that appears after stent placement This study is based upon the hypothesis that stopping MYC protein production in the vessel will help reduce restenosis vessel re-narrowing
AVI BioPharma Inc has utilized its proprietary antisense chemistry to design a drug that interferes with MYC production
This study will evaluate the safety and potential effectiveness of RESTEN-MP to reduce in-stent restenosis following balloon angioplasty and stent placement The post-dose follow-up period is up to six-months
RESTEN-MP is administered at the time a stent is successfully placed in a coronary artery and again 24 hours later via slow-push intravenous administration
There is a substantial body of literature suggesting that local MYC protein production in the injured coronary artery is a major stimulus and potential cause of restenosis that appears after stent placement This study is based upon the hypothesis that stopping MYC protein production in the vessel will help reduce restenosis vessel re-narrowing
AVI BioPharma Inc has utilized its proprietary antisense chemistry to design a drug that interferes with MYC production
This study will evaluate the safety and potential effectiveness of RESTEN-MP to reduce in-stent restenosis following balloon angioplasty and stent placement The post-dose follow-up period is up to six-months
RESTEN-MP is administered at the time a stent is successfully placed in a coronary artery and again 24 hours later via slow-push intravenous administration
Detailed Description:
The process of restenosis the re-narrowing of a coronary artery lumen following a revascularization procedure begins at the time of percutaneous coronary intervention PCI Restenosis has long been seen as a major impediment of effective long-term interventional cardiology necessitating repeated procedures to deal with in situ recurrent stenosis of the original targeted vessel The restenosis rates are between 30 to 50 of patients treated with balloon angioplasty and between 15 to 30 of patients treated with bare metal stents There is currently high enthusiasm for drug-eluting stents already approved for the market and which have an overall restenosis rate of 3 as reported in published reports for most clinical trial patient populations However there are subsets of patients eg diabetic patients and patients with diffuse small vessel disease that have restenosis rates around 10 despite the use of drug-eluting stents It is probably too early to conclude that the currently approved drug-eluting stents are a panacea to relieve coronary arterial obstruction due to atherosclerotic heart disease In fact with the increased usage of the current drug-eluting stents on the market there are reports of problems such as late stent malposition subacute and late thromboses and aneurysm formations due to the vessel toxicity associated with this method of treatment There remains a definite need for a simple safe and durable solution to restenosis
The development of devices such as intravascular ultrasound has led to a greater understanding of restenosis mechanisms especially after coronary artery stenting It is presumed that the pathogenesis of coronary artery restenosis after a revascularization procedure entails two major processes The first component viz recoil and remodeling involves the mechanical collapse and constriction of the treated vessel however coronary stents provide luminal scaffolding that eliminates recoil and remodeling The second component of coronary artery restenosis after a revascularization procedure is the endothelial response to injury Whereas the former focus in modulating the pathophysiological mechanisms involved in restenosis centered mainly on inhibition of platelet aggregation and function current targets of pharmaceutical agents for this condition have shifted to inhibitors of the cell cycle smooth muscle cell proliferation and migration synthesis of extra-cellular matrix and inflammatory mediators Many different agents are currently being evaluated in pre-clinical and clinical studies
AVI-4126 the active ingredient of RESTEN-MP is a proprietary antisense drug designed to interrupt the translation of the human c-myc gene by mRNA Therefore the basis for this study is to ascertain if RESTEN-MP is safe and has a therapeutic benefit Slow-push intravenous administration of RESTEN-MP in pharmacological doses in the restenosis porcine model prevented subsequent in-stent stenosis
This clinical study will evaluate the safety and potential effectiveness of RESTEN-MP to reduce in-stent restenosis following balloon angioplasty In order to objectively assess the therapeutic value of RESTEN-MP compared to other drugs used in combination with coronary artery stents and to utilize a sensitive method to assess the effectiveness of RESTEN-MP as a neointimal hyperplasia inhibitor late loss between the time of stent placement and 6 months later is the therapeutic endpoint in this study
The development of devices such as intravascular ultrasound has led to a greater understanding of restenosis mechanisms especially after coronary artery stenting It is presumed that the pathogenesis of coronary artery restenosis after a revascularization procedure entails two major processes The first component viz recoil and remodeling involves the mechanical collapse and constriction of the treated vessel however coronary stents provide luminal scaffolding that eliminates recoil and remodeling The second component of coronary artery restenosis after a revascularization procedure is the endothelial response to injury Whereas the former focus in modulating the pathophysiological mechanisms involved in restenosis centered mainly on inhibition of platelet aggregation and function current targets of pharmaceutical agents for this condition have shifted to inhibitors of the cell cycle smooth muscle cell proliferation and migration synthesis of extra-cellular matrix and inflammatory mediators Many different agents are currently being evaluated in pre-clinical and clinical studies
AVI-4126 the active ingredient of RESTEN-MP is a proprietary antisense drug designed to interrupt the translation of the human c-myc gene by mRNA Therefore the basis for this study is to ascertain if RESTEN-MP is safe and has a therapeutic benefit Slow-push intravenous administration of RESTEN-MP in pharmacological doses in the restenosis porcine model prevented subsequent in-stent stenosis
This clinical study will evaluate the safety and potential effectiveness of RESTEN-MP to reduce in-stent restenosis following balloon angioplasty In order to objectively assess the therapeutic value of RESTEN-MP compared to other drugs used in combination with coronary artery stents and to utilize a sensitive method to assess the effectiveness of RESTEN-MP as a neointimal hyperplasia inhibitor late loss between the time of stent placement and 6 months later is the therapeutic endpoint in this study
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