Ignite Creation Date:
2024-05-05 @ 12:07 PM
Last Modification Date:
2024-10-26 @ 9:20 AM
Study NCT ID:
NCT00244647
Status:
TERMINATED
Last Update Posted:
2008-04-10
First Post:
2005-10-25
Brief Title:
A Phase 1b Study Evaluating RESTEN-MP in Subjects With Focal de Novo Stenosis
Sponsor:
Sarepta Therapeutics Inc
Organization:
Sarepta Therapeutics Inc
Study Overview
Official Title:
A Phase 1b Randomized Single Blind Study Evaluating RESTEN-MP in Subjects With Focal de Novo Stenosis
Status:
TERMINATED
Status Verified Date:
2008-04
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 has 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 pharmacokinetics and potential effectiveness of a single intravenous slow-push dose of RESTEN-MP at the time of stent placement to reduce in-stent restenosis following balloon angioplasty and stent placement The post-dose follow-up period is up to six-months
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 has 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 pharmacokinetics and potential effectiveness of a single intravenous slow-push dose of RESTEN-MP at the time of stent placement to reduce in-stent restenosis following balloon angioplasty and stent placement The post-dose follow-up period is up to six-months
Detailed Description:
The process of restenosis following a revascularization procedure begins at the time of percutaneous coronary intervention PCI Restenosis has long been seen 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 interfere with the ability of human c-myc gene to translate mRNA into MYC protein Slow-push intravenous administration of RESTEN-MP in pharmacological doses in the restenosis porcine model prevented subsequent in-stent stenosis
In addition to the standard safety assessments assessments of the potential therapeutic value of RESTEN-MP as a neointimal hyperplasia inhibitor include late loss between the time of stent placement and 6 months thereafter
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 interfere with the ability of human c-myc gene to translate mRNA into MYC protein Slow-push intravenous administration of RESTEN-MP in pharmacological doses in the restenosis porcine model prevented subsequent in-stent stenosis
In addition to the standard safety assessments assessments of the potential therapeutic value of RESTEN-MP as a neointimal hyperplasia inhibitor include late loss between the time of stent placement and 6 months thereafter
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