NCT01269242

The Effects of Bindarit in Preventing Stent Restenosis

A Pilot Study to Evaluate the Efficacy and Safety of Different Bindarit Dosages in Preventing Stent Restenosis

• Status: Completed
• Phase: Phase 2
• Study type: Interventional
• Enrollment: 148 (actual)
• Sponsor: Aziende Chimiche Riunite Angelini Francesco S.p.A · Industry
• Sex: All
• Age: 19 Years
• Healthy volunteers: Not accepted

Summary

The main study objective is to assess the efficacy and safety of different bindarit dosages compared to placebo in preventing restenosis, in patients submitted to coronary stenting and using a bare metal stent (Vision BMS, by Abbott).

Detailed description

Coronary artery disease is caused by the gradual build-up of fatty deposits in coronary arteries (atherosclerosis). A diminished blood flow may cause chest pain (angina), shortness of breath or other symptoms. A complete blockage can cause a heart attack. Angioplasty and stenting techniques are safe and effective procedures performed to unblock coronary arteries. However, a recurrent problem after angioplasty is the occurrence of a new blockage, usually within 6 to 9 months after the initial procedure. This phenomenon, called "restenosis", is a body's response to the injury of the angioplasty and does not mean a progression of coronary artery disease.The pathophysiology of restenosis is complex and has as yet not been fully clarified. Serial studies have shown that in-stent restenosis is almost exclusively caused by neointimal hyperplasia and tissue proliferation occurring in site or adjacent to the stent sites. Histological studies confirmed that neointimal hyperplasia post-stent implantation is related to vessel injury during the procedure. Chemokines have been implicated in the pathogenesis of vascular injury. In this context, MCP-1 which shows a potent chemotactic action on monocytes, can amplify the inflammatory response through the recruitment of additional monocytes. In addition, MCP-3 is known to share some key biological features with MCP-1. It has been proved that MCP-1 directly induces human vascular smooth muscle proliferation acting at this level as a potent mitogen, and that anti-MCP-1 gene therapy inhibits restenotic changes (neointimal hyperplasia) in animals after balloon injury. An evidence of a critical increase in circulating MCP-1 after coronary angioplasty was reported. It was more evident and prolonged in patients with restenosis rather than in non-restenotic patients, in which only a transient increases in plasma MCP-1 has been demonstrated. Since these chemokines showed to play a main role in the appearance and worsening of the restenosis process, a selective inhibitor of MCP-1 and other members of monocyte chemotactic protein subfamily of CC inflammatory chemokines (MCP-3/CCL7, MCP-2/CCL8), such as bindarit, may have a potential therapeutic use in preventing restenosis by inhibiting the VSMC proliferation, and without affecting the important process of re-endothelization.

Conditions

• Coronary Restenosis

Interventions

Type	Name	Description
DRUG	bindarit	300 mg bid, that is one 300 mg tablet twice a day for 6 months;
DRUG	bindarit	600 mg bid, that is two 300 mg tablets twice a day for 6 months
DRUG	placebo	bindarit-matching placebo tablets for 6 months.

Timeline

• Start date: 2009-01-01
• Primary completion: 2011-01-01
• Completion: 2011-04-01
• First posted: 2011-01-04
• Last updated: 2016-08-05

Locations

1 site across 1 country: Italy