Data presented today at the European Society of Cardiology Congress demonstrates the effectiveness of a peptide called FX06 in preventing cardiac damage resulting from treatment following a heart attack.
While reperfusion is well established as a standard of care, it paradoxically causes additional damage to heart muscle in patients surviving from these attacks - a phenomenon termed "reperfusion injury". FX06 is a novel compound intended to prevent that damage.
Professor Dan Atar, the Coordinating Investigator of the F.I.R.E. (FX06 In ischemia and REperfusion) trial, a Phase II clinical study of FX06, will present the results of the trial at
12-noon on September 2nd in the Hot Line III Session at the European Society of Cardiology Congress in Munich, Germany.
"Re-establishment of blood flow, either by catheter-based balloon-intervention (PCI) or by thrombolysis, is necessary and life-saving in the treatment of acute myocardial infarctions. However, such interventions can lead to further damage to the heart muscle due to blood vessel dysfunction and inflammation," said Dan Atar, Professor of Cardiology at the Aker University Hospital, University of Oslo, Norway. "Based on the F.I.R.E. results, FX06 has been shown to reduce damage to the heart muscle by inhibiting inflammation and protecting vascular function. We predict that FX06 may become a novel treatment for STEMI patients undergoing PCI, representing a major advance in acute cardiac care."
The Phase II clinical trial of FX06 (F.I.R.E. study) was completed in March 2008, with data indicating a statistically significant reduction in myocardial necrosis following intravenous application of FX06 concurrent with reperfusion. FX06 is a peptide that binds to VE-cadherin, a target on the surfaces of endothelial cells, which form the inner cell layer of blood vessels, thereby preserving blood vessel function. This leads to reduced inflammation, reduced oedema and reduced infarct sizes.
About the study: