(BUSINESS WIRE)-- Stealth Peptides Inc. (Stealth), a privately held biopharmaceutical company developing innovative mitochondrial therapies for diseases with unmet medical needs, reported today on a presentation of Bendavia study findings by cardiologist Dr. Robert Kloner, who presented data from three independent labs during the American Heart Association's (AHA) annual meeting. Bendavia(TM) is a novel compound that targets the mitochondrion to treat mitochondrial dysfunction including ischemia reperfusion and microvascular injuries. AHA is a U.S. nonprofit organization that focuses on cardiac care worldwide with a goal of reducing morbidity and mortality caused by cardiovascular diseases, the leading cause of death worldwide. The 2011 AHA annual meeting was held November 12 through 16 in Orlando, Florida, and centered on state of the art scientific advances for cardiovascular medicine and biology.
Dr. Kloner presented animal data on Bendavia from his group and two other independent laboratories led by Dr. Robert Gorman at the University of Pennsylvania and Dr. David Brown at East Carolina University. The research studied reperfusion injury and Bendavia's ability to preserve viable and compromised myocardium, while independently reducing the area of microvascular dysfunction associated with the "no-reflow" phenomenon.
The no-reflow phenomenon was originally described by Dr. Kloner more than three decades ago and has more recently been shown to be an independent determinate of mortality and morbidity of acute myocardial infarction (AMI) patients.
The findings showed Bendavia's cardioprotective effects and potential to reduce reperfusion and microvascular injuries in a variety of cellular and whole animal models. Dr. Kloner concluded that Bendavia protected cardiomyocytes along with reducing infarct size and limiting no-reflow when given after ischemia but prior to reperfusion, making Bendavia an attractive candidate for clinical studies in cardiac ischemia reperfusion injury.
The initial clinical program for Bendavia is the treatment of ischemia reperfusion and microvascular injuries, common complications of interventional procedures for AMI, coronary bypass surgery and renal transplantation. Standard animal models for such interventional procedures demonstrate Bendavia's beneficial biologic effects and confirm the significance of its novel mechanism of action, which preserves mitochondrial function under pathological conditions for ischemia reperfusion and microvascular injuries.
Contrary to prior therapeutic strategies for ischemia reperfusion injury and AMI that focused on uni-targeted pathways, Bendavia and its mitochondrial directed actions address the more complicated, multifactorial nature of disease. Specifically, Bendavia appears to maintain electron transport chain efficiencies under substantial oxidative stress, thereby preserving mitochondrial respiration and adenosine triphosphate levels and preventing mitochondrial swelling and depolarization. Bendavia also appears to be a strong neurologic and ophthalmologic protectant in preclinical models and holds promise as a treatment for disorders such as Alzheimer's disease and diabetic retinopathy.
Stealth's CEO Travis Wilson remarked, "Stealth is excited about the data showing Bendavia as a candidate for such common cardiovascular diseases as AMI and heart failure. Based on the successful conclusion of our Phase I clinical studies with Bendavia and encouraging preclinical data for several chronic and acute conditions, we feel that Bendavia has the potential to be a significant advancement to the treatment of cardio-renal, neurologic and ophthalmologic disorders including rare and orphan mitochondrial diseases."Stealth is currently initiating a multinational Phase II clinical study with Bendavia focused on ischemia reperfusion and microvascular injuries for patients experiencing acute ST-segment elevation myocardial infarction (STEMI). Stealth's Phase II clinical trial is termed EMBRACE-STEMI(TM) for the Evaluation of the Myocardial effects of Bendavia for reducing Reperfusion injury in patients with Acute Coronary Events.