CytRx drug may help reduce heart attack and stroke damage
The data, published by researchers collaborating with Biorex R&D Company (the company from which CytRx purchased iroxanadine), demonstrated that iroxanadine protects human endothelial cells that line the walls of blood vessels in an in vitro cellular model. Normally, when oxygen is restored to oxygen-starved endothelial cells the resulting oxidative cell damage triggers programmed cell death, or apoptosis, resulting in death of the endothelial cells. However, the research showed that cells treated with iroxanadine showed significantly less cell death under those conditions, even when the drug was added 20 hours after onset of oxygen deprivation. "If iroxanadine behaves in patients as it did in this cell culture model, the drug could help prevent oxidative damage to endothelial cells that occurs as a result of ischemia/reperfusion from stroke or heart attack," said Dr Louis Ignarro, Nobel Laureate and world acclaimed expert in the field of cardiovascular disease. "Although this won't necessarily prevent damage to the target tissue supplied by the blood vessel, it could prevent the failure of the blood vessel barrier that results in complications such as thrombosis (generation of blood clots) and edema (accumulation of fluid)." Iroxanadine is believed to activate the expression of molecular chaperone proteins that repair or degrade damaged proteins in stressed cells. The company plans to seek a corporate partner to develop iroxanadine for cardiovascular indications, and also plans to evaluate the drug candidate in pre-clinical animal models for other indications thought to be caused by damage to endothelial cells, such as diabetic foot ulcers.