Indication

• Acute myocardial infarction is caused by necrosis of the myocardium due to interruption of blood flow through the coronary arteries. At the time of onset, about one-third of patients die before arriving at the hospital, and the in-hospital mortality rate is 5-10%.
• The current best treatment is to recanalize the coronary artery within 2 hours after occlusion to minimize the infarct area. However, edema, bleeding, and inflammation caused by oxidative stress during blood flow reperfusion account for 30-40% of myocardial damage.
• Endothelial dysfunction plays a key role in both the initiation and progression of MI injury. Therefore, a promising therapeutic strategy which protects cardiac micro-vessels is required for preventing lethal myocardial I/R injury.
• CU101 is a new treatment to reduce cardiac tissue damage due to reperfusion by protecting cardiac microvascular endothelial cells in the early stage of ischemia/reperfusion.

Unmet Needs

• After surgical recanalization of the coronary arteries, mortality and cardiac dysfunction are reported in approximately 10-20% of cases.
• The current standard treatment is to minimize the infarct area by recanalizing the coronary artery within 2 hours after occlusion. However, edema, bleeding, and inflammation caused by oxidative stress during reperfusion account for 30-40% of myocardial damage.

Mechanism of Action

• Protects myocardium and improves cardiac function by preventing cardiac edema and inflammation by stabilizing cardiac micro-vessel and reducing ROS production
• Fundamentally blocks hyper-permeability by stabilizing endothelial cell junctions by modifying the actin structure of vascular endothelial cells 

Efficacy

Inhibition of cardiomyocyte necrosis in the Rat MI model

Excellent early myocardial cell protection effect in short-term model

Blocking edema in Rat MI model

Significant reduction in cardiac edema caused by I/R injury

Attenuation of inflammatory response in the Rat MI model

Significant decrease in endothelial cell adhesion protein expression and neutrophil influx after I/R injury

Inhibition of myocardial necrosis in the Mini-Pig MI model

Identical effect confirmed in pig (large animal) MI model and rat MI model