CAMI103 Midkine Protein for Heart Attack

The death of heart muscle cells (cardiomyocytes) is the major cause of loss of heart function from heart attack (also known as acute myocardial infarction, or AMI). Cell death occurs within 24-48 hours after heart attack through a process called apoptosis. Preventing this apoptosis represents a promising therapeutic approach to rescue the heart from post-heart attack damage.

Midkine is a potent anti-apoptotic growth factor. Cellmid scientists made the important discovery that during AMI, cardiomyocytes produce midkine. MK production by cardiomyocytes (‘endogenous MK’) during AMI is an attempt by these cells to save themselves from cell death. Endogenous MK can reduce cell death, but its effectiveness is limited by the small quantity and slow speed at which it is produced. However, if MK is added to cardiomyocytes by intravenous infusion or catheter (‘exogenous MK’) this protective effect is greatly enhanced. Using animal models, Cellmid has confirmed that a single dose of extraneous MK reduces cardiomyocyte death, thereby limiting infarct size and minimising damage to the heart muscle. Reducing heart damage results in preserved cardiac function, and consequently to improved post-AMI survival.

Cellmid has a pre-clinical program underway to evaluate MK protein for treatment of AMI in collaboration with cardiovascular specialists Pharmahungary.