As expected, all injured hearts showed some spontaneous arrhythmias, particularly around the time of infarction and transplantation. Importantly, there was no significant difference in the incidence of either spontaneous or induced arrhythmias between the recipients of GRNCM1 and vehicle, demonstrating the lack of arrhythmogenic potential of GRNCM1 in this setting of myocardial infarction.

Geron is currently conducting studies of GRNCM1 in a swine model of myocardial infarction to further assess preclinical safety and efficacy of GRNCM1 in an additional animal model with a cardiovascular system of similar size and structure to humans.

Previously, Geron scientists and collaborators from the University of Washington Medical School showed that when GRNCM1 was transplanted into a rodent model of acute myocardial infarction, human cardiac grafts survived in the infarct zone. Analysis by echocardiography and MRI showed significantly improved cardiac structure and contractile function compared to controls. These data were published in the journal Nature Biotechnology.

According to the American Heart Association, congestive heart failure, a common consequence of heart muscle or valve damage, affects approximately 5.8 million people in the United States and approximately half of those diagnosed will die within five years. Each year over 1.2 million people have a heart attack, which is the primary cause of heart muscle damage. GRNCM1 could treat heart failure by replacing damaged myocardium with new viable cardiac cells to restore cardiac function.

SOURCE Geron Corporation