Geron (GERN) Preclinical Study Data of GRNCM1
GRNCM1, a cardiomyocyte product derived from human embryonic stem cells (hESCs), in a small animal model of acute heart damage was administered by injection into the heart which resulted in greater resistance to induced arrhythmias, halted adverse cardiac remodeling and preserved mechanical function compared to controls.
- The results suggest that GRNCM1 positively impacts cardiac function through several mechanisms, leading to overall increased cardiac output and decreased arrhythmias in the acute infarct setting;
- GERN is developing GRNCM1 for the treatment of myocardial disease;
- A guinea pig model was used to assess the potential for arrhythmias from GRNCM1 because the animal’s heart rate and electrophysiology are more similar to humans than other small animal models;
- Myocardial infarction was induced by cryo-injury; 7 days after injury, GRNCM1 was administered into the heart. In the control groups, ventricular tachycardia was induced in 61.5% (8/13) of animals that received non-cardiac cells and 50% (7/14) that received vehicle only. In contrast, ventricular tachycardia was induced in only 6% (1/15) of animals that received GRNCM1, suggesting a protective effect against arrhythmias in this acute model.
The Bottom Line: The current data suggests that GRNCM1 halts the remodeling process and preserves cardiac function. GERN used a guinea pig model of acute cardiac injury and found that, recipients of hESC-cardiomyocytes showed fewer induced arrhythmias 1 month after transplantation. These results are important because following an acute myocardial infarction patients are at an elevated risk of cardiac arrhythmias, which can be fatal. A cardiac arrhythmia is an abnormality of the heart rhythm, which can cause the heart to pump less efficiently. According to the AHA, congestive heart failure, a common consequence of heart muscle or valve damage, affects approximately 5M people in the US and it is estimated that every year about 1M people will have a heart attack, which is the primary cause of heart muscle damage.