N-Methylmoranoline dose-dependently decreases the α-1,6-glucosidase activity in rabbit heart extract. The myocardial uptake of a considerable amount of N-Methylmoranoline is sufficient to fully inhibit alpha-1,6-glucosidase. Preischemic treatment with 25, 50, and 100 mg/kg of N-Methylmoranoline dose-dependently reduces the infarct size without altering the blood pressure or heart rate. MOR-14 significantly increases levels of PKC-ε in the particulate fraction at 20 and 30?min of ischaemia and in the cytosolic fraction at 30?min of ischaemia.

N-Methylmoranoline decreases the alpha-1,6-glucosidase activity to approximately 20%, reduces the glycogen breakdown, and attenuates the lactate accumulation at both 10 and 30 minutes of ischemia. MOR-14 is protective against postischemic left ventricular dysfunction through the inhibition of glycogenolysis in the isolated rat heart.