N-Methylmoranoline (MOR 14) is an α-glucosidase inhibitor.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Arai M, et al. N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly reduced infarct size in rabbit hearts. Circulation. 1998 Apr 7;97(13):1290-7.  [Content Brief]

  . Arai M, et al. Role of protein kinase C in the reduction of infarct size by N-methyl-1-deoxynojirimycin, an alpha-1,6-glucosidase inhibitor. Br J Pharmacol. 2001 Jul;133(5):635-42.  [Content Brief]

  . Nishida Y, et al. N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly improves postischemic left ventricular dysfunction. Heart Vessels. 2000;15(6):268-73.  [Content Brief]