N-Methylmoranoline  (Synonyms: MOR 14; N-Methyl-1-deoxynojirimycin; N-Methylmoranolin)

The inhibitory action of N-Methylmoranoline against myocardial α-1,6-glucosidase is first examined in rabbit heart extracts. The substrate mixture contained 44 mM glycylglycine (pH 6.5), 12.5% rabbit liver glycogen, 2.5 mM [¹⁴C]glucose (20 μCi/μM), 2.1 mM EDTA, 4.1 mM mercaptoethanol, 0.02% gelatin, and N-Methylmoranoline (0, 0.01, 0.03, 0.1, 0.3, or 1.0 μM). This solution (16 μL) is warmed at 30°C for 2 minutes, and the reaction is then initiated by the addition of 4 μL of the rabbit heart homogenate. The reaction is stopped 60 minutes later by the addition of 20 μL of 0.2N HCl. An aliquot (30 μL) is spotted onto a Whatman GF/A glass fiber disk. The disk is immediately washed in 66% ethanol for 20 minutes three times each and dipped in 15 mL of acetone for 10 minutes. Then the disk is dried, and the [¹⁴C] activity incorporated into glycogen is measured with a liquid scintillation counter^[1].

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

Rabbits: To investigate the infarct size-reducing effect of N-Methylmoranoline, 54 rabbits are assigned randomly into drug treatment or saline control groups. There are four drug treatment groups, ie, three preischemic treatment groups given 100 mg/kg, 50 mg/kg, or 25 mg/kg of N-Methylmoranoline 10 minutes before ischemia, and one prereperfusion treatment group given 100 mg/kg of the drug 5 minutes before reperfusion. In all treatments, the injected volume is <1 mL/kg body wt. After the treatment, the coronary artery is occluded for 30 minutes and reperfused. The blood pressure and heart rate are monitored throughout the experiment until 20 minutes after reperfusion and are recorded at baseline, at 0, 1, 3, 5, 10, 20, and 30 minutes of ischemia, and at 5, 10, and 20 minutes of reperfusion^[1].

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

• [1]. 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]

  [2]. 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]

  [3]. 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]