N-Methylmoranoline (MOR 14)
(Synonyms: 丙二腈,MOR 14; N-Methyl-1-deoxynojirimycin; N-Methylmoranolin) 目录号 : GC30637
An inhibitor of glycoprotein processing and α-glucosidases
Cas No.:69567-10-8
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Kinase experiment: | 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]. |
Animal experiment: | 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]. |
References: [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. | |
N-Methyldeoxynojirimycin is an inhibitor of α-glucosidases and glycoprotein processing.1 It inhibits the rabbit intestinal α-glucosidases sucrase and maltase (IC50s = 0.068 and 0.46 ?g/ml, respectively) and R. niveus glucoamylase (IC50s = 1.6 and 4.7 ?g/ml with starch or maltose as substrates, respectively).2 It is selective for these enzymes over β-glucosidase (IC50 = 363 ?g/ml). N-Methyldeoxynojirimycin inhibits highly pathogenic avian influenza (HPAI) oligosaccharide processing in HPAI-infected chicken embryo cells.1 It reduces the cytopathic effect of HIV in infected Karpas-45 T cells.3 N-Methyldeoxynojirimycin also inhibits postprandial increases in blood glucose levels in sucrose-loaded rats (ED50 = 5.8 mg/kg).
1.Romero, P.A., Datema, R., and Schwarz, R.T.N-Methyl-1-deoxynojirimycin, a novel inhibitor of glycoprotein processing, and its effect on fowl plague virus maturationVirology130(1)238-242(1983) 2.Yoshikuni, Y.Inhibition of intestinal α-glucosidase activity and postprandial hyperglycemia by moranoline and its N-alkyl derivativesAgric. Biol. Chem.52(1)121-128(1988) 3.Karpas, A., Fleet, G.W.J., Dwek, R.A., et al.Aminosugar derivatives as potential anti-human immunodeficiency virus agentsProc. Natl. Acad. Sci. USA85(23)9229-9233(1988)
| Cas No. | 69567-10-8 | SDF | |
| 别名 | 丙二腈,MOR 14; N-Methyl-1-deoxynojirimycin; N-Methylmoranolin | ||
| Canonical SMILES | O[C@@H]1[C@@H](CO)N(C)C[C@H](O)[C@H]1O | ||
| 分子式 | C7H15NO4 | 分子量 | 177.2 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.6433 mL | 28.2167 mL | 56.4334 mL |
| 5 mM | 1.1287 mL | 5.6433 mL | 11.2867 mL |
| 10 mM | 0.5643 mL | 2.8217 mL | 5.6433 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly reduced infarct size in rabbit hearts
Background: N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, reduces the glycogenolytic rate by inhibiting the alpha-1,6-glucosidase of glycogen-debranching enzyme in the liver, in addition to possessing an antihyperglycemic action by blocking alpha-1,4-glucosidase in the intestine. Because the reduction of the glycogenolytic rate may be one of the mechanisms of myocardial protection in ischemic preconditioning, the compounds inhibiting myocardial alpha-1,6-glucosidase may be protective against ischemic damage. Thus, we investigated whether MOR-14 could inhibit alpha-1,6-glucosidase and reduce the infarct size in rabbit hearts without collateral circulation. Methods and results: MOR-14 dose-dependently decreased the alpha-1,6-glucosidase activity in rabbit heart extract. A tracer study demonstrated the myocardial uptake of a considerable amount of MOR-14 sufficient to fully inhibit alpha-1,6-glucosidase. To assess the infarct size-reducing effect of MOR-14, 54 rabbits were subjected to 30-minute coronary occlusion followed by 48-hour reperfusion. Preischemic treatment with 25, 50, and 100 mg/kg of MOR-14 dose-dependently reduced the infarct size (to 26+/-4%, 19+/-3%, and 14+/-2% of the area at risk, respectively), compared with the saline control (45+/-5%) without altering the blood pressure or heart rate. Another 40 rabbits given 100 mg of MOR-14 or saline 10 minutes before ischemia were euthanized at 10 or 30 minutes of ischemia for biochemical analysis. MOR-14 decreased the alpha-1,6-glucosidase activity to approximately 20% in vivo, reduced the glycogen breakdown, and attenuated the lactate accumulation at both 10 and 30 minutes of ischemia. Conclusions: Preischemic treatment with MOR-14 preserved glycogen, attenuated the accumulation of lactate, and reduced the myocardial infarct size by 69%. This cardioprotective effect was independent of changes of blood pressure and heart rate or regional blood flow. It may be associated with alpha-1,6-glucosidase inhibition, because MOR-14 markedly decreased the alpha-1,6-glucosidase activity in the heart.
N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly improves postischemic left ventricular dysfunction
We examined whether pharmacological inhibition of glycogenolysis by N-methyl-1-deoxynojirimycin (MOR-14), a new compound which reduces the glycogenolytic rate by inhibiting the alpha-1,6-glucosidase activity of the glycogen-debranching enzyme, can protect the heart against postischemic left ventricular dysfunction. The hearts of male Sprague-Dawley rats were excised, and perfused on a Langendorff apparatus with Krebs-Henseleit solution with a gas mixture of 95% O2 and 5% CO2. The hearts were paced at 320 beats/min except during the ischemia. Left ventricular developed pressure (LVDP, mmHg), +/-dP/dt (mmHg/s), and coronary flow (ml/min) were continuously monitored. All hearts were perfused for a total of 120 min including a 30-min preischemic period followed by a 30-min episode of global ischemia and 60 min reperfusion. with or without 0.5 or 2 mM of MOR-14 during the 30-min preischemic period or the first 30 min of reperfusion. In another series of experiments, the myocardial content of glycogen and lactate was measured during the 30-min episode of ischemia in groups treated with and without 2mM of MOR-14. Preischemic but not postischemic treatment with MOR-14 significantly improved LVDP and +/-dP/dt without altering coronary flow during reperfusion in a dose-dependent manner. MOR-14 significantly preserved the glycogen content and significantly attenuated the lactate accumulation during the 30-min episode of ischemia. Preischemic treatment with MOR-14 is protective against postischemic left ventricular dysfunction through the inhibition of glycogenolysis in the isolated rat heart.
Sexual Contact as Risk Factor for Campylobacter Infection, Denmark
Campylobacteriosis is a disease of worldwide importance, but aspects of its transmission dynamics, particularly risk factors, are still poorly understood. We used data from a matched case-control study of 4,269 men who have sex with men (MSM) and 26,215 controls, combined with national surveillance data on Campylobacter spp., Salmonella spp., and Shigella spp., to calculate matched odds ratios (mORs) for infection among MSM and controls. MSM had higher odds of Campylobacter ( mOR 14, 95% CI 10-21) and Shigella (mOR 74, 95% CI 27-203) infections, but not Salmonella (mOR 0.2, 95% CI 0-13), and were less likely than controls to have acquired Campylobacter infection abroad (χ2 = 21; p<0.001). Our results confirm that sexual contact is a risk factor for campylobacteriosis and also suggest explanations for unique features of Campylobacter epidemiology. These findings provide a baseline for updating infection risk guidelines to the general population.
Inhibitors of oligosaccharide processing
Role of protein kinase C in the reduction of infarct size by N-methyl-1-deoxynojirimycin, an alpha-1,6-glucosidase inhibitor
Preischaemic treatment with N-methyl-1-deoxynojirimycin (MOR-14), an alpha-1,6-glucosidase inhibitor, attenuates glycogenolysis and lactate accumulation during ischaemia and markedly reduces infarct size in rabbit hearts. In the present study, we have investigated whether protein kinase C (PKC), a principal mediator of ischaemic preconditioning, is also involved in the cardioprotective effect of MOR-14. To assess the effect of PKC inhibition on infarct size in MOR-14-treated hearts, 38 rabbits were subjected to 30 min of ischaemia followed by 48 h of reperfusion. Infarct size, as a per cent of area at risk, was significantly smaller in rabbits administered 100 mg kg(-1) of MOR-14 10 min before ischaemia (17+/-2%, n=10), than in a control group (46+/-5%, n=10). This beneficial effect of MOR-14 was abolished when 5 mg kg(-1) of chelerythrine, a PKC inhibitor, was given 10 min prior to MOR-14 injection (39+/-4%, n=10), although chelerythrine alone did not alter infarct size (43+/-4%, n=8). Further, chelerythrine had no effect on MOR-14-induced attenuation of glycogen breakdown and lactate accumulation in hearts excised at 30 min of ischaemia. Immunoblot analysis of PKC in homogenates of Langendorff-perfused rabbit hearts revealed that MOR-14 significantly increased levels of PKC-epsilon in the particulate fraction at 20 and 30 min of ischaemia and in the cytosolic fraction at 30 min of ischaemia. Taken as a whole, our data suggest that PKC acts downstream of the inhibition of glycogenolysis by MOR-14 to reduce infarct size. Thus, activation of PKC is a more direct mediator of the cardioprotection afforded by MOR-14 than is inhibition of glycogenolysis.