N-Methylnicotinamide
(Synonyms: N-甲基烟酰胺) 目录号 : GC40994
An isomer of nicotinamide
Cas No.:114-33-0
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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N-Methylnicotinamide is an isomer of nicotinamide. N-methylnicotinamide (20 mg/animal) increases urinary excretion of nicotinamide, 1-methylnicotinamide , 1-methyl-2-pyridone-5-carboxamide, and 1-methyl-4-pyridone-3-carboxamide in mice in similar ratios as those excreted following nicotinamide administration. It is also found in human urine.
| Cas No. | 114-33-0 | SDF | |
| 别名 | N-甲基烟酰胺 | ||
| Canonical SMILES | O=C(NC)C1=CC=CN=C1 | ||
| 分子式 | C7H8N2O | 分子量 | 136.2 |
| 溶解度 | DMF: 15 mg/ml,DMSO: 15 mg/ml,Ethanol: 2.5 mg/ml,PBS (pH 7.2): 10 mg/ml | 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 7.3421 mL | 36.7107 mL | 73.4214 mL |
| 5 mM | 1.4684 mL | 7.3421 mL | 14.6843 mL |
| 10 mM | 0.7342 mL | 3.6711 mL | 7.3421 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。
Structure of N-Methylnicotinamide
Acta Crystallogr C 1990 Sep 15;46 ( Pt 9):1723-5.PMID:2150911DOI:10.1107/s0108270190000658.
C7H8N2O, Mr = 136.2, monoclinic, P21/a, a = 7.055 (1), b = 9.849 (6), c = 10.066 (4) A, beta = 100.47 (2) degrees, V = 687.5 (5) A3, Z = 4, Dm = 1.32, Dx = 1.315 g cm-3, Cu K alpha, lambda = 1.5418 A, mu = 7.09 cm-1, F(000) = 288, T = 294 K, R = 0.048 for 1134 reflections [I greater than 3 sigma(I)]. The N-methylcarboxamide group is extended with the keto O(7) transoid to C(2) [C(2)--C(3)--C(7)--O(7) +/- 158.9 (3), C(3)--C(7)--N(7)--C(8) +/- 177.1 (3), C(2)--C(3)--C(7)--N(7) +/- 23.2 (3) and C(4)--C(3)--C(7)--N(7) +/- 158.2 (3) degrees]. The dihedral angle between the planes of the pyridine ring and the carboxamide plane is 22 degrees. The molecules are linked together by N--H...O hydrogen bonds involving the amino N(7) and the carbonyl O(7) atoms.
N-Methylnicotinamide inhibits arterial thrombosis in hypertensive rats
J Physiol Pharmacol 2007 Sep;58(3):515-27.PMID:17928647doi
There are few findings indicating that nicotinamide may potentially influence intravascular thrombosis. Interestingly, N-Methylnicotinamide, one of the metabolites of nicotinamide - could be more potent than its parent compound. In the present study we have investigated the influence of N-Methylnicotinamide on arterial thrombosis in normotensive and renovascular hypertensive rats. The contribution of platelets, coagulation and fibrinolytic systems in the mode of N-Methylnicotinamide action was also determined. Furthermore, we examined the role of nitric oxide/prostacyclin in the mechanisms of N-Methylnicotinamide action. N-Methylnicotinamide, but not nicotinamide, administered intravenously into renovascular hypertensive rats developing electrically induced arterial thrombosis caused dose-dependent decrease of thrombus weight, collagen-induced platelet aggregation and plasma antigen/activity of plasminogen activator inhibitor - 1, without changing of occlusion time, routine coagulation parameters and plasma activity of tissue plasminogen activator. Indomethacin - an inhibitor of prostacyclin synthesis, completely abolished the antithrombotic and antiplatelet effect of N-Methylnicotinamide, and the plasma level of 6-keto-PGF(1alpha) , prostacyclin metabolite, increased simultaneously with the inhibition of thrombus formation. Our study shows that N-Methylnicotinamide via production/release of prostacyclin inhibits arterial thrombosis development. The antithrombotic effect of N-Methylnicotinamide is accompanied by platelet inhibition and enhanced fibrinolysis, due to the decrease production of plasminogen activator inhibitor - 1.
N-Methylnicotinamide and nicotinamide N-methyltransferase are associated with microRNA-1291-altered pancreatic carcinoma cell metabolome and suppressed tumorigenesis
Carcinogenesis 2014 Oct;35(10):2264-72.PMID:25115443DOI:10.1093/carcin/bgu174.
The cell metabolome comprises abundant information that may be predictive of cell functions in response to epigenetic or genetic changes at different stages of cell proliferation and metastasis. An unbiased ultra-performance liquid chromatography-mass spectrometry-based metabolomics study revealed a significantly altered metabolome for human pancreatic carcinoma PANC-1 cells with gain-of-function non-coding microRNA-1291 (miR-1291), which led to a lower migration and invasion capacity as well as suppressed tumorigenesis in a xenograft tumor mouse model. A number of metabolites, including N-Methylnicotinamide, involved in nicotinamide metabolism, and l-carnitine, isobutyryl-carnitine and isovaleryl-carnitine, involved in fatty acid metabolism, were elevated in miR-1291-expressing PANC-1. Notably, N-Methylnicotinamide was elevated to the greatest extent, and this was associated with a sharp increase in nicotinamide N-methyltransferase (NNMT) mRNA level in miR-1291-expressing PANC-1 cells. In addition, expression of NNMT mRNA was inversely correlated with pancreatic tumor size in the xenograft mouse model. These results indicate that miR-1291-altered PANC-1 cell function is associated with the increase in N-Methylnicotinamide level and NNMT expression, and in turn NNMT may be indicative of the extent of pancreatic carcinogenesis.
N-Methylnicotinamide protects against endothelial dysfunction and attenuates atherogenesis in apolipoprotein E-deficient mice
Mol Nutr Food Res 2016 Jul;60(7):1625-36.PMID:26887666DOI:10.1002/mnfr.201501019.
Scope: Epidemiological studies have demonstrated that N-Methylnicotinamide (MNA) may exert antithrombotic and anti-inflammatory effects on the endothelium. However, the exact role of MNA in endothelial function remains uncertain. Methods and results: Apolipoprotein E-deficient (apoE(-/-) ) mice fed with a high-fat, high-cholesterol diet (HCD) and human umbilical vein endothelial cells (HUVECs) were used to explore the role of MNA in endothelial function and its underlying mechanism. The endothelium-dependent vasorelaxation to acetylcholine in the aortas of low and high dose MNA-fed apoE(-/-) mice was improved by 24 and 36% (p < 0.05), respectively, compared with high-fat, HCD-fed control. MNA significantly increased nitric oxide/cyclic guanosinemonophosphate levels and decreased asymmetric dimethylarginine (ADMA) concentrations by induction of dimethylarginine dimethylaminohydrolase (DDAH)2 both in aorta and endothelial cells. Neither the activity nor the protein expression of DDAH1 was influenced upon MNA treatment. Then, DDAH2 depletion by RNA interference in HUVECs abolished the protective effect of MNA on endothelial function. Mechanically, this could be attributed to a direct modulation of the methylation level of DDAH2 gene promoter region by MNA. Conclusions: The present study reveals a novel mechanism through which MNA improves endothelial dysfunction and attenuates atherogenesis via the modulation of ADMA-DDAH axis.
N-Methylnicotinamide excretion and affective disorders
Psychol Med 1976 May;6(2):265-70.PMID:137411DOI:10.1017/s0033291700013817.
N-Methylnicotinamide urinary output is examined in 38 healthy volunteers, 52 patients with secondary affective disorders (SAD), 55 patients with primary affective disorders (PAD) and 46 healthy first-degree relatives of PAD patients. The results indicate (1) that in PAD patients and their first-degree relatives the frequency of low N1-MN excretion was significantly higher (P less than 0-001) than in healthy controls and in patients with secondary affective disorders, and (2) that PAD patients have a consistently low N1-MN output, at all times constant and independent of the clinical phases of the disease. These findings provide evidence that the low N1-MN levels may represent an index of a biological background linked to a high morbidity risk for primary affective disorders. The theoretical implications deriving from these data are briefly discussed.