Nicotinamide N-oxide
(Synonyms: 烟酰胺-N-氧化物) 目录号 : GC36737
A metabolite of nicotinamide
Cas No.:1986-81-8
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: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nicotinamide N-oxide is a metabolite of nicotinamide .1 It is formed via oxidation of nicotinamide by the cytochrome P450 (CYP) isoform CYP2E1. Nicotinamide N-oxide (30 mM) inhibits proliferation and induces reduction of nitroblue tetrazolium , indicating cell differentiation, in HL-60 promyelocytic leukemia cells.2 Urine levels of nicotinamide N-oxide are elevated in a mouse model of high-fat diet-induced obesity.3
1.Real, A.M., Hong, S., and Pissios, P.Nicotinamide N-oxidation by CYP2E1 in human liver microsomesDrug Metab. Dispos.41(3)550-553(2013) 2.Iwata, K., Ogata, S., Okumura, K., et al.Induction of differentiation in human promyelocytic leukemia HL-60 cell line by niacin-related compoundsBiosci. Biotechnol. Biochem.67(5)1132-1135(2003) 3.Jung, J.Y., Kim, I.Y., Kim, Y.N., et al.1H NMR-based metabolite profiling of diet-induced obesity in a mouse modeBMB Rep.45(7)419-424(2012)
| Cas No. | 1986-81-8 | SDF | |
| 别名 | 烟酰胺-N-氧化物 | ||
| Canonical SMILES | O=C(C1=C[N+]([O-])=CC=C1)N | ||
| 分子式 | C6H6N2O2 | 分子量 | 138.12 |
| 溶解度 | DMSO: 6.6 mg/mL (47.78 mM) | 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 | 7.2401 mL | 36.2004 mL | 72.4008 mL |
| 5 mM | 1.448 mL | 7.2401 mL | 14.4802 mL |
| 10 mM | 0.724 mL | 3.62 mL | 7.2401 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。
Nicotinamide N-oxide Attenuates HSV-1-Induced Microglial Inflammation through Sirtuin-1/NF-κB Signaling
Int J Mol Sci 2022 Dec 16;23(24):16085.PMID:36555725DOI:10.3390/ijms232416085.
HSV-1 is a typical neurotropic virus that infects the brain and causes keratitis, cold sores, and occasionally, acute herpes simplex encephalitis (HSE). The large amount of proinflammatory cytokines induced by HSV-1 infection is an important cause of neurotoxicity in the central nervous system (CNS). Microglia, as resident macrophages in CNS, are the first line of defense against neurotropic virus infection. Inhibiting the excessive production of inflammatory cytokines in overactivated microglia is a crucial strategy for the treatment of HSE. In the present study, we investigated the effect of Nicotinamide N-oxide (NAMO), a metabolite mainly produced by gut microbe, on HSV-1-induced microglial inflammation and HSE. We found that NAMO significantly inhibits the production of cytokines induced by HSV-1 infection of microglia, such as IL-1β, IL-6, and TNF-α. In addition, NAMO promotes the transition of microglia from the pro-inflammatory M1 type to the anti-inflammatory M2 type. More detailed studies revealed that NAMO enhances the expression of Sirtuin-1 and its deacetylase enzymatic activity, which in turn deacetylates the p65 subunit to inhibit NF-κB signaling, resulting in reduced inflammatory response and ameliorated HSE pathology. Therefore, Sirtuin-1/NF-κB axis may be promising therapeutic targets against HSV-1 infection-related diseases including HSE.
The intestinal microbial metabolite Nicotinamide N-oxide prevents herpes simplex encephalitis via activating mitophagy in microglia
Gut Microbes 2022 Jan-Dec;14(1):2096989.PMID:35793266DOI:10.1080/19490976.2022.2096989.
Herpes simplex encephalitis (HSE), a complication of herpes simplex virus type I (HSV-1) infection causes neurological disorder or even death in immunocompromised adults and newborns. However, the intrinsic factors controlling the HSE outcome remain unclear. Here, we show that HSE mice exhibit gut microbiota dysbiosis and altered metabolite configuration and tryptophan-nicotinamide metabolism. HSV-1 neurotropic infection activated microglia, with changed immune properties and cell numbers, to stimulate antiviral immune response and contribute substantially to HSE. In addition, depletion of gut microbiota by oral antibiotics (ABX)-treatment triggered the hyper-activation of microglia, which in turn enhanced inflammatory immune response, and cytokine production, resulting in aggregated viral burden and HSE pathology. Furthermore, exogenous administration of Nicotinamide N-oxide (NAMO), an oxidative product of nicotinamide derived from gut microbiota, to ABX-treated or untreated HSE mice significantly diminished microglia-mediated proinflammatory response and limited HSV-1 infection in CNS. Mechanistic study revealed that HSV-1 activates microglia by increasing mitochondrial damage via defective mitophagy, whereas microbial metabolite NAMO restores NAD+-dependent mitophagy to inhibit microglia activation and HSE progression. NAMO also prevented neuronal cell death triggered by HSV-1 infection or microglia-mediated microenvironmental toxicity. Finally, we show that NAMO is mainly generated by neomycin-sensitive bacteria, especially Lactobacillus_gasseri and Lactobacillus_reuteri. Together, these data demonstrate that gut microbial metabolites act as intrinsic restrictive factors against HSE progression via regulating mitophagy in microglia, implying further exploration of bacterial or nutritional approaches for treating neurotropic virus-related neurodegenerative diseases.
Nicotinamide N-oxide reductase activity in bovine and rabbit eyes
Invest Ophthalmol Vis Sci 1987 Jul;28(7):1204-6.PMID:2954926doi
The Nicotinamide N-oxide reductase activity of a variety of ocular tissues was investigated. The 9,000g supernatant of ciliary body, retinal pigment epithelium-choroid, iris, retina and cornea, but not lens, exhibited reductase activity under anaerobic conditions when supplemented with 2-hydroxypyrimidine, an electron donor of aldehyde oxidase. Among these tissues, the highest activity was observed with ciliary body. When the 9,000g supernatant of ciliary body was fractionated, the 2-hydroxypyrimidine-linked reductase activity was mainly associated with the cytosolic fraction and was markedly inhibited by menadione, an inhibitor of aldehyde oxidase. Similarly, in the presence of 2-hydroxypyrimidine, the cytosolic fraction of rabbit ciliary body exhibited Nicotinamide N-oxide reductase activity which was susceptible to inhibition by menadione. These facts strongly suggest that aldehyde oxidase present in mammalian eyes is involved in the reduction of Nicotinamide N-oxide to nicotinamide.
Simultaneous measurement of nicotinamide and its catabolites, Nicotinamide N-oxide, N(1)-methyl-2-pyridone-5-carboxamide, and N(1)-methyl-4-pyridone-3-carboxamide, in mice urine
Biosci Biotechnol Biochem 2014;78(8):1306-9.PMID:25130730DOI:10.1080/09168451.2014.918495.
Nicotinamide N-oxide is a major nicotinamide catabolite in mice but not in humans and rats. A high-performance liquid chromatographic method for the simultaneous measurement of nicotinamide, Nicotinamide N-oxide, N(1)-methyl-2-pyridone-5-carboxamide, and N(1)-methyl-4-pyridone-3-carboxamide in mice urine was developed by modifying the mobile phase of a reported method for measurement of Nicotinamide N-oxide.
Effects of excess nicotinamide administration on the urinary excretion of Nicotinamide N-oxide and nicotinuric acid by rats
Biosci Biotechnol Biochem 2004 Jan;68(1):44-50.PMID:14745162DOI:10.1271/bbb.68.44.
We investigated a useful chemical index for an excessive nicotinamide intake and how this excessive nicotinamide intake affects the tryptophan-nicotinamide metabolism in rats. Weaning rats were fed on a tryptophan-limited and nicotinic acid-free diet containing no, 0.003%, 0.1%, 0.2%, or 0.3% nicotinamide for 21 days. Urine samples were collected on the last day and analyzed the intermediates and metabolites on the tryptophan-nicotinamide pathway. Nicotinamide N-oxide, nicotinic acid and nicotinuric acid, metabolites of nicotinamide, were detected when nicotinamide at more than 0.1% had been taken. An intake of nicotinamide of more than 0.1% increased the urinary excretion of quinolinic acid, an intermediate on the pathway. Nicotinamide N-oxide and nicotinuric acid increased with increasing dietary concentration of nicotinamide. These results show that the measurements of Nicotinamide N-oxide and nicotinuric acid in urine would be useful indices for an excessive nicotinamide intake.