β-Nicotinamide mononucleotide(Synonyms: 烟酰胺单核苷酸; β-NM; NMN)

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β-Nicotinamide mononucleotide (Synonyms: 烟酰胺单核苷酸; β-NM; NMN) 纯度: 99.47%

β-nicotinamide mononucleotide (β-NM) 是烟酰胺磷酸核糖转移酶 (NAMPT) 反应的产物，NAD+ 的关键中间体。β-nicotinamide mononucleotide 的作用包括其在细胞生化功能、心脏保护、糖尿病、阿尔茨海默病和肥胖相关并发症中的作用。

β-Nicotinamide mononucleotide(Synonyms: 烟酰胺单核苷酸; β-NM; NMN)

β-Nicotinamide mononucleotide Chemical Structure

CAS No. : 1094-61-7

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500 mg ￥5700 In-stock
1 g ￥8550 In-stock
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生物活性

β-nicotinamide mononucleotide (β-NM) is a product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and a key NAD+ intermediate. The pharmacological activities of β-nicotinamide mononucleotide include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer’s disease, and complications associated with obesity[1].

IC50 & Target

Human Endogenous Metabolite

 

体外研究
(In Vitro)

β-nicotinamide mononucleotide has several beneficial pharmacological activities. Mostly mediated by its involvement in NAD+ biosynthesis, the pharmacological activities of NMN include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer’s disease, and complications associated with obesity[1].
The intracellular NAD+ levels are significantly decreased by knockdown or knockout of Nampt (Nampt KD or Nampt KO) or treatment with Nampt inhibitor FK866, whereas NAD+ levels are dramatically increased by supplement of NAD+ precursors NAM or NMN (0.5-1 mM). NAD+ precursor NMN treatment inhibited CD8+ T cells activation and function[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

β-Nicotinamide mononucleotide (500 mg/kg; i.p.; 3 times per week for 7-10 week) prevents mtDNA damage and Dox-induced cardiac dysfunction[3].
Nampt KO markedly inhibits tumor progression, whereas Nampt metabolite β-Nicotinamide mononucleotide (300 mg/kg body weight; i.p.; once every two days for 2 weeks) significantly promotes tumor growth in C57BL/6 mice (bearing wildtype Hepa1-6 cells). The reduction and increase in NAD+ level of respective Nampt KO and β-Nicotinamide mononucleotide-treated tumors are confirmed[2].
β-nicotinamide mononucleotide ameliorates glucose intolerance by restoring NAD+ levels in HFD-induced T2D mice. β-nicotinamide mononucleotide also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation[4].

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

Animal Model: C57BL6 mice (p53−/− mice)[3]
Dosage: 500 mg/kg
Administration: I.p.; 3 times per week for 7-10 week
Result: Prevented the significant decline in cardiac function of Dox-treated p53−/− mice (study week 7 versus 10) along with rescuing the decreased mitochondrial respiration and tissue ATP depletion caused by Doxorubicin (Dox).

分子量

334.22

Formula

C11H15N2O8P
CAS 号

1094-61-7
中文名称

β-烟酰胺单核苷酸；烟酰胺单核苷酸
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
溶解性数据
In Vitro: 

H2O : 83.33 mg/mL (249.33 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.9920 mL 14.9602 mL 29.9204 mL
5 mM 0.5984 mL 2.9920 mL 5.9841 mL
10 mM 0.2992 mL 1.4960 mL 2.9920 mL

*

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, 6 months; -20°C, 1 month (protect from light)。-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。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂： PBS

    Solubility: 100 mg/mL (299.20 mM); Clear solution; Need ultrasonic

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Poddar SK, et al. Nicotinamide Mononucleotide: Exploration of Diverse Therapeutic Applications of a Potential Molecule. Biomolecules. 2019;9(1):34. Published 2019 Jan 21.

    [2]. Lv H, et al. NAD+ Metabolism Maintains Inducible PD-L1 Expression to Drive Tumor Immune Evasion [published online ahead of print, 2020 Nov 3]. Cell Metab. 2020;S1550-4131(20)30554-4.

    [3]. Li J, et al. p53 prevents doxorubicin cardiotoxicity independently of its prototypical tumor suppressor activities. Proc Natl Acad Sci U S A. 2019;116(39):19626-19634.

    [4]. Yoshino J, et al Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011;14(4):528-536.