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。
| 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 |
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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].
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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].
| 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). |
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| 结构分类 | - Ketones, Aldehydes, Acids
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| 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 | 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℃, 6 months; -20℃, 1 month (protect from light)。-80℃ 储存时，请在 6 个月内使用，-20℃ 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本网站选购。 |
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