β-烟酰胺单核苷酸-烟酰胺单核苷酸

中文名称:

β-烟酰胺单核苷酸

中文同义词:

Β-烟酰胺单核苷酸 ?NMN,烟酰胺单核苷酸;A-烟酰胺单核苷酸;Β-烟酰胺单核苷酸(烟酰胺核苷酸);烟酰胺核苷酸(Β-NMN);烟酰胺核苷酸(BETA-NMN);烟酰胺核苷酸;NMN(Β-烟酰胺单核苷酸;Β-烟酰胺单核苷酸

英文名称:

β-Nicotinamide Mononucleotide

英文同义词:

BETA-NMN;BETA-NICOTINAMIDE MONONUCLEOTIDE;BETA-NICOTINAMIDE RIBOSE MONOPHOSPHATE;3-(aminocarbonyl)-1-(5-O-phosphonato-beta-D-ribofuranosyl)pyridinium;B-NICOTINAMIDE MONONUCLEOTIDE;NMN;NICOTINAMIDE-1-IUM-1-BETA-D-RIBOFURANOSIDE 5-PHOSPHATE;NICOTINAMIDE RIBOTIDE

CAS号:

1094-61-7

分子式:

C11H15N2O8P

分子量:

334.22

EINECS号:

214-136-5

相关类别:

甾体;化妆品原料;辅酶及核苷酸原料;杂化;原药中间体;中药对照品;抗衰老研究，抗衰老保健品原料;酶;原料药;医药原料;原料;食品添加剂;保健品原料;辅酶;中间体;试剂;医药原料中间体;保健品;医药保健品;医药原料药;有机原料;合成;营养剂;植提 核苷类;化工中间体;化工原料;分析试剂标准品;辅酶核糖核苷核酸系列;化工产品原料药;医药化工原料;成品;β-烟酰胺单核苷酸;杂化;新品;其他原料;有机中间体;日用化学品-化妆品原料;产品2;化妆品原料-功能性原料;抗衰;调节剂;精细化工;Amines;Aromatics;Bases Related Reagents;Intermediates Fine Chemicals;Nicotine Derivatives;Nucleotides;Pharmaceuticals;nicotinamide mononucleotide;API;BETA-NICOTINAMI;标准品;芳烃;大货;医药化工原料;原料药-保健品添加;有机化工原料;化工材料;农药、医药;保健品添加剂;功能性食品添加;化学中间体;核苷系列;化工原料

Mol文件:

1094-61-7.mol

熔点 

166 °C(dec.)

储存条件 

2-8°C

Merck 

13,6697

BRN 

3570187

InChIKey

DAYLJWODMCOQEW-TURQNECASA-N

简介

β-烟酰胺单核苷酸-烟酰胺单核苷酸又叫β-烟酰胺单核苷酸(NMN)，是辅酶I的合成底物，同时NMN也被用于抗衰老研究。日本庆应义塾大学和美国华盛顿大学合作，正在对β-NMN的抗衰老效果和安全性进行人体临床试验。研究表明，β-NMN对胰岛素的分泌也能起到调节作用，对mRNA的表达水平也有影响，β-NMN在医疗治疗领域有着广泛的应用前景。

来源

烟酰胺单核苷酸（Nicotinamide mononucleotide），简称NMN，是人体内固有的物质，也富含在一些水果和蔬菜中，包括西兰花、卷心菜等。

生理功能

在哺乳动物体内，β-烟酰胺单核苷酸由烟酰胺(Nicotinamide，Nam)在Nampt（体内一种蛋白酶）的催化下生成，随后烟酰胺单核苷酸在烟酰胺单核苷酸腺苷转移酶的催化下生成NAD+。烟酰胺单核苷酸是补充NAD+直接的方式。烟酰胺单核苷酸正是通过显著提升细胞内DNA损伤的修复能力，最终实现了逆转衰老的效果。 烟酰胺单核苷酸会转化成体内能量代谢必不可少的“烟酰胺腺嘌呤二核苷酸(NAD)”物质。在小鼠试验中，证实烟酰胺单核苷酸可激活体内一种叫做乙酰化酶的基因，以此发挥延年益寿和治疗糖尿病等效果。NAD是人体原本可以生成的物质，研究证实体内的NAD含量会随着年龄的增加而减少。;

抗衰老作用机制

β-烟酰胺单核苷酸是人体内长寿蛋白的辅因子NAD+的前体物质。NAD+是三羧酸循环的重要辅酶，促进糖、脂肪、氨基酸的代谢，参与能量的合成；NAD+又是辅酶I消耗酶的唯一底物（DNA修复酶PARP的唯一底物、长寿蛋白Sirtuins的唯一底物、环ADP核糖合成酶CD38/157的唯一底物）。 NAD+参与人体新陈代谢的方方面面，是关键性的辅酶，缺了NAD+，新陈代谢就不行了，老年人缺少了NAD+，于是各种大大小小的毛病就来了，通过额外补充NAD+，可以全面抗衰老。

生物活性

Nicotinamide mononucleotide (β-NM, NMN)是NAD+的关键前体之一，也是NAMPT反应的产物，通过烟酰胺单核苷酸腺苷酸转移酶转化为NAD+。

靶点

Human Endogenous Metabolite

Human Endogenous Metabolite

体外研究

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, Alzheimers disease, and complications associated with obesity. 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.

体内研究

β-Nicotinamide mononucleotide (500 mg/kg; i.p.; 3 times per week for 7-10 week) prevents mtDNA damage and Dox-induced cardiac dysfunction. 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. 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. Animal Model: C57BL6 mice (p53 −/− mice) 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).

Animal Model:

C57BL6 mice (p53 −/− mice)

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).

WGK Germany 

3

F 

8-10-21