1094-61-7

1094-61-7 - Names and Identifiers

Name	beta-nicotinamide mononucleotide
Synonyms	NMN BETA-NMN NICOTINAMIDE RIBOTIDE Nicotinamide mononucleotide B-NICOTINAMIDE MONONUCLEOTIDE β-Nicotinamide mononucleotide beta-nicotinamide mononucleotide BETA-NICOTINAMIDE MONONUCLEOTIDE BETA-NICOTINAMIDE RIBOSE MONOPHOSPHATE 3-carbamoyl-1-(5-O-phosphonopentofuranosyl)pyridinium NICOTINAMIDE-1-IUM-1-BETA-D-RIBOFURANOSIDE 5'-PHOSPHATE 3-(aminocarbonyl)-1-(5-O-phosphonato-beta-D-ribofuranosyl)pyridinium 3-(Aminocarbonyl)-1-(5-O-phosphonato-beta-D-ribofuranosyl)pyridinium 3-carbamoyl-1-[5-O-(hydroxyphosphinato)-beta-D-ribofuranosyl]pyridinium Pyridinium, 3-(aminocarbonyl)-1-(5-O-phosphono-beta-D-ribofuranosyl)-, inner salt
CAS	1094-61-7
EINECS	214-136-5
InChI	InChI=1/C11H15N2O8P/c12-10(16)6-2-1-3-13(4-6)11-9(15)8(14)7(21-11)5-20-22(17,18)19/h1-4,7-9,11,14-15H,5H2,(H3-,12,16,17,18,19)/t7-,8-,9-,11-/m1/s1

1094-61-7 - Physico-chemical Properties

Molecular Formula	C11H15N2O8P
Molar Mass	334.22
Melting Point	166 °C(dec.)
Solubility	Soluble in PBS (10 mg/ml).
Appearance	White to white-like powder
Storage Condition	-20 ℃, nitrogen storage
MDL	MFCD00038748
Use	A product of the eNAMPT reaction and a NAD intermediate

1094-61-7 - Upstream Downstream Industry

Downstream Products

25 MG -NICOTINAMIDE ADENINE DINUCLEOTIDEPHOSPHATE REDUCED.NA4-SALT AN.GR.

1094-61-7 - Reference

Reference

1. Sun, Dongxue, et al. "Coupling p-Hydroxybenzoate Hydroaxylase with the Photoresponsive Nanozyme for Universal Dehydrogenase-Based Bioassays." Sensors and Actuators B: Chemical 327 (2021): 128859.https://doi.org/10.1016/j.snb.2020.128859

1094-61-7 - Nature

melting point	166 °C(dec.)
storage conditions	-20°C
Merck	13,6697
BRN	3570187
InChIKey	DAYLJWODMCOQEW-TURQNECASA-N

Last Update：2024-04-10 22:29:15

1094-61-7 - Introduction

β-nicotinamide mononucleotide-nicotinamide mononucleotide is also called β-nicotinamide mononucleotide (NMN), which is the synthetic substrate of coenzyme I, and NMN is also used in anti-aging research. Japan's Keio University and the University of Washington in the United States are cooperating to conduct human clinical trials on the anti-aging effect and safety of β-NMN. Studies have shown that β-NMN can also regulate the secretion of insulin and affect the expression level of mRNA. β-NMN has a broad application prospect in the field of medical treatment.
β-nicotinamide mononucleotide is the product and key NAD intermediate of the extracellular nicotinamide phosphoribosyltransferase (eNAMPT) reaction. It improves glucose tolerance by restoring NAD levels in HFD-induced T2D mice. It also enhances liver insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response and circadian rhythm in part through SIRT1 activation.

Last Update：2024-04-10 22:29:15

1094-61-7 - Application

source

nicotinamide mononucleotide (Nicotinamide mononucleotide), referred to as NMN, is an inherent substance in the human body and is also rich in some fruits and vegetables, including broccoli, cabbage, etc.

physiological function

in mammals, β-nicotinamide mononucleotide is generated by nicotinamide (Nicotinamide,Nam) under the catalysis of Nampt (a protease in vivo), and then nicotinamide mononucleotide is generated by nicotinamide mononucleotide adenosine transferase Under the catalysis of NAD. Nicotinamide mononucleotide is a direct way to supplement NAD. Nicotinamide mononucleotide can significantly improve the repair ability of intracellular DNA damage, and finally achieve the effect of reversing aging.

Nicotinamide mononucleotide will be converted into the "nicotinamide adenine dinucleotide (NAD)" substance essential for energy metabolism in the body. In mouse experiments, it was confirmed that nicotinamide mononucleotide can activate a gene called acetylase in the body to prolong life and treat diabetes. NAD is a substance that can be produced in the human body. Studies have confirmed that the content of NAD in the body will decrease with age.;

anti-aging mechanism

β-nicotinamide mononucleotide is the precursor of NAD, the cofactor of longevity protein in human body. NAD is an important coenzyme in the tricarboxylic acid cycle, which promotes the metabolism of sugar, fat and amino acids and participates in the synthesis of energy. NAD is also the only substrate of coenzyme I consuming enzyme (the only substrate of DNA repair enzyme PARP, the only substrate of longevity protein Sirtuins, and the only substrate of cyclic ADP ribose synthase CD38/157).

NAD participates in all aspects of human metabolism and is a key coenzyme. Without NAD, metabolism will not work. The elderly lack NAD, so various problems, large and small, will come. By supplementing NAD, it can resist aging in an all-round way.

biological activity

Nicotinamide mononucleotide (β-NM, NMN) is one of the key precursors of NAD and the product of NAMPT reaction, which is converted to NAD by nicotinamide mononucleotide adenylate transferase.

Last Update：2025-08-19 16:24:40

1094-61-7 - Introduction

target

Human Endogenous Metabolite

in vitro study

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.

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.

in vivo studies

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:	C 7BL6 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).

Last Update：2024-04-10 22:29:15

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