β-Nicotinamide mononucleotide

Research use only, not for human use.

Nicotinamide ribotide (NMN) is an important intermediate metabolite in the nicotinate and nicotinamide metabolism pathway.

Nicotinamide ribotide (NMN) is an important intermediate metabolite in the nicotinate and nicotinamide metabolism pathway. Mammals predominantly use nicotinamide rather than nicotinic acid as a precursor for NAD biosynthesis. Instead of the deamidation to nicotinic acid nicotinamide is directly converted to NMN by nicotinamide phosphoribosyltransferase (NAMPT EC 2.4.2.12). The enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT EC 2.7.7.1) which is a member of the nucleotidyltransferase alpha/beta-phosphodiesterase superfamily catalyzes the reaction NMN + ATP <=> Nicotinamide adenine dinucleotide (NAD) + PPi representing the final step in the biosynthesis of NAD. NAD is a molecule that plays a fundamental role as a cofactor in cellular redox reactions. Thus NMN is an important metabolite for the maintenance of normal NAD biosynthesis. Circulating NMN levels may play an important role in regulating cell function in physiological and pathophysiological conditions.

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.

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).

β-NM

Others

Other Targets

Others

——

——

1094-61-7

334.22

C11H15N2O8P

>98% (HPLC)

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

NC(=O)c1ccc[n+](c1)[C@@H]1O[C@H](COP(O)([O-])=O)[C@@H](O)[C@H]1O

((2R3S4R5R)-5-(3-carbamoylpyridin-1-ium-1-yl)-34-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

(-20℃)

With Ice Pack

≥ 2 years