β-Nicotinamide mononucleotide  (Synonyms: β-NM; NMN)

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].

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.

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.

334.22

Solid

C₁₁H₁₅N₂O₈P

1094-61-7

NC(C1=C[N+]([C@@H]2O[C@H](COP(O)([O-])=O)[C@@H](O)[C@H]2O)=CC=C1)=O

Room temperature in continental US; may vary elsewhere.

4°C, protect from light

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

• [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]