Home>>Signaling Pathways>> Proteases>> Endogenous Metabolite>>β-Nicotinamide mononucleotide

β-Nicotinamide mononucleotide

Catalog No.: GC16971

β-nicotinamide mononucleotide is a product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and a key NAD+ intermediate.

β-Nicotinamide mononucleotide Chemical Structure

Size Price Stock Qty
100mg
$37.00
In stock
500mg
$71.00
In stock

Customer Reviews

Based on customer reviews.

Tel: (626) 353-8530 Email: sales@glpbio.com

Sample solution is provided at 25 µL, 10mM.

Product Documents

Quality Control & SDS

View current batch:

Protocol

Cell experiment [1]:

Cell lines

Hepa1-6 cells

Preparation Method

β-Nicotinamide mononucleotide was added to the cell medium

Reaction Conditions

0.5-1 mMβ-Nicotinamide mononucleotide

Applications

Intracellular NAD + levels were significantly reduced by knocking down or knocking down Nampt or treated with the Nampt inhibitor FK866, whereas NAD + levels were significantly increased by supplementation with NAD + precursors NAM or β-Nicotinamide mononucleotide.

Animal experiment [2]:

Animal models

Nampt+/- female mice

Preparation Method

For GTTs, mice were injected with PBS or β-Nicotinamide mononucleotide (500 mg/kg body weight) and fasted for 14 hrs; dextrose (3 g/kg body weight) was then injected intraperitoneally.

Dosage form

500 mg/kg β-Nicotinamide mononucleotide for 0、15、30、60,120min

Applications

After β-Nicotinamide mononucleotide administration, there was no difference in blood glucose levels in GTTs between Nampt+/- and control female mice. In addition, β-Nicotinamide mononucleotide-treated Nampt+/- and control mice also had similar plasma insulin levels at each time point. β-Nicotinamide mononucleotide administration corrects the defect in GSIS observed in Nampt+/- mice.

References:

[1]: Lv H, Lv G, et,al. NAD+ Metabolism Maintains Inducible PD-L1 Expression to Drive Tumor Immune Evasion. Cell Metab. 2021 Jan 5;33(1):110-127.e5. doi: 10.1016/j.cmet.2020.10.021. Epub 2020 Nov 9. PMID: 33171124.
[2]: Revollo JR, KÖrner A, et,al. Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme. Cell Metab. 2007 Nov;6(5):363-75. doi: 10.1016/j.cmet.2007.09.003. PMID: 17983582; PMCID: PMC2098698.

Background

β-nicotinamide mononucleotide 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].

Intracellular NAD + levels were significantly reduced by knocking down or knocking down Nampt or treated with the Nampt inhibitor FK866, whereas NAD + levels were significantly increased by supplementation with NAD + precursors NAM or β-Nicotinamide mononucleotide [3].Treatment of β-nicotinamide mononucleotide, a precursor of NAD+, to HEK293 cells activated and improved the rate of mtDNA replication by increasing nucleotides in mitochondria and decreasing their degradation products: nucleosides. β-Nicotinamide mononucleotide metabolism plays a role in supporting mtDNA replication by maintaining the nucleotide pool balance in the mitochondria[7].

After β-Nicotinamide mononucleotide administration, there was no difference in blood glucose levels in GTTs between Nampt+/- and control female mice. In addition, β-Nicotinamide mononucleotide-treated Nampt+/- and control mice also had similar plasma insulin levels at each time point. β-Nicotinamide mononucleotide administration corrects the defect in GSIS observed in Nampt+/- mice[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].In a mouse model induced by doxorubicin administered in divided low doses as in the clinics, supplementing mice with a precursor of NAD+ prevented the mtDNA depletion and cardiac dysfunction[5].When investigated whether β-Nicotinamide mononucleotide is superior to nicotinamide (Nam) as a precursor of NAD+ in whole animal experiments. β-Nicotinamide mononucleotide is retained in the body for longer than Nam[6].

References:
[1]: Poddar SK, Sifat AE, et,al. Nicotinamide Mononucleotide: Exploration of Diverse Therapeutic Applications of a Potential Molecule. Biomolecules. 2019 Jan 21;9(1):34. doi: 10.3390/biom9010034. PMID: 30669679; PMCID: PMC6359187.
[2]: Revollo JR, KÖrner A, et,al. Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme. Cell Metab. 2007 Nov;6(5):363-75. doi: 10.1016/j.cmet.2007.09.003. PMID: 17983582; PMCID: PMC2098698.
[3]: Lv H, Lv G, et,al. NAD+ Metabolism Maintains Inducible PD-L1 Expression to Drive Tumor Immune Evasion. Cell Metab. 2021 Jan 5;33(1):110-127.e5. doi: 10.1016/j.cmet.2020.10.021. Epub 2020 Nov 9. PMID: 33171124.
[4]:Yoshino J, Mills KF, et,al. Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011 Oct 5;14(4):528-36. doi: 10.1016/j.cmet.2011.08.014. PMID: 21982712; PMCID: PMC3204926.
[5]: Li J, Wang PY, et,al. p53 prevents doxorubicin cardiotoxicity independently of its prototypical tumor suppressor activities. Proc Natl Acad Sci U S A. 2019 Sep 24;116(39):19626-19634. doi: 10.1073/pnas.1904979116. Epub 2019 Sep 5. PMID: 31488712; PMCID: PMC6765288.
[6]: Kawamura T, Mori N, et,al. β-Nicotinamide Mononucleotide, an Anti-Aging Candidate Compound, Is Retained in the Body for Longer than Nicotinamide in Rats. J Nutr Sci Vitaminol (Tokyo). 2016;62(4):272-276. doi: 10.3177/jnsv.62.272. PMID: 27725413.
[7]:Cros C, Margier M, et,al. Nicotinamide Mononucleotide Administration Triggers Macrophages Reprogramming and Alleviates Inflammation During Sepsis Induced by Experimental Peritonitis. Front Mol Biosci. 2022 Jun 27;9:895028. doi: 10.3389/fmolb.2022.895028. PMID: 35832733; PMCID: PMC9271973.

Chemical Properties

Cas No. 1094-61-7 SDF
Synonyms N/A
Chemical Name ((2R,3S,4R,5R)-3,4-dihydroxy-5-(3-(hydroxy(imino)methyl)pyridin-1-ium-1-yl)tetrahydrofuran-2-yl)methyl hydrogen phosphate
Canonical SMILES N=C(O)C1=C[N+]([C@@]2([H])[C@@](O)([H])[C@@](O)([H])[C@@](O2)([H])COP(O)([O-])=O)=CC=C1
Formula C11H16N2O8P M.Wt 334.22
Solubility ≥ 33.4mg/mL in Water Storage 4°C, protect from light
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.

  • Molarity Calculator

  • Dilution Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
**When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / CoA (available online).

Calculate

Research Update

Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women

Science2021 Jun 11;372(6547):1224-1229.PMID: 33888596DOI: 10.1126/science.abe9985

In rodents, obesity and aging impair nicotinamide adenine dinucleotide (NAD+) biosynthesis, which contributes to metabolic dysfunction. Nicotinamide mononucleotide (NMN) availability is a rate-limiting factor in mammalian NAD+ biosynthesis. We conducted a 10-week, randomized, placebo-controlled, double-blind trial to evaluate the effect of NMN supplementation on metabolic function in postmenopausal women with prediabetes who were overweight or obese. Insulin-stimulated glucose disposal, assessed by using the hyperinsulinemic-euglycemic clamp, and skeletal muscle insulin signaling [phosphorylation of protein kinase AKT and mechanistic target of rapamycin (mTOR)] increased after NMN supplementation but did not change after placebo treatment. NMN supplementation up-regulated the expression of platelet-derived growth factor receptor ¦ and other genes related to muscle remodeling. These results demonstrate that NMN increases muscle insulin sensitivity, insulin signaling, and remodeling in women with prediabetes who are overweight or obese (clinicaltrial.gov NCT03151239).

Effect of oral administration of nicotinamide mononucleotide on clinical parameters and nicotinamide metabolite levels in healthy Japanese men

Endocr J2020 Feb 28;67(2):153-160.PMID: 31685720DOI: 10.1507/endocrj.EJ19-0313

Recent studies have revealed that decline in cellular nicotinamide adenine dinucleotide (NAD+) levels causes aging-related disorders and therapeutic approaches increasing cellular NAD+ prevent these disorders in animal models. The administration of nicotinamide mononucleotide (NMN) has been shown to mitigate aging-related dysfunctions. However, the safety of NMN in humans have remained unclear. We, therefore, conducted a clinical trial to investigate the safety of single NMN administration in 10 healthy men. A single-arm non-randomized intervention was conducted by single oral administration of 100, 250, and 500 mg NMN. Clinical findings and parameters, and the pharmacokinetics of NMN metabolites were investigated for 5 h after each intervention. Ophthalmic examination and sleep quality assessment were also conducted before and after the intervention. The single oral administrations of NMN did not cause any significant clinical symptoms or changes in heart rate, blood pressure, oxygen saturation, and body temperature. Laboratory analysis results did not show significant changes, except for increases in serum bilirubin levels and decreases in serum creatinine, chloride, and blood glucose levels within the normal ranges, independent of the dose of NMN. Results of ophthalmic examination and sleep quality score showed no differences before and after the intervention. Plasma concentrations of N-methyl-2-pyridone-5-carboxamide and N-methyl-4-pyridone-5-carboxamide were significantly increased dose-dependently by NMN administration. The single oral administration of NMN was safe and effectively metabolized in healthy men without causing any significant deleterious effects. Thus, the oral administration of NMN was found to be feasible, implicating a potential therapeutic strategy to mitigate aging-related disorders in humans.

Long-Term Administration of Nicotinamide mononucleotide Mitigates Age-Associated Physiological Decline in Mice

Cell Metab2016 Dec 13;24(6):795-806.PMID: 28068222DOI: 10.1016/j.cmet.2016.09.013

NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans.

Nicotinamide mononucleotide Supplementation Reverses the Declining Quality of Maternally Aged Oocytes

Cell Rep2020 Aug 4;32(5):107987.PMID: 32755581DOI: 10.1016/j.celrep.2020.107987

Advanced maternal age is highly associated with a decline in oocyte quality, but effective approaches to improve it have still not been fully determined. Here, we report that in vivo supplementation of nicotinamide mononucleotide (NMN) efficaciously improves the quality of oocytes from naturally aged mice by recovering nicotinamide adenine dinucleotide (NAD+) levels. NMN supplementation not only increases ovulation of aged oocytes but also enhances their meiotic competency and fertilization ability by maintaining the normal spindle/chromosome structure and the dynamics of the cortical granule component ovastacin. Moreover, single-cell transcriptome analysis shows that the beneficial effect of NMN on aged oocytes is mediated by restoration of mitochondrial function, eliminating the accumulated ROS to suppress apoptosis. Collectively, our data reveal that NMN supplementation is a feasible approach to protect oocytes from advanced maternal age-related deterioration, contributing to the improvement of reproductive outcome of aged women and assisted reproductive technology.

Nicotinamide mononucleotide: Exploration of Diverse Therapeutic Applications of a Potential Molecule

Biomolecules2019 Jan 21;9(1):34.PMID: 30669679DOI: 10.3390/biom9010034

Nicotinamide mononucleotide (NMN) is a nucleotide that is most recognized for its role as an intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis. Although the biosynthetic pathway of NMN varies between eukaryote and prokaryote, two pathways are mainly followed in case of eukaryotic human-one is through the salvage pathway using nicotinamide while the other follows phosphorylation of nicotinamide riboside. Due to the unavailability of a suitable transporter, NMN enters inside the mammalian cell in the form of nicotinamide riboside followed by its subsequent conversion to NMN and NAD+. This particular molecule has demonstrated several beneficial pharmacological activities in preclinical studies, which suggest its potential therapeutic use. 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 recent groundbreaking discovery of anti-ageing activities of this chemical moiety has added a valuable essence in the research involving this molecule. This review focuses on the biosynthesis of NMN in mammalian and prokaryotic cells and mechanism of absorption along with the reported pharmacological activities in murine model.

Reviews

Review for β-Nicotinamide mononucleotide

Average Rating: 5 ★★★★★ (Based on Reviews and 3 reference(s) in Google Scholar.)

5 Star
100%
4 Star
0%
3 Star
0%
2 Star
0%
1 Star
0%
Review for β-Nicotinamide mononucleotide

GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.

Required fields are marked with *

You may receive emails regarding this submission. Any emails will include the ability to opt-out of future communications.