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| 50mg |
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| 500mg |
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Purity: ≥98%
β-nicotinamide mononucleotide (also known as 'NMN', 'NAMN', and 'β-NMN') is a nucleotide intermediate derived from ribose and nicotinamide and is used in NAD+ biosynthesis produced from nicotinamide (NAM) and phosphoribosyl pyrophosphate (PRPP) by nicotinamide phosphoribosyl transferase enzyme with no toxicity. Like nicotinamide riboside , NMN is a derivative of niacin , and humans have enzymes that can use NMN to generate nicotinamide adenine dinucleotide (NADH).
| ln Vitro |
β-Nicotinamide mononucleotide has numerous advantageous pharmacological properties. Participation in NAD+ production is the primary mechanism by which NMN carries out its pharmacological effect. This mechanism is involved in cell biochemical processes, cardioprotection, diabetes, Alzheimer's disease, and issues connected to obesity [1]. While NAD+ levels were dramatically decreased by providing the NAD+ precursor NAM or NMN (0.5–1 mM), intracellular NAD+ levels were significantly decreased by knocking down or knocking out Nampt (KD or KO) or by treatment with the Nampt inhibitor FK866. Boost. CD8+ T cell activation and activity are inhibited by treatment with the NAD+ precursor NMN [2].
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| ln Vivo |
Dox-induced cardiac dysfunction and mtDNA damage are prevented by β-nicotinamide mononucleotide (500 mg/kg; intraperitoneal injection; three times a week for 7–10 weeks) [3]. While Nampt metabolite β-nicotinamide mononucleotide (300 mg/kg body weight; i.p.; every two days for two weeks) greatly enhanced tumor growth in C57BL/6 mice (carrying wild-type type Hepa1-6 cells), Nampt KO considerably prevented tumor progression. shown variations in NAD+ levels in tumors treated with β-nicotinamide mononucleotide and Nampt KO [2]. In HFD-induced T2D animals, β-nicotinamide mononucleotide restores NAD+ levels, thereby mitigating glucose intolerance. Additionally, by partially activating SIRT1, β-nicotinamide mononucleotide improves hepatic insulin sensitivity and restores gene expression linked to oxidative stress, inflammatory response, and circadian rhythms [4].
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| Animal Protocol |
Animal/Disease Models: C57BL6 mice (p53−/− mice) [3]
Doses: 500 mg/kg Route of Administration: intraperitoneal (ip) injection; 3 times a week for 7-10 weeks Experimental Results: Protection against Dox-treated p53−/− The cardiac function of mice Dramatically diminished (weeks 7 and 10 of the study), while the doxorubicin (Dox)-induced attenuation of mitochondrial respiration and tissue ATP depletion were rescued). |
| References |
[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.
[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. [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. [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. |
| Molecular Formula |
C11H15N2O8P
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|---|---|
| Molecular Weight |
334.2192
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| CAS # |
1094-61-7
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| SMILES |
O=P(OC[C@H]1O[C@@H]([N+]2=CC=CC(C(N)=O)=C2)[C@H](O)[C@@H]1O)([O-])O
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| InChi Key |
DAYLJWODMCOQEW-TURQNECASA-N
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| InChi Code |
InChI=1S/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
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| Chemical Name |
((2R,3S,4R,5R)-5-(3-carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate
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| Synonyms |
β-nicotinamide mononucleotide; NMN; β-Nicotinamide mononucleotide; Nicotinamide Mononucleotide; β-NMN; β-NM;
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~83.33 mg/mL (~249.33 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (299.20 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9920 mL | 14.9602 mL | 29.9204 mL | |
| 5 mM | 0.5984 mL | 2.9920 mL | 5.9841 mL | |
| 10 mM | 0.2992 mL | 1.4960 mL | 2.9920 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution 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 stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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