1. Metabolic Enzyme/Protease Epigenetics Cell Cycle/DNA Damage
  2. Endogenous Metabolite Sirtuin
  3. Nicotinic acid mononucleotide

Nicotinic acid mononucleotide acts as a SARM1 inhibitor and a NAD+ biosynthesis intermediate, with an IC50 value of 93.3 μM against SARM1. Nicotinic acid mononucleotide exerts axon-protective effects, delays axonal degeneration, elevates NAD+ levels, enhances Sirt1 activity, improves myocardial capillary density and alleviates myocardial fibrosis. Nicotinic acid mononucleotide reverses diabetic cardiomyopathy in diabetic mice by increasing myocardial NAD+ levels. Nicotinic acid mononucleotide is applicable to research related to cancer, multiple sclerosis, diabetic cardiomyopathy, neurodegenerative diseases and Huntington's disease.

For research use only. We do not sell to patients.

Nicotinic acid mononucleotide

Nicotinic acid mononucleotide Chemical Structure

CAS No. : 321-02-8

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10 mM * 1 mL in Water
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Based on 1 publication(s) in Google Scholar

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1 Publications Citing Use of MCE Nicotinic acid mononucleotide

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Description

Nicotinic acid mononucleotide acts as a SARM1 inhibitor and a NAD+ biosynthesis intermediate, with an IC50 value of 93.3 μM against SARM1. Nicotinic acid mononucleotide exerts axon-protective effects, delays axonal degeneration, elevates NAD+ levels, enhances Sirt1 activity, improves myocardial capillary density and alleviates myocardial fibrosis. Nicotinic acid mononucleotide reverses diabetic cardiomyopathy in diabetic mice by increasing myocardial NAD+ levels. Nicotinic acid mononucleotide is applicable to research related to cancer, multiple sclerosis, diabetic cardiomyopathy, neurodegenerative diseases and Huntington's disease[1][2][3][4].

In Vitro

Nicotinic acid mononucleotide (0-250 μM; assay duration) inhibits the NAD+ hydrolase activity of full-length human SARM1 by binding to its N-terminal ARM domain; its IC50 is 93.3 μM in the absence of NMN, while this inhibitory effect is attenuated in the presence of 5 μM NMN (IC50 = 147.2 μM)[1].
Nicotinic acid mononucleotide delays axonal degeneration of mammalian axons by restoring reduced intracellular NAD+ levels[3].
Nicotinic acid mononucleotide (NAM) increases the expression of Sirt1 and the phosphorylation level of eNOS in human umbilical vein endothelial cells (HUVECs) treated with high glucose[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Nicotinic acid mononucleotide (NAM) (400 mg/kg/day; i.p.; daily; 8 weeks) partially reverses streptozotocin (HY-13753)-induced diabetic cardiomyopathy in diabetic mice by increasing myocardial NAD+ levels, improving cardiac function and ultrastructure, enhancing capillary density, alleviating fibrosis, and restoring Sirt1 expression[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (8-week-old male; streptozotocin-induced diabetic)[4]
Dosage: 400 mg/kg/day
Administration: i.p.; daily; 8 weeks
Result: Partially increased myocardial NAD+ levels in diabetic mice.
Partially reversed impaired left ventricular ejection fraction (LVEF) and fractional shortening (FS) relative to untreated diabetic mice.
Improved myocardial ultrastructural abnormalities (reduced Z-line misalignment, mitochondrial swelling, and myofibril disorganization).
Increased myocardial capillary density relative to untreated diabetic mice.
Reduced myocardial expression of fibrosis markers TGF-β1 and collagen I relative to untreated diabetic mice.
Restored myocardial Sirt1 mRNA and protein expression relative to untreated diabetic mice.
Had no effect on blood glucose or body weight in diabetic mice, and no significant effect on interventricular septal thickness (IVSD) or left ventricular posterior wall thickness (LVPWD).
Molecular Weight

335.20

Formula

C11H14NO9P

CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O[C@@H]1[C@H](O)[C@@H](COP(O)(O)=O)O[C@H]1[N+]2=CC=CC(C([O-])=O)=C2

Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : 10 mg/mL (29.83 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.9833 mL 14.9165 mL 29.8329 mL
5 mM 0.5967 mL 2.9833 mL 5.9666 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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This equation is commonly abbreviated as: C1V1 = C2V2

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Purity & Documentation
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
H2O 1 mM 2.9833 mL 14.9165 mL 29.8329 mL 74.5823 mL
5 mM 0.5967 mL 2.9833 mL 5.9666 mL 14.9165 mL
10 mM 0.2983 mL 1.4916 mL 2.9833 mL 7.4582 mL
15 mM 0.1989 mL 0.9944 mL 1.9889 mL 4.9722 mL
20 mM 0.1492 mL 0.7458 mL 1.4916 mL 3.7291 mL
25 mM 0.1193 mL 0.5967 mL 1.1933 mL 2.9833 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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Product Name:
Nicotinic acid mononucleotide
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HY-128700
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