321-02-8
321-02-8
Chemical Structure
Nicotinic acid mononucleotide
- CAS No.: 321-02-8
- Formula:C11H14NO9P
- Molecular Weight:335.20
IUPAC Name: 1-((2R,3R,4S,5R)-3,4-dihydroxy-5-((phosphonooxy)methyl)tetrahydrofuran-2-yl)pyridin-1-ium-3-carboxylate
InChIKey: JOUIQRNQJGXQDC-ZYUZMQFOSA-N
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
Biological Activity: 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].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Nicotinic acid mononucleotide | 98.08% | 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. | ||||||||||||||||||||
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Uridine 5'-monophosphate | 99.92% | Uridine 5'-monophosphate (5'-Uridylic acid) is an orally active mitochondrial ATP-dependent potassium channel activator that has a protective effect on the heart. Uridine 5'-monophosphate can promote the synthesis of CDP-choline and induce apoptosis in intestinal epithelial cells, which is beneficial for gut development and reduces diarrhea. | ||||||||||||||||||||
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Nicotinamide riboside | Nicotinamide riboside, an orally active NAD+ precursor, increases NAD+ levels and activates SIRT1 and SIRT3. Nicotinamide riboside is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities. Nicotinamide riboside reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease. | |||||||||||||||||||||
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Nicotinamide riboside chloride | 99.90% | Nicotinamide riboside Chloride, an orally active NAD+ precursor, increases NAD+ levels and activates SIRT1 and SIRT3. Nicotinamide riboside Chloride is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities. Nicotinamide riboside Chloride reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease. | ||||||||||||||||||||
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Nicotinamide riboside malate | 98.04% | Nicotinamide riboside malate, an orally active NAD+ precursor, increases NAD+ levels and activates SIRT1 and SIRT3. Nicotinamide riboside malate is a source of vitamin B3 (niacin) and enhances oxidative metabolism, protection against high fat diet-induced metabolic abnormalities. Nicotinamide riboside malate reduces cognitive deterioration in a transgenic mouse model of Alzheimer’s disease. | ||||||||||||||||||||
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Sulfo-ara-F-NMN | 99.18% | Sulfo-ara-F-NMN (CZ-48) is a mimetic of nicotinamide mononucleotide (NMN). Sulfo-ara-F-NMN acts selectively, activating SARM1 but inhibiting CD38 (IC50 around 10 μM). Sulfo-ara-F-NMN induces intracellular cyclic ADP-ribose (cADPR) production. | ||||||||||||||||||||
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Im-NMN | Im-NMN is a monomeric raw material that can be used for nucleic acid synthesis. | |||||||||||||||||||||
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Fosribnicotinamide (Standard) | 99.76% | Fosribnicotinamide (Standard) (β-Nicotinamide mononucleotide (Standard)) is the analytical standard of Fosribnicotinamide (HY-F0004 ). This product is intended for research and analytical applications. Fosribnicotinamide is a product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and a key NAD+ intermediate. The pharmacological activities of Fosribnicotinamide include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer's disease, and complications associated with obesity. | ||||||||||||||||||||
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Cytidine 5'-monophosphate | 99.82% | Cytidine 5'-monophosphate (5'-Cytidylic acid) is a nucleotide which is used as a monomer in RNA. Cytidine 5'-monophosphate consists of the nucleobase cytosine, the pentose sugar ribose, and the phosphate group. | ||||||||||||||||||||
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Nicotinic acid riboside | 99.90% | Nicotinic acid riboside is a NAD+ precursor in human cells. Nicotinic acid riboside is an authentic intermediate of human NAD+ metabolism. | ||||||||||||||||||||
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Cytarabine 5’-monophosphate | 98.04% | Cytarabine 5′-monophosphate is a metabolite of the nucleoside analog Cytarabine (HY-13605), catalyzed by deoxycytidine kinase. Cytarabine 5′-monophosphate is incorporated into DNA by DNA polymerase α, which reduces the rate of DNA synthesis. At a concentration of 15 mM, Cytarabine 5′-monophosphate inhibits nuclear and mitochondrial DNA replication in Saccharomyces cerevisiae (S. cerevisiae). Additionally, Cytarabine 5′-monophosphate (3.5-75.1 mg/kg) improves survival in leukemia mice (L1210 mice). Cytarabine 5′-monophosphate can be used in cancer research. | ||||||||||||||||||||
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References
- [1]. Sasaki Y, et al. Nicotinic acid mononucleotide is an allosteric SARM1 inhibitor promoting axonal protection. Exp Neurol. 2021;345:113842. [Content Brief]
- [2]. O'Hara JK, et al. Targeting NAD+ metabolism in the human malaria parasite Plasmodium falciparum. PLoS One. 2014;9(4):e94061. Published 2014 Apr 18. [Content Brief]
- [3]. Khan JA, et al. Nicotinamide adenine dinucleotide metabolism as an attractive target for drug discovery. Expert Opin Ther Targets. 2007;11(5):695-705. [Content Brief]
- [4]. Zeng F, et al. ACMSD mediated de novo NAD+ biosynthetic impairment in cardiac endothelial cells as a potential therapeutic target for diabetic cardiomyopathy. Diabetes Res Clin Pract. 2023;206:111014. [Content Brief]
