7694-45-3 Purity
95%
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Specification
Although baseline requirements for nicotinamide adenine dinucleotide (NAD) synthesis can be met by dietary tryptophan or less than 20 mg of niacin daily (composed of niacin and/or nicotinamide), increasing evidence suggests that NAD synthesis rates may be substantially increased. Beneficial in protection against neurodegeneration, Candida glabrata infection, and possibly enhancing reverse cholesterol transport. The unique and tissue-specific biosynthetic and/or ligand activities of tryptophan, niacin, nicotinamide, and the newly identified NAD precursor nicotinamide riboside account for vitamin-specific effects and side effects. As current data suggest that nicotinamide riboside may be the only vitamin precursor that supports neuronal NAD synthesis, the prospect of nicotinamide riboside supplementation in humans is raised and areas for future research are suggested.
NR is a newly discovered salvageable precursor of NAD that is found in milk. Studies in Saccharomyces cerevisiae have shown that, like Na and Nam, NR is a NAD precursor that helps maintain intracellular NAD concentrations and improves NAD-dependent activities in cells, including Sir2-dependent gene silencing and lifespan. NR can be converted to NAD via the Nrk pathway, which is induced by axotomy in dorsal root ganglion (DRG) neurons, or via the actions of nucleoside phosphorylases and nicotinamide rescue. Studies have also shown that the same two pathways required for NR rescue in yeast cells can also be used for NaR rescue. In yeast cells, NR clearly qualifies as a vitamin, as it can rescue growth of strains deficient in de novo synthesis, improve Sir2 function (8), and utilize dedicated transporters.
Nicotinamide, the amide form of vitamin B (niacin), has long been implicated in neuronal development, survival, and function in the central nervous system (CNS), with implications for neuronal death and neuroprotection. Research investigates the role of nicotinamide in neuronal health within the CNS, with an emphasis on studies that have shown neuroprotective effects. Nicotinamide appears to play a role in protecting neurons from traumatic injury, ischemia, and stroke, and has been implicated in 3 key neurodegenerative diseases: Alzheimer's, Parkinson's, and Huntington's. A key factor is the bioavailability of nicotinamide, with low concentrations causing neurological deficits and dementia and high concentrations potentially causing neurotoxicity. Finally, potential mechanisms of action for nicotinamide are discussed, including general maintenance of cellular energy levels and more specific inhibition of molecules such as the nicotinamide adenine dinucleotide-dependent deacetylase Sirtuin 1 (SIRT1).
Many studies suggest that nicotinamide is essential for the growth and maintenance of the CNS, promoting neuronal differentiation and neuronal survival, respectively. For example, nicotinamide appears to enhance and accelerate the conversion of embryonic stem cells to neural progenitor cells and the differentiation of neurons from precursor cells, suggesting that it plays a key role in neural development. Considerable evidence suggests that NAD+ metabolism has a direct impact on the survival of neurons in the central nervous system. NAD+ is an important substrate for 3 major enzyme classes: the sirtuin family (SIRTs), poly (ADP-ribose) polymerases (PARPs) and related adenosine diphosphate (ADP)-ribosyltransferases (ARTs), and cyclic ADP-ribose (cADPR) synthases, CD38, and CD157. Nicotinamide is a byproduct of SIRT, PARP, and ART activity. Nicotinamide can inhibit the activity of these enzymes by binding to NAD+. In addition, neurons contain only low levels of the enzyme NAMPT, which is required for the first step in the conversion of nicotinamide to NAD+, which may reduce its availability in these cells. NAD+ levels decrease with age, which may be related to reduced NAMPT levels. Further evidence supporting this comes from studies where the aminopropylcarbazole chemicals of the P7C3 class were found to exert neuroprotective effects in PD, stroke, and ALS models via activation of NAMPT.
The molecular formula of Nicotinamide is C6H6N2O.
Some synonyms for Nicotinamide are niacinamide, 3-Pyridinecarboxamide, and Nicotinic acid amide.
The molecular weight of Nicotinamide is 122.12 g/mol.
Nicotinamide was created on September 16, 2004, and modified on October 21, 2023.
The primary significance of Nicotinamide is in the prevention and/or cure of blacktongue and pellagra.
Nicotinamide functions as an EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor, a metabolite, a cofactor, an antioxidant, a neuroprotective agent, an EC 3.5.1.98 (histone deacetylase) inhibitor, an anti-inflammatory agent, a Sir2 inhibitor, a Saccharomyces cerevisiae metabolite, an Escherichia coli metabolite, a mouse metabolite, a human urinary metabolite, and a geroprotector.
The IUPAC name of Nicotinamide is pyridine-3-carboxamide.
The InChI of Nicotinamide is InChI=1S/C6H6N2O/c7-6(9)5-2-1-3-8-4-5/h1-4H,(H2,7,9).
The InChIKey of Nicotinamide is DFPAKSUCGFBDDF-UHFFFAOYSA-N.
The CAS number of Nicotinamide is 98-92-0.
Reference: [1]Biochemical Journal,1949,vol. 44,p. 506 - 509
Reference: [1] Journal of the American Chemical Society, 1944, vol. 66, p. 1479,1482
[2] Journal of Organic Chemistry, 1954, vol. 19, p. 1633,1636[3] Org. Synth. Coll., 1963, vol. Vol. IV, p. 166
Reference: [1] Journal of the American Chemical Society, 1944, vol. 66, p. 1479,1482
Reference: [1] ACS Catalysis, 2016, vol. 6, # 1, p. 47 - 54
[2] Chemical Science, 2017, vol. 8, # 5, p. 3576 - 3585
Reference: [1]Justus Liebigs Annalen der Chemie,1959,vol. 621,p. 106,119
Reference: [1]Roczniki Chemii,1953,vol. 27,p. 396,401
Chem.Abstr.,1955,p. 1033
[2]Indian Journal of Chemistry - Section B Organic and Medicinal Chemistry,2005,vol. 44,p. 158 - 162
[3]Journal of Chemical Sciences,2014,vol. 126,p. 1285 - 1290
* For details of the synthesis route, please refer to the original source to ensure accuracy.