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Nicotinamide
Nicotinamide Chemical Structure

Nicotinamide

Catalog NO.: B0005-464879 CAS NO.: 98-92-0 Brand: BOC Sciences

Category
Natural Compounds
Chemical Family/Application
Alkaloids
Molecular Formula
C18H34O5
Molecular Weight
330.5

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WARNING: Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

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  • kg to MT scale
  • GMP batches production
  • Over 20 years of experience
  • HPAPI production with OEL < 1 μg/m³
  • Cleanroom Class 100 to Class 100,000
  • Special type of reactions in cGMP workshop
  • Cleaning level: Class A B C
  • cGMP synthesis workshop
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Product Description

Nicotinamide, a water-soluble vitamin, is an active component of coenzymes NAD and NADP, and also acts as an activator of sirtuins.

Quantity
Kilos
Boiling Point
334 °C
Melting Point
128-131 °C
Density
1.4 g/cm3
InChI Key
DFPAKSUCGFBDDF-UHFFFAOYSA-N
InChI
InChI=1S/C6H6N2O/c7-6(9)5-2-1-3-8-4-5/h1-4H,(H2,7,9)
SMILES
CCCCC[C@@H]([C@H](/C=C/[C@H](CCCCCCCC(=O)O)O)O)O
Stability
Stable under recommended storage conditions
HPLC
HNMR
MS

Enhanced SIRT6 activity abrogates the neurotoxic phenotype of astrocytes expressing ALS-linked mutant SOD1

Benjamin A. Harlan; Mariana Pehar; Kelby M. Killoy; Marcelo R. Vargas

The FASEB Journal

All chemicals and reagents were obtained from **** unless otherwise specified. Culture media and serum were obtained from ****. Primers and a mouse Nrf2 small interfering RNA (siRNA) (5′-AUAUACGCAGGAGAGGUAAGAAUAA-3′) were obtained from ****. Mouse SIRT6 siRNAs (L-061392-01) were obtained from ****. NR was obtained from BOC Sciences (Shirley, NY, USA).

Nicotinamide riboside regulates inflammation and mitochondrial markers in AML12 hepatocytes

Hee Jae Lee; Soo Jin Yang

Nutrition Research and Practice

Steatosis was induced by treating AML12 cells with 250 µM palmitic acid (****) for 48 h. The cells were treated with phosphate-buffered saline (PBS) or NR (10 µM and 10 mM; BOC Sciences, Shirley, NY, USA) for 24 h. Morphological changes in the cells were captured using a Leica DM IL LED (****) and TrueChrome Metrics (****).

NCT NumberTitleCondition Or DiseasePhaseStart DateSponsorStatus
NCT03975777Time-course of Mitochondrial Biogenic Gene and Protein Expression in Exercised Human Skeletal MuscleMitochondrial BiogenesisNot ApplicableJune 1, 2019Brendon Gurd, PhD,Brendon Gurd, PhDRecruiting
NCT03060772A Study of Pleiotropic Pioglitazone Effects on the Alcoholic Lung (APPEAL Study) (APPEAL)AlcoholismPhase 2January 3, 2018Emory University,Emory UniversityRecruiting
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1. Photoprotective effects of nicotinamide
Diona L. Damian*. Photochem. Photobiol. Sci., 2010, 9, 578–585
Nicotinamide intake, deficiency and pharmacology Nicotinamide and nicotinic acid (niacin, which is converted to nicotinamide in vivo; Fig. 1) are most abundant in foods such as meats, legumes, nuts, grains, coffee and tea, andinniacin-fortified cereals. Nicotinamide is also manufactured in the liver from tryptophan, which is found in eggs, dairy products, fish, meat and soybeans and comprises up to 2% of total dietary protein. The tryptophan pathway provides ~50%of total niacin requirements. Recommended daily nicotinamide intake for adults is ～15 mg, and typical commercially available daily supplement doses range from 20–500 mg.
2. Sirtuin mechanism and inhibition: explored with Ne-acetyl-lysine analogs
Brett M. Hirsch and Weiping Zheng*. Mol. BioSyst., 2011, 7, 16–28
Multiple transcriptional coactivators such as p300, cAMP-response element binding protein (CREB) binding protein (CBP), and p300/CBP-associated factor (PCAF) were shown to possess an intrinsic protein acetyltransferase activity. The yeast transcriptional repressors reduced potassium dependency 3 (Rpd3), histone deacetylase 1 (Hda1), and silent information regulator 2 (Sir2) were shown to possesses a protein deacetylase activity. While acetyl-coenzyme A (AcCoA) is used as the universal cofactor to donate the acetyl group during lysine Ne-acetylation catalyzed by all the protein acetyltransferases, the enzymatic lysine Ne-deacetylation is accomplished by the deacetylase enzymes that use either Zn2+ or b-nicotinamide adenine dinucleotide (β-NAD+ or just NAD+ as used below throughout this article) as the catalytic cofactor. While the Zn2+-containing metallo-deacetylases catalyze the Zn2+-assisted hydrolysis of the amide bond of the acetyl-lysine side chain to afford the deacetylated product and acetic acid, the NAD+-dependent deacetylases achieve the deacetylation of the acetyl-lysine side chain by catalyzing the ultimate transfer of the acetyl group onto the 2’-OH of the nicotinamide ribose of NAD+, which is coupled to the cleavage of nicotinamide from NAD+, thus affording three enzymatic products, i.e. nicotinamide, the deacetylated product, and 2’-O-acetyl-ADP-ribose (20 -O-AADPR) (Fig. 1). Rpd3 and Hda1 are the two founding members of the Zn+-containing protein deacetylase enzyme family that also includes the eleven human homologs (HDAC1-11, HDAC stands for histone deacetylase). Sir2 is the founding member of the NAD+-dependent protein deacetylase enzyme family that is also known as the sirtuin family.
3. Protection effect of nicotinamide on cardiomyoblast hypoxia/re-oxygenation injury: study of cellular mitochondrial metabolism
He Wang, Xiaoping Liang,* Guoan Luo, Mingyu Ding and Qionglin Liang*. Mol. BioSyst., 2016, 12, 2257—2264
Nicotinamide, the amide form of nicotinic acid, is the precursor of the coenzymeβNAD, which is an important currency for cell energy metabolism. The protective properties of nicotinamide in enhancement of cell survival as well as longevity, especially in neuroprotection, have been widely discussed. It has been proved to be neuroprotective by poly(ADP-ribose)polymerase inhibition and lipid peroxidation. Furthermore, a nicotinamide-rich diet could up-regulate SUR2A and ATP-sensitive K+ channels in H/R injured mice, thus increasing cardiac resistance to H/R. It has also been proved that nicotinamide could increase the membrane potential of mitochondria, thus improving mitochondrial stress in cardiomyocytes. However, little is known about the role of nicotinamide in metabolism regulation during cardiac H/R injury. We suppose that nicotinamide may preserve mitochondrial NAD-linked respiration and regulate cellular metabolism, especially the mitochondrial metabolism (Fig. 1).
Preparing Stock Solutions
ConcentrationVolumeMass1 mg5 mg10 mg
1 mM8.1887 mL40.9433 mL81.8867 mL
5 mM1.6377 mL8.1887 mL16.3773 mL
10 mM0.8189 mL4.0943 mL8.1887 mL
50 mM0.1638 mL0.8189 mL1.6377 mL
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