| CAS NO: | 98-92-0 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 1g | 电议 |
| 5g | 电议 |
| 10g | 电议 |
| 25g | 电议 |
| 50g | 电议 |
| Molecular Weight (MW) | 122.12 |
|---|---|
| Formula | C6H6N2O |
| CAS No. | 98-92-0 |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 24 mg/mL (196.52 mM) |
| Water: 24 mg/mL (196.52 mM) | |
| Ethanol: 24 mg/mL (196.52 mM) | |
| Other info | Chemical Name: 3-Pyridinecarboxylic acid amide InChi Key: DFPAKSUCGFBDDF-UHFFFAOYSA-N InChi Code: InChI=1S/C6H6N2O/c7-6(9)5-2-1-3-8-4-5/h1-4H,(H2,7,9) SMILES Code: O=C(C1=CC=CN=C1)N |
| Synonyms | Niacinamide, Vitamin PP, Nicotinic acid amide; Vitamin B3 |
| In Vitro | In vitro activity: Nicotinamide strongly inhibits yeast silencing, increases rDNA recombination, and shortens replicative life span to that of a sir2 mutant. Nicotinamide abolishes silencing and leads to an eventual delocalization of Sir2 even in G(1)-arrested cells, demonstrating that silent heterochromatin requires continual Sir2 activity. Nicotinamide results in a twofold increase in DNA content and a threefold increase in insulin content in the fetal cells. Nicotinamide induces differentiation and maturation of human fetal pancreatic islet cells. Nicotinamide regulates sirtuins by switching between deacetylation and base exchange. Nicotinamide switching is quantitated for the Sir2s from Archeaglobus fulgidus (Sir2Af2), Saccharomyces cerevisiae (Sir2p), and mouse (Sir2alpha). Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization in Alzheimer's disease transgenic mice, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increases acetylated alpha-tubulin, a primary substrate of SirT2, and MAP2c in Alzheimer's disease transgenic mice, both of which are linked to increased microtubule stability. Nicotinamide fosters DNA integrity and maintains phosphatidylserine membrane asymmetry to prevent cellular inflammation, cellular phagocytosis and vascular thrombosis. Nicotinamide both prevents and reverses neuronal and vascular cell injury. Cell Assay: Previous findings suggested that nicotinamide had a protective effect against PARP-1-induced astrocyte death. The transporter-mediated uptake of nicotinamide, which was extracellular pH-sensitive and common to N-methylnicotinamide, was found to be critical for prevention of PARP-1-triggered cell death. |
|---|---|
| In Vivo | Type 2 diabetes was induced in Wistar rats by streptozotocin followed by nicotinamide. Test compounds and standard treatment were continued for 15 days. Results showed that there was significant normalisation of liver antioxidant enzymes compared to diabetic rats, suggesting all the tested compounds were beneficial in reducing oxidative stress |
| Animal model | Rats and Mice: Normal and streptozotocin-nicotinamide induced adult male diabetic rats receive quercetin (10, 25 and 50 mg/kg/bw) orally, and cause significant decrease in FBG and cardiac injury marker levels with increased in insulin levels[2]. Nicotinamide improves maternal hypertension, proteinuria, and glomerular endotheliosis in RUPP mice. Moreover, nicotinamide prolongs pregnancies, and improves survival and growth of the embryos in RUPP PE mice |
| Formulation & Dosage | 10, 25 and 50 mg/kg; oral |
| References | J Biol Chem. 2002 Nov 22;277(47):45099-107; ScientificWorldJournal. 2014;2014:854267; Life Sci. 2010 Apr 24;86(17-18):676-82. |
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