规格 | 价格 | 库存 | 数量 |
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10 mM * 1 mL in DMSO |
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500mg |
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1g |
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5g |
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10g |
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25g |
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Other Sizes |
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体外研究 (In Vitro) |
体外活性:烟酰胺强烈抑制酵母沉默,增加 rDNA 重组,并缩短 Sir2 突变体的复制寿命。即使在 G(1) 停滞的细胞中,烟酰胺也会消除沉默并导致 Sir2 最终离域,这表明沉默的异染色质需要持续的 Sir2 活性。烟酰胺导致胎儿细胞中 DNA 含量增加两倍,胰岛素含量增加三倍。烟酰胺诱导人胎儿胰岛细胞的分化和成熟。烟酰胺通过在脱乙酰化和碱基交换之间切换来调节去乙酰化酶。对来自古球菌 (Sir2Af2)、酿酒酵母 (Sir2p) 和小鼠 (Sir2alpha) 的 Sir2s 的烟酰胺转换进行定量。烟酰胺以类似于抑制 SirT1 的方式选择性地减少与阿尔茨海默病转基因小鼠中微管解聚相关的 tau 蛋白 (Thr231) 的特定磷酸种类。烟酰胺还显着增加阿尔茨海默病转基因小鼠中乙酰化 α-微管蛋白(SirT2 的主要底物)和 MAP2c,这两者都与增加微管稳定性有关。烟酰胺促进 DNA 完整性并维持磷脂酰丝氨酸膜不对称性,以防止细胞炎症、细胞吞噬作用和血管血栓形成。烟酰胺可以预防和逆转神经元和血管细胞损伤。细胞测定:先前的研究结果表明烟酰胺对 PARP-1 诱导的星形胶质细胞死亡具有保护作用。转运蛋白介导的烟酰胺摄取对细胞外 pH 值敏感,并且是 N-甲基烟酰胺所共有的,被发现对于预防 PARP-1 触发的细胞死亡至关重要。
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体内研究 (In Vivo) |
在 Wistar 大鼠中先使用链脲佐菌素,然后使用烟酰胺诱导 2 型糖尿病。测试化合物和标准治疗持续15天。结果显示,与糖尿病大鼠相比,肝脏抗氧化酶显着正常化,表明所有测试的化合物都有益于减少氧化应激
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动物实验 |
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参考文献 |
J Biol Chem.2002 Nov 22;277(47):45099-107.
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分子式 |
C6H6N2O
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分子量 |
122.12
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CAS号 |
98-92-0
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相关CAS号 |
Nicotinamide;98-92-0
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SMILES |
O=C(C1=C([H])N=C([H])C([H])=C1[H])N([H])[H]
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别名 |
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存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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溶解度 (体外) |
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制备储备液 | 1 mg | 5 mg | 10 mg | |
1 mM | 8.1887 mL | 40.9433 mL | 81.8867 mL | |
5 mM | 1.6377 mL | 8.1887 mL | 16.3773 mL | |
10 mM | 0.8189 mL | 4.0943 mL | 8.1887 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;
3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);
4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。
计算结果:
工作液浓度: mg/mL;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL ddH2O,混匀澄清。
(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
(2) 一定要按顺序加入溶剂 (助溶剂) 。
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT04843553 | Completed | Drug: Oral Nicotinamide | Actinic Keratoses | Rhode Island Hospital | October 14, 2016 | Early Phase 1 |
NCT06007391 | Not yet recruiting | Drug: Nicotinamide | Nicotinamide Adverse Reaction | University Hospital, Angers | September 2023 | Phase 2 Phase 3 |
NCT03789175 | Completed Has Results | Dietary Supplement: Nicotinamide Riboside (NR) |
Cancer Skin Fibroblasts |
National Heart, Lung, and Blood Institute (NHLBI) |
March 25, 2019 | Phase 1 Phase 2 |
NCT03432871 | Completed | Dietary Supplement: Nicotinamide Riboside |
Mitochondrial Diseases Mitochondrial Myopathies |
Cambridge University Hospitals NHS Foundation Trust |
December 8, 2017 | Not Applicable |
The NAD+ salvage pathway.Nicotinamide generated by Sir2 is converted into nicotinic acid by Pnc1 and subsequently back into NAD+ in three steps.YNR073C and YEL070W are putative NAD+glycohydrolases. Question marks represent enzymes present in bacteria without obvious homologs in yeast. Abbreviations:NAD +, nicotinamide adenine dinucleotide;NaMN, nicotinic acid mononucleotide; NaAD, desamido-NAD+; NADP +, nicotinamide adenine dinucleotide phosphate. td> |
Localization of Sir2-GFP in the presence of nicotinamide (NAM). A, wild-type strains containing SIR2-GFP (YDS1078), SIR3-GFP(YDS1099), or GFP-SIR4 (YDS1097), and an isogenicsir2 derivative expressing SIR3-GFP (YDS1109), were grown for the indicated times in the presence of 5 mmnicotinamide. GFP fluorescence was detected in live cells.B, the SIR2-GFP strain was deleted forHML(YDS1784) arrested in G1 by 10 μg/ml α-factor and treated with 0 or 5 mm nicotinamide. Times indicated are post-nicotinamide treatment. td> |
Model for noncompetitive inhibition of Sirs by nicotinamide. A, the Sir2 family of deacetylases contains an NAD+ binding pocket divided into three distinct regions. The adenine-ribose moiety of NAD+binds the A site whereas, in the absence of acetylated substrate, the nicotinamide moiety is bound to the B site. B, in the presence of an acetyllysine (K) a rotation around a phosphodiester bond of the pyrophosphate moiety would position the nicotinamide group near the C site where hydrolysis and subsequent nicotinamide release may take place. C, when present at elevated levels, free nicotinamide may bind to the C site preventing the conformational change and hydrolysis of NAD+. td> |