Neocuproine
(Synonyms: 新铜试剂) 目录号 : GC40639
A chelating agent
Cas No.:484-11-7
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Neocuproine is a phenanthroline compound that is used as a chelating agent in a wide array of transition metal-catalyzed reactions. It can also be used in the synthesis of aryl ketones.
| Cas No. | 484-11-7 | SDF | |
| 别名 | 新铜试剂 | ||
| Canonical SMILES | CC1=NC2=C(C=C1)C=CC3=CC=C(C)N=C32 | ||
| 分子式 | C14H12N2 | 分子量 | 208.3 |
| 溶解度 | DMF: 25 mg/ml,DMSO: 25 mg/ml,DMSO:PBS(pH 7.2) (1:4): 0.2 mg/ml,Ethanol: 10 mg/ml | 储存条件 | Store at RT |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 4.8008 mL | 24.0038 mL | 48.0077 mL |
| 5 mM | 0.9602 mL | 4.8008 mL | 9.6015 mL |
| 10 mM | 0.4801 mL | 2.4004 mL | 4.8008 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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，
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 saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Neocuproine as a Redox-Active Ligand Platform on Iron and Cobalt
Inorg Chem 2019 Jul 15;58(14):9057-9066.PMID:31247828DOI:10.1021/acs.inorgchem.9b00531.
A family of bis(Neocuproine) complexes of Fe2+ and Co2+ have been investigated for Neocuproine redox noninnocence. A series of redox isomers of M(Neocuproine)2n+ (where n = 2, 1, 0 for Co and n = 2, 0 for Fe) have been synthesized and thoroughly characterized. The electronic structure of these complexes has been rigorously investigated using a variety of techniques, including X-ray absorption spectroscopy, Mössbauer spectroscopy, X-ray diffraction, electron paramagnetic resonance spectroscopy, and magnetic measurements. All of these techniques are consistent with ligand-based reduction events to generate radical Neocuproine complexes. Thus, Neocuproine adds to a growing family of chelating N-donor type ligands that participate in redox noninnocence and may be useful for future catalyst and reaction design.
Neocuproine ablates melanocytes in adult zebrafish
Zebrafish 2008 Dec;5(4):257-64.PMID:19133824DOI:10.1089/zeb.2008.0540.
The simplest regeneration experiments involve the ablation of a single cell type. While methods exist to ablate the melanocytes of the larval zebrafish,(1,2) no convenient method exists to ablate melanocytes in adult zebrafish. Here, we show that the copper chelator Neocuproine (NCP) causes fragmentation and disappearance of melanin in adult zebrafish melanocytes. Adult melanocytes expressing eGFP under the control of a melanocyte-specific promoter also lose eGFP fluorescence in the presence of NCP. We conclude that NCP causes melanocyte death. This death is independent of p53 and melanin, but can be suppressed by the addition of exogenous copper. NCP is ineffective at ablating larval melanocytes. This now provides a tool for addressing questions about stem cells and the maintenance of the adult pigment pattern in zebrafish.
Neocuproine, a selective Cu(I) chelator, and the relaxation of rat vascular smooth muscle by S-nitrosothiols
Br J Pharmacol 1997 Jul;121(6):1047-50.PMID:9249237DOI:10.1038/sj.bjp.0701218.
1. A study has been made of the effect of Neocuproine, a specific Cu(I) chelator, on vasodilator responses of rat isolated perfused tail artery to two nitrosothiols: S-nitroso-N-acetyl-D,L-penicillamine (SNAP) and S-nitroso-glutathione (GSNO). 2. Bolus injections (10 microl) of SNAP or GSNO (10(-7)-10(-3) M) were delivered into the lumen of perfused vessels pre-contracted with sufficient phenylephrine (1-7 microM) to develop pressures of 100-120 mmHg. Two kinds of experiment were made: SNAP and GSNO were either (a) pre-mixed with Neocuproine (10(-4) M) and then injected into arteries; or (b) vessels were continuously perfused with Neocuproine (10(-5) M) and then injected with either pure SNAP or GSNO. 3. In each case, Neocuproine significantly attenuated vasodilator responses to both nitrosothiols, although the nature of the inhibitory effect differed in the two types of experiment. We conclude that the ability of exogenous nitrosothiols to relax vascular smooth muscle in our ex vivo model is dependent upon a Cu(I) catalyzed process. Evidence is presented which suggests that a similar Cu(I)-dependent mechanism is responsible for the release of NO from endogenous nitrosothiols and that this process may assist in maintaining vasodilator tone in vivo.
Neocuproine, a copper (I) chelator, potentiates purinergic component of vas deferens contractions elicited by electrical field stimulation
Pharmacology 2005 Oct;75(2):69-75.PMID:16020948DOI:10.1159/000087007.
Effects of the specific copper (I) chelator, Neocuproine, on the purinergic and adrenergic components of nerve-evoked contractions were investigated in the prostatic rat vas deferens. Electrical field stimulation (EFS; 4 Hz) induced bimodal contractions of vas deferens tissue in the presence of alpha1-adrenoceptor antagonist prazosin (to isolate the purinergic component) or purinoceptor antagonist suramin (to isolate the adrenergic component). Neocuproine significantly potentiated the purinergic component of the contractile responses to EFS. However, the same agent failed to elicit any significant effect on the adrenergic component of nerve-evoked contractions. The copper (II) chelator cuprizone could not affect the purinergic component of contractions. The potentiating effect of Neocuproine which was reversible after washout of the drug, did not occur following the application of the pre-prepared neocuproine-copper (I) complex. A nitric oxide synthase inhibitor, L-nitroarginine; a cyclooxygenase inhibitor, indomethacin or an alpha2-adrenoceptor antagonist, yohimbine, failed to alter the responses to Neocuproine on the purinergic component of the contraction to EFS. Neocuproine did not elicit any significant effect on preparations in which the purinergic receptors were desensitized with alpha,beta-methylene ATP. In conclusion, our results suggest that Neocuproine potentiates the purinergic component of rat vas deferens contractions elicited by EFS, presumably by facilitating purinergic neurotransmission and that copper (I)-sensitive mechanisms can modulate purinergic transmission in this tissue.
Protective effects of Neocuproine copper chelator against oxidative damage in NSC34 cells
Mutat Res Genet Toxicol Environ Mutagen 2018 Dec;836(Pt B):62-71.PMID:30442347DOI:10.1016/j.mrgentox.2018.06.019.
In this work, we aim to provide evidence for the protective effect of a copper chelator, Neocuproine (NeoCu), against the oxidative stress in NSC34 cells, which inhibits biomolecule oxidation and cell death. Results obtained with the comet assay allowed to determine the increase in oxidized purines and pyrimidines by H2O2 exposure, and their changes after the addition of NeoCu. We also observed a higher ATP7b activity in nuclei and a higher Cu concentration inside the cells, proving that the NeoCu acts directly in DNA to promote cell recovery in oxidative stress conditions, also observed in Reactive Oxygen Species (ROS) detection assay by Flow Cytometry. Based on these results, we propose that NeoCu is a promising drug for the protection of motor neuron cells during oxidative stress caused by neurodegenerative diseases in this system.