2,6-Dichlorodiphenylamine
(Synonyms: 2,6-二氯-N-苯基苯胺,2,6-Dichloro-N-phenylaniline) 目录号 : GC60466
2,6-Dichlorodiphenylamine是双氯芬酸钠的结构类似物，具有抗白色念珠菌活性。DiclofenacSodium是一种有效的，非选择性抗炎剂，为 COX的抑制剂，在CHO细胞中，对人COX-1和COX-2的 IC50值分别为4和1.3nM。
Cas No.:15307-93-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2,6-Dichlorodiphenylamine is an analogue of Diclofenac Sodium and has anti-Candida albicans activity. Diclofenac Sodium is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC50s of 4 and 1.3 nM for human COX-1 and COX-2 in CHO cells.
[1]. Makoto Urai,et al. Potent Drugs That Attenuate anti-Candida Albicans Activity of Fluconazole and Their Possible Mechanisms of Action. J Infect Chemother. 2014 Oct;20(10):612-5.
| Cas No. | 15307-93-4 | SDF | |
| 别名 | 2,6-二氯-N-苯基苯胺,2,6-Dichloro-N-phenylaniline | ||
| Canonical SMILES | ClC1=C(NC2=CC=CC=C2)C(Cl)=CC=C1 | ||
| 分子式 | C12H9Cl2N | 分子量 | 238.11 |
| 溶解度 | 储存条件 | 4°C, protect from light | |
| 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.1997 mL | 20.9987 mL | 41.9974 mL |
| 5 mM | 0.8399 mL | 4.1997 mL | 8.3995 mL |
| 10 mM | 0.42 mL | 2.0999 mL | 4.1997 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。
[Analysis of 1-(2,6-dichlorophenyl)-2-indolone and related materials by high performance liquid chromatography]
Se Pu 2000 Jan;18(1):55-6.PMID:12541457doi
The separation of 1-(2,6-dichlorophenyl)-2-indolone (DCI) and related materials in the synthesis of medical intermediate DCI from 2, 6-dichlorophenol and phenylamine was investigated with high performance liquid chromatography under different chromatographic conditions. The results showed that DCI and related materials were in baseline separation by using CLC-CN(150 mm x 6.0 mm i.d., 7 microns) as column, MeOH-H2O(6:4, V/V) as mobile phase and a flow-rate at 1 mL/min. A rapid, accurate and reproducible HPLC method for determining DCI was developed. Fine and crude DCI samples were detected, results showed that N-(2,6-dichlorodiphenyl)-chloracetyl amide (CBCC) was the main impurity in fine sample, and CBCC and 2,6-Dichlorodiphenylamine were the main impurities in the crude one.
Potent drugs that attenuate anti-Candida albicans activity of fluconazole and their possible mechanisms of action
J Infect Chemother 2014 Oct;20(10):612-5.PMID:25009090DOI:10.1016/j.jiac.2014.06.004.
Fluconazole (FLCZ) is a first-line drug for treating Candida albicans infections, but clinical failure due to reduced sensitivity is a growing concern. Our previous study suggested that certain drug combinations pose a particular challenge in potently reducing FLCZ's anti-C. albicans activity, and cyclooxygenase inhibitors formed the major group of these attenuating drugs in combination with FLCZ. In this study, we examined the effects of diclofenac sodium (DFNa) and related compounds in combination with FLCZ against C. albicans, and investigated their possible mechanisms of interaction. DFNa, ibuprofen, and omeprazole elevated the minimum inhibitory concentration (MIC) of FLCZ by 8-, 4-, and 4-fold, respectively; however, loxoprofen sodium and celecoxib did not. An analogue of DFNa, 2,6-Dichlorodiphenylamine, also elevated the MIC by 4-fold. Gene expression analysis revealed that diclofenac sodium induced CDR1 efflux pump activity, but not CDR2 activity. In addition, an efflux pump CDR1 mutant, which was manipulated to not be induced by DFNa, showed less elevation of MIC compared to that shown by the wild type. Therefore, DFNa and related compounds are potent factors for reducing the sensitivity of C. albicans to FLCZ partly via induction of an efflux pump. Although it is not known whether such antagonism is relevant to the clinical treatment failure observed, further investigation of the molecular mechanisms underlying the reduction of FLCZ's anti-C. albicans activity is expected to promote safer and more effective use of the drug.
Inhibition by non-steroidal anti-inflammatory drugs of compound action potentials in frog sciatic nerve fibers
Biomed Pharmacother 2018 Jul;103:326-335.PMID:29665554DOI:10.1016/j.biopha.2018.04.041.
Aims: Although antinociception produced by non-steroidal anti-inflammatory drugs (NSAIDs) is partly attributed to nerve conduction inhibition, this has not been thoroughly examined yet. The aim of the present study was to reveal quantitatively how various types of NSAIDs affect compound action potentials (CAPs), a measure of nerve conduction. Main methods: CAPs were recorded from the frog sciatic nerve by using the air-gap method. Key findings: Soaking the sciatic nerve with acetic acid-based NSAIDs (diclofenac and aceclofenac) reduced the peak amplitude of CAP in a concentration-dependent manner; their IC50 values were 0.94 and 0.47 mM, respectively. Other acetic acid-based NSAIDs (indomethacin, acemetacin and etodolac) also inhibited CAPs [the extent of inhibition: some 40% (1 mM), 40% (0.5 mM) and 15% (1 mM), respectively], except for sulindac and felbinac at 1 mM that had no effects on CAP peak amplitudes. A similar inhibition was produced by fenamic acid-based NSAIDs [tolfenamic acid (IC50 = 0.29 mM), meclofenamic acid (0.19 mM), flufenamic acid (0.22 mM) and mefenamic acid] which are similar in chemical structure to diclofenac and aceclofenac; their derivatives (2,6-Dichlorodiphenylamine and N-phenylanthranilic acid) also inhibited. On the other hand, salicylic acid-based (aspirin), propionic acid-based (ketoprofen, naproxen, ibuprofen, loxoprofen and flurbiprofen) and enolic acid-based (meloxicam and piroxicam) NSAIDs had no effects on CAP peak amplitudes. Significance: At least a part of antinociception produced by NSAIDs used as a dermatological drug to alleviate pain may be attributed to their inhibitory effects on nerve conduction, which depend on the chemical structures of NSAIDs.