30267-40-4

Basic information

• Product Name: 1-(2,6-Dichlorophenyl)-1,3-Dihydro-5-Hydroxy-2H-Indol-2-One
• Synonyms: 1-(2,6-Dichlorophenyl)-1,3-Dihydro-5-Hydroxy-2H-Indol-2-One;2H-Indol-2-one,1-(2,6-dichlorophenyl)-1,3-dihydro-5-hydroxy-
• CAS NO: 30267-40-4
• Molecular Formula: C₁₄H₉Cl₂NO₂
• Molecular Weight: 294.13276
• Mol File: 30267-40-4.mol
• Article Data: 8

Chemical Properties

• Boiling Point: 517.7 °C at 760 mmHg
• Flash Point: 266.9 °C
• Appearance: /
• Density: 1.511 g/cm³
• PKA: 9.65±0.20(Predicted)
• CAS DataBase Reference: 1-(2,6-Dichlorophenyl)-1,3-Dihydro-5-Hydroxy-2H-Indol-2-One(CAS DataBase Reference)
• NIST Chemistry Reference: 1-(2,6-Dichlorophenyl)-1,3-Dihydro-5-Hydroxy-2H-Indol-2-One(30267-40-4)
• EPA Substance Registry System: 1-(2,6-Dichlorophenyl)-1,3-Dihydro-5-Hydroxy-2H-Indol-2-One(30267-40-4)

Safety Data

• Hazardous Substances Data: 30267-40-4(Hazardous Substances Data)

Usage

General Description

1-(2,6-Dichlorophenyl)-1,3-Dihydro-5-Hydroxy-2H-Indol-2-One, also known as SU 101, is a chemical compound that is commonly used as a pesticide and insecticide. It belongs to the class of chemicals called indoles, which are known for their biological activity and are used in various pharmaceutical and agricultural applications. This particular compound is a white crystalline solid, and its structure includes a 2H-indol-2-one core with a hydroxy group and dichlorophenyl substituents. It is effective at controlling a wide range of pests on crops and in urban environments, and is used in formulations for a variety of applications, including sprays, dusts, and baits. Additionally, the hydroxy group in its structure gives it potential as a pharmaceutical ingredient for the development of new drugs.

Upstream product

• 30118-47-9 <2-(2,6-Dichlor-anilino)-5-methoxy-phenyl>-essigsaeure 
• 207395-03-7 N-(chloroacetyl)-2',6'-(dichlorophenyl)-4-(methoxyphenyl)amine 
• 69002-84-2 2-(2-((2,6-dichlorophenyl)amino)-5-hydroxyphenyl)acetic acid 
• 696-62-8 para-iodoanisole 
• 30124-19-7 2',6'-(dichlorophenyl)-4-(methoxyphenyl)amine 
• 608-31-1 2,6-Dichloroaniline 
• 3776-30-5 2,2,6,6-tetrachlorocyclohexanone 
• 104-94-9 4-methoxy-aniline 
• 207395-01-5 N-(p-methoxyphenyl)-2,2,6,6-tetrachlorocyclohexaneimine 
• 100-02-7 4-nitro-phenol 
• 100-17-4 para-methoxynitrobenzene 
• 15307-86-5 [2-(2,6-dichloroanilino)phenyl]acetic acid 
• 15362-40-0 1-(2,6-dichlorophenyl)indolin-2-one 

Downstream Products

• 69002-84-2 2-(2-((2,6-dichlorophenyl)amino)-5-hydroxyphenyl)acetic acid 
• 1285680-62-7 C₁₅H₁₃Cl₂NO₃ 

Relevant articles and documents

Site-Selective C?H Oxygenation via Aryl Sulfonium Salts

Herein, we report a two-step process forming arene C?O bonds in excellent site-selectivity at a late-stage. The C?O bond formation is achieved by selective introduction of a thianthrenium group, which is then converted into C?O bonds using photoredox chemistry. Electron-rich, -poor and -neutral arenes as well as complex drug-like small molecules are successfully transformed into both phenols and various ethers. The sequence differs conceptually from all previous arene oxygenation reactions in that oxygen functionality can be incorporated into complex small molecules at a late stage site-selectively, which has not been shown via aryl halides.

Diclofenac derivatives with insulin-sensitizing activity

A series of diclofenac derivatives were synthesized. The insulin-sensitizing activity of 28 new compounds was evaluated in 3T3-L1 cells. The compounds 10a and 10f exhibited similar insulin-sensitizing activity with positive drug rosiglitazone.

Diclofenac toxicity to hepatocytes: A role for drug metabolism in cell toxicity

Diclofenac, a 2-arylacetic acid, nonsteroidal anti-inflammatory drug, has been reported to cause adverse hepatic effects in certain individuals. To discriminate among possible mechanisms of hepatotoxicity, we examined the effects of diclofenac on human and rat hepatocytes and hepatic cell lines (HepG2, FaO), investigated the major biochemical events in the course of diclofenac cytotoxicity (calcium homeostasis, lipid peroxidation, and mitochondrial dysfunction), and investigated whether cytotoxicity could be related to drug metabolism by cytochrome P-450. Acute diclofenac-induced toxicity in hepatocytes was preluded by a decrease in ATP levels, whereas no significant oxidative stress (decrease in glutathione and lipid peroxidation) or increase in intracellular calcium concentration could be observed at early incubation stages. Diclofenac was more cytotoxic to drug metabolizing cells (rat and human primary cultured hepatocytes) than to nonmetabolizing cell lines (HepG2, FaO). Despite the fact that diclofenac itself was effective in impairing ATP synthesis by mitochondria, we found evidence that toxicity was also related to drug metabolism and was reduced by the addition of cytochrome P-450 inhibitors (proadifen and ketoconazole) to culture medium. The in vitro cytotoxicity correlated well with the formation by hepatocytes of 5- hydroxydiclofenac and, in particular, N,5-dihydroxydiclofenac, a minor metabolite first characterized in this article. Hepatic microsomes showed the ability to both oxidize 5-hydroxydiclofenac to N,5-dihydroxydiclofenac and back reduce the latter to 5-hydroxydiclofenac with the consumption of NADPH. The experimental results suggest that the toxic effect of diclofenac on hepatocytes may be caused by drug-induced mitochondrial impairment, together with a futile consumption of NADPH.