40411-25-4

Usage

Chemical Properties

clear colorless liquid

InChI:InChI=1/C9H9NO/c1-2-8-5-3-4-6-9(8)10-7-11/h3-6H,2H2,1H3

Upstream product

• 578-54-1 ortho-ethylaniline 
• 503-38-8 trichloromethyl chloroformate 
• 32315-10-9 bis(trichloromethyl) carbonate 
• 121-44-8 triethylamine 
• 75-44-5 phosgene 
• 530-62-1 1,1'-carbonyldiimidazole 
• 2860-30-2 N-(2-ethylphenyl)formamide 
• 511302-92-4 1-(2-bromoethyl)-2-isocyanatobenzene 

Downstream Products

• 38145-71-0 1-{[(E)-4-Chloro-2-methyl-phenylimino]-methyl}-3-(2-ethyl-phenyl)-1-methyl-urea 
• 64393-36-8 1-(2-Aethyl-phenyl)-3-cyclopropyl-harnstoff 
• 34126-75-5 3-(2-ethyl-phenyl)-6,7-dihydro-5H-cyclopenta[e][1,3]oxazine-2,4-dione 
• 128255-28-7 (2-Ethyl-phenyl)-carbamic acid 2-piperidin-1-yl-ethyl ester; hydrochloride 
• 195523-40-1 butyl (2-ethylphenyl)carbamate 
• 27058-78-2 isopropyl (2-ethylphenyl)carbamate 
• 1582273-46-8 phenethyl (2-ethylphenyl)carbamate 
• 93731-23-8 1,3-bis(2-ethylphenyl)urea 

Relevant academic research and scientific papers

Phenylquinoline transient receptor potential vanilloid 1 antagonists for the treatment of pain: Discovery of 1-(2-phenylquinoline-4-carbonyl)-N-(4-(trifluoromethyl)phenyl)pyrrolidine-3-carboxamide

Reported herein is the design, synthesis, and pharmacologic characterization of a class of TRPV1 antagonists constructed on a phenylquinoline platform that evolved from Cinchophen lead. This design composes three sections: a phenylquinoline headgroup attached to an aliphatic carboxamides, which is tethered at a phenyl tail group. Optimization of this design led to the identification of 37, comprising a pyrrolidine linker and a trifluoromethyl–phenyl tail. In the TRPV1 functional assay, using cells expressed hTRPV1, 37 antagonized capsaicin-induced Ca2+ influx, with an IC50 value of 10.2 nM. In the complete mice analgesic model, 37 exhibited better antinociceptive activity than the positive control BCTC in diverse pain models. All of these results suggested that 37 could be considered as a lead candidate for the further development of antinociceptive drugs.

With anti-tumor effect of a quinazoline-urea derivative and its application (by machine translation)

The present invention relates to a of the general formula (II) anti-tumor function of said quinazoline-urea derivative and its application. The definition of the substituent in the general formula (II) in the specification. This invention, in order to SUO draw non-Buddhist nun and Geftinat compounds as the precursor, retention of SUO draw non-Buddhist nun the pharmocology-carbamido; at the same time, such as in reserved [...] EGFR-TKIs Geftinat, synthesis, and obtain a series of quinazoline-urea derivatives, by the in vitro activity tests, some compounds exhibit excellent anti-tumor activity, such derivatives have high research and utility value. (II). (by machine translation)

Synthesis of unsymmetrical phenylurea derivatives via oxidative cross coupling of aryl formamides with amines under metal-free conditions

A new synthetic approach for phenylurea derivatives involving the cross coupling of N-aryl formamides with amines through the formation of isocyanate intermediates in the presence of hypervalent iodine reagents is described.

Metal free oxidative coupling of aryl formamides with alcohols for the synthesis of carbamates

A direct transformation of N-aryl formamides to the corresponding carbamates via the formation of isocyanate intermediates is achieved in good yields using hypervalent iodine as an oxidant. This journal is

A simple and efficient synthesis of diaryl ureas with reduction of the intermediate isocyanate by triethylamine

Thirty symmetrical diaryl urea derivatives were synthesised in moderate to excellent yields from arylamine and triphosgene with triethylamine as a reducing agent for the intermediate, isocyanate. It was significant that part of the products could be collected in almost quantitative yield without column chromatography. The procedure under mild reaction conditions was tolerant of a wide range of functional groups. The structures of the compounds were determined by NMR, MS and X-ray crystallographic analyses.

Structural optimization of a CXCR2-directed antagonist that indirectly inhibits γ-secretase and reduces Aβ

Amyloid β (Aβ), a key molecule in the pathogenesis of Alzheimer's disease (AD), is derived from the amyloid precursor protein (APP) by sequential proteolysis via β- and γ-secretases. Because of their role in generation of Aβ, these enzymes have emerged as important therapeutic targets for AD. In the case of γ-secretase, progress has been made towards designing potent inhibitors with suitable pharmacological profiles. Direct γ-secretase inhibitors are being evaluated in clinical trials and new strategies are being explored to block γ-secretase activity indirectly as well. In this regard, we have previously reported an indirect regulation of γ-secretase through antagonism of CXCR2, a G-protein coupled receptor (GPCR). We demonstrated that N-(2-hydroxy-4-nitrophenyl)-N′-(2-bromophenyl)urea (SB225002), a selective inhibitor of CXCR2 also plays a role in an indirect inhibition of γ-secretase. Furthermore, we reported a ～5-fold difference in the selective inhibition of APP versus Notch processing via γ-secretase following treatment with SB225002. Herein we describe the synthesis and optimization of SB225002. By determination of the structure-activity relationship (SAR), we derived small molecules that inhibit Aβ40 production with IC50 values in the sub-micromolar range in a cell-based assay and also validated the potential of CXCR2 as a new target for therapeutic intervention in AD.

Radical ring closures of 4-isocyanato carbon-centered radicals

The 2-(2-isocyanatophenyl)ethyl radical was generated from the corresponding bromide with tributyltin and tris(trimethylsilyl)silyl radicals and shown to ring close in the 6-endo-mode to afford 3,4-dihydro-1H-quinolin-2-one as the major product. Cyclization in the 5-exo-mode to produce 2,3-dihydroindole-1-carbaldehyde, after hydrogen abstraction, was a minor reaction. Rate constants for the two processes were estimated and compared with reaction enthalpies computed by the DFT method.

Anti-viral method

PCT No. PCT/US97/07431 Sec. 371 Date Jan. 6, 1999 Sec. 102(e) Date Jan. 6, 1999 PCT Filed May 2, 1997 PCT Pub. No. WO97/41846 PCT Pub. Date Nov. 13, 1997The present invention provides compounds which inhibit an envelope virus by inhibiting the fusion of the virus with the host cell. The virus may be inhibited in an infected cell, a cell susceptible of infection or a mammal in need thereof.

Substituted N-phenylcarbamates as histamine H3 receptor antagonists with improved in vivo potency

Novel substituted N-phenylcarbamates as derivatives of 3-(1 H-imidazol- 4-yl)propanol were prepared and tested for their antagonist potency in vitro and in vivo at histamine H3 receptors. Structural modifications with different alkyl and acetyl moieties were performed in an attempt to optimize pharmacodynamic and pharmacokinetic effects. Most compounds are active in a functional test for histamine H3 receptors on rat cerebral cortex synaptosomes as well as in a peripheral model on guinea pig ileum. But only carbamates without too bulky lipophilic residues showed pronounced to high antagonist potency on the enhancement of endogenous histamine in brain after p.o. administration to mice (ED50 values of 5.5 to 0.86 mg · kg-1). The tested compounds presented weak activities at histamine H1, H2, and muscarinic M3 receptors thus demonstrating their H3-receptor selectivity.

Urea, thiourea and guanidine compounds and their use as anti-viral agents

The present invention provides compounds which inhibit an envelope virus by inhibiting the fusion of the virus with the host cell. The virus may be inhibited in an infected cell, a cell susceptible of infection or a mammal in need thereof.