167415-27-2

Basic information

• Product Name: 4-BROMO-2,5-DIFLUORONITROBENZENE
• Synonyms: BUTTPARK 29\01-58;4-BROMO-2,5-DIFLUORONITROBENZENE;1-BROMO-2,5-DIFLUORO-4-NITROBENZENE;2,5-Difluoro-4-bromonitrobenzene;5-Bromo-1,4-difluoro-2-nitrobenzene
• CAS NO: 167415-27-2
• Molecular Formula: C₆H₂BrF₂NO₂
• Molecular Weight: 237.99
• Mol File: 167415-27-2.mol

Chemical Properties

• Melting Point: 55 °C
• Boiling Point: 262.379 °C at 760 mmHg
• Flash Point: 112.483 °C
• Appearance: /
• Density: 1.891 g/cm³
• Vapor Pressure: 0.0178mmHg at 25°C
• Refractive Index: 1.556
• Storage Temp.: Sealed in dry,Room Temperature
• BRN: 7411347
• CAS DataBase Reference: 4-BROMO-2,5-DIFLUORONITROBENZENE(CAS DataBase Reference)
• NIST Chemistry Reference: 4-BROMO-2,5-DIFLUORONITROBENZENE(167415-27-2)
• EPA Substance Registry System: 4-BROMO-2,5-DIFLUORONITROBENZENE(167415-27-2)

Safety Data

• Hazard Codes: Xi,T
• Statements: 36/37/38-20/21/22
• Safety Statements: 26-36/37/39-36/37
• HazardClass: IRRITANT, TOXIC
• Hazardous Substances Data: 167415-27-2(Hazardous Substances Data)

Usage

Chemical Properties

light yellow solid

InChI:InChI=1/C6H2BrF2NO2/c7-3-1-5(9)6(10(11)12)2-4(3)8/h1-2H

Upstream product

• 399-94-0 2-bromo-1,4-difluorobenzene 
• 540-36-3 para-difluorobenzene 

Downstream Products

• 172921-32-3 2,5-difluoro-4-nitrobenzonitrile 
• 944805-22-5 5-bromo-4-fluoro-2-nitrophenol 
• 1037364-36-5 2-amino-5-bromo-4-fluorophenol 
• 1607486-17-8 6-(benzylthio)-5-fluorobenzo[d]oxazol-2(3H)-one 
• 1607486-18-9 (R)-tert-butyl 8-(1-(6-(benzylthio)-5-fluoro-2-oxobenzo[d]oxazol-3(2H)-yl)ethyl)-3,4-dihydroisoquinoline-2(1H)-carboxylate 
• 1393685-65-8 8-(2,5-difluoro-4-nitrophenyl)-1,4-dioxa-spiro[4.5]dec-7-ene 
• 1393685-67-0 4-(4-amino-2,5-difluorophenyl)cyclohexanone 
• 1393686-10-6 4-(1,4-dioxa-spiro[4.5]dec-7-en-8-yl)-2,5-difluoro-phenylamine 
• 1407965-47-2 4-(4-amino-2,5-difluoro-phenyl)cyclohexanone O-[1-(4-trifluoromethyl-pyrimidin-2-yl)piperidin-4-yl]oxime 
• 1393685-66-9 4-(1,4-dioxa-spiro[4.5]dec-8-yl)-2,5-difluorophenylamine 
• 1393685-92-1 4-[4-(4-amino-2,5-difluorophenyl)cyclohexylideneaminooxy]piperidin-1-carboxylic acid isopropyl ester 
• 1393685-68-1 4-[4-(4-amino-2,5-difluorophenyl)cyclohexylideneaminooxy]piperidin-1-carboxylic acid tert-butyl ester 
• 1393683-88-9 4-(4-{2,5-difluoro-4-[(3-hydroxy-azetidine-1-carbonyl)amino]phenyl}cyclohexylideneaminooxy)piperidine-1-carboxylic acid tert-butyl ester 
• 1394121-29-9 N-(5-bromo-4-fluoro-2-nitrophenyl)-2-chloropyrimidin-4-amine 

Relevant articles and documents

A 2, 5 - difluoro -4 - nitro benzoic acid (by machine translation)

The invention discloses a 2, 5 - difluoro - 4 - nitro-benzoic acid industrial preparation method. The 2, 5 - difluoro - 4 - nitro-benzoic acid industrial preparation method, the initial raw materials to the difluoro, through the bromo, nitration, carbonitriding, the hydrolysis of the four-step reaction synthesis of 2, 5 - difluoro - 4 - nitro-benzoic acid. The got in the course of 2, 5 - difluoro - 4 - nitrobenzoic acid as white powdery solid, purity 98.5%, each step the raw material conversion rate respectively reaches 100%, the total yield of the whole process 44.6%. (by machine translation)

POLYCYCLIC PYRAZOLINONE DERIVATIVE AND HERBICIDE COMPRISING SAME AS EFFECTIVE COMPONENT THEREOF

Provided are a polycyclic pyrazolinone derivative indicated by general formula (1) (in the formula, R1, X1, X2, X3, and Y indicate the definitions provided in the Specification) and a herbicide comprising same as effective component thereof.

PYRAZOLINE-3-ON DERIVATIVE AND HERBICIDE CONTAINING THE SAME AS ACTIVE INGREDIENT

PROBLEM TO BE SOLVED: To provide a compound having excellent weed controlling effect and useful as an active ingredient of a herbicide. SOLUTION: There are provided a pyrazoline-3-on derivative represented by the following formula (1), where R1

PYRAZOLINONE DERIVATIVE, MANUFACTURING METHOD THEREFOR AND HERBICIDE CONTAINING THE SAME AS ACTIVE INGREDIENT

PROBLEM TO BE SOLVED: To provide a compound having excellent weed controlling effect and useful as an active ingredient of a herbicide. SOLUTION: There are provided a pyrazolinone derivative represented by the formula (1), a manufacturing method therefor and herbicide containing the same. (1), where R1 is a halogen atom, R2 and R3 are integrally a trimethylene group (-(CH2)3-), a tetramethylene group (-(CH2)4-), a pentamethylene group (-(CH2)5-) or an oxydiethylene group (-(CH2)2O(CH2)2-), R4 is H or a halogen atom, R5 is a halogen atom, Ar is 3-oxo-1,4-benzoxazine-5-yl group, a 2,2-difluoro-3-oxo-1,4-benzoxazine-5-yl group or a 3,4-dihydro-2-oxo quinoxaline-5-yl group. SELECTED DRAWING: None COPYRIGHT: (C)2016,JPOandINPIT

Heterocyclic compound

The present invention relates to compound (I) or a salt thereof which has a ROR γ t inhibitory action. wherein each symbol is as defined in the specification.

TRPV4 ANTAGONISTS

The present invention relates to spirocarbamate compounds of Formula (I) in which R1, (R2)Y, R3, R4, X and A have the meanings given in the specification. The invention further provides pharmaceutical compositions containing the compounds or pharmaceutically acceptable salts thereof and relates to their use of these compounds as TRPV4 antagonists in treating or preventing conditions associated with TRPV4 imbalance.

TRPV4 ANTAGONISTS

The present invention relates to spirocarbamate analogs, pharmaceutical compositions containing them and their use as TRPV4 antagonists.

PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR MODULATORS

The present invention is directed to a compound of formula (I), or a pharmaceutically acceptable salt, solvate hydrate or stereoisomer thereof, which is useful in treating or preventing disorders mediated by a peroxisome proliferator activated receptor (PPAR) such as syndrome X, type II diabetes, hyperglycemia, hyperlipidemia, obesity, coagaulopathy, hypertension, arteriosclerosis, and other disorders related to syndrome X and cardiovascular diseases.

Alkyl, azido, alkoxy, and fluoro-substituted and fused quinoxalinediones

Methods of treating or preventing neuronal loss associated with stroke, ischemia, CNS trauma, hypoglycemia, and surgery, as well as treating neurodegenerative diseases including Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and Down's syndrome, treating or preventing the adverse consequences of the hyperactivity of the excitatory amino acids, as well as treating anxiety, chronic pain, convulsions, and inducing anesthesia are disclosed by administering to an animal in need of such treatment an alkyl or azido-substituted 1,4-dihydroquinoxaline-2,3-dione or pharmaceutically acceptable salts thereof, which have high binding to the glycine receptor.

Synthesis and structure-activity relationships of substituted 1,4- dihydroquinoxaline-2,3-diones: Antagonists of N-methyl-D-aspartate (NMDA) receptor glycine sites and non-NMDA glutamate receptors

A series of mono-, di-, tri-, and tetrasubstituted 1,4- dihydroquinoxaline-2,3-diones (QXs) were synthesized and evaluated as antagonists at N-methyl-D-aspartate (NMDA)/glycine sites and α-amino-3- hydroxy-5-methylisoxazole-4-propionic acid-preferring non-NMDA receptors. Antagonist potencies were measured by electrical assays in Xenopus oocytes expressing rat whole brain poly(A)+ RNA. Trisubstituted QXs 17a (ACEA 1021), 17b (ACEA 1031), 24a, and 27, containing a nitro group in the 5 position and halogen in the 6 and 7 positions, displayed high potency (K(b) ~ 6-8 nM) at the glycine site, moderate potency at non-NMDA receptors (K(b) = 0.9-1.5 μM), and the highest (120-250-fold) selectivity in favor of glycine site antagonism over non-NMDA receptors. Tetrasubstituted QXs 17d,e were more than 100-fold weaker glycine site antagonists than the corresponding trisubstituted QXs with F being better tolerated than Cl as a substituent at the 8 position. Di- and monosubstituted QXs showed progressively weaker antagonism compared to trisubstituted analogues. For example, removal of the 5-nitro group of 17a results in a ~100-fold decrease in potency (10a,b,z), while removal of both halogens from 17a results in a ~3000-fold decrease in potency (10v). In terms of steady-state inhibition, most QX substitution patterns favor antagonism at NMDA/glycine sites over antagonism at non-NMDA receptors. Among the QXs tested, only 17i was slightly selective for non- NMDA receptors.