168966-54-9

Basic information

• Product Name: 1,2-Benzenediamine,3,4,5-trifluoro-(9CI)
• Synonyms: 1,2-Benzenediamine,3,4,5-trifluoro-(9CI);3,4,5-Trifluorobenzene-1,2-diamine;3,4,5-Trifluorophenylene-1,2-diamine, 1,2-Diamino-3,4,5-trifluorobenzene;1,2-Benzenediamine, 3,4,5-trifluoro-
• CAS NO: 168966-54-9
• Molecular Formula: C₆H₅F₃N₂
• Molecular Weight: 162.1125096
• Product Categories: HALIDE
• Mol File: 168966-54-9.mol

Chemical Properties

• Appearance: /
• Storage Temp.: under inert gas (nitrogen or Argon) at 2–8 °C
• CAS DataBase Reference: 1,2-Benzenediamine,3,4,5-trifluoro-(9CI)(CAS DataBase Reference)
• NIST Chemistry Reference: 1,2-Benzenediamine,3,4,5-trifluoro-(9CI)(168966-54-9)
• EPA Substance Registry System: 1,2-Benzenediamine,3,4,5-trifluoro-(9CI)(168966-54-9)

Safety Data

• Hazardous Substances Data: 168966-54-9(Hazardous Substances Data)

Usage

Common uses

Production of polymers
Production of dyes
Manufacture of pharmaceuticals
Manufacture of agrochemicals

Hazardous properties

Skin and eye irritant
Respiratory irritant or lung damage at high concentrations
Potentially harmful if swallowed
Adverse effects on liver and kidneys

Environmental impact

Harmful to aquatic life
Long-lasting effects on the environment

Safety precautions

Proper handling and disposal procedures
Minimize impact on human health and the environment

Upstream product

• 882068-89-5 C₆H₃F₃N₂O₂ 
• 64-17-5 ethanol 
• 365-29-7 N-(2,3,4-trifluorophenyl)acetamide 
• 148416-38-0 6-nitro-2,3,4-trifluoroaniline 
• 3862-73-5 2,3,4-trifluoroaniline 

Downstream Products

• 1196131-58-4 5,6,7-triifluoro-2-phenyl-1H-benzimidazole 

Relevant articles and documents

Chemoenzymatic Synthesis and Antiherpes Activity of 5-Substituted 4,6-Difluorobenzimidazoles Ribo- and 2′-Deoxyribonucleosides

A series of 5,6-disubstituted benzimidazole nucleosides, obtained earlier, did not show any significant antiviral activity at relatively low cytotoxicity in vitro. In the course of our research we have succeeded in introducing an additional fluorine atom

One-Step Sixfold Cyanation of Benzothiadiazole Acceptor Units for Air-Stable High-Performance n-Type Organic Field-Effect Transistors

Reported here is a new high electron affinity acceptor end group for organic semiconductors, 2,1,3-benzothiadiazole-4,5,6-tricarbonitrile (TCNBT). An n-type organic semiconductor with an indacenodithiophene (IDT) core and TCNBT end groups was synthesized

Synthesis and potent antifungal activity against Candida species of some novel 1H-benzimidazoles

(Chemical Equation Presented) A series of 47 novel N1-alkylated- 2-aryl-5(6)-substituted-1H-benzimidazoles and their three novel indole analogues were synthesized and evaluated for in vitro antifungal activities against Candida species by the tube dilution method. The results showed that compounds 79 and 80, having pyridine at the position C-2, of benzimidazoles exhibited the greatest activity with MIC values of 6.25-3.12 μg/mL. Indole analogues 108-110 have no inhibitory activity.

Benzimidazole derivatives for the treatment of viral infections

According to a first aspect of the invention there is provided compounds of formula (I): wherein: R1is hydroxy; O-acetyl; or a halo atom; R2is hydroxy; O-acetyl; or a halo atom; R3is hydrogen; a halo atom; azido; C2-6alkenyl; C2-6alkynyl; C6-14aryl C2-6alkenyl; C6-14arylC2-6alkynyl —NR8R9(where R8and R9may be the same or different and are hydrogen, C1-8alkyl, cyanoC1-8alkyl, hydroxyC1-8alkyl, haloC1-8alkyl, C3-7cycloalkyl, C1-8alkylC3-7cycloalkyl, C2-6alkenyl, C3-7cycloalkylC1-8alkyl, C2-6alkynyl, C6-14aryl, C6-14arylC1-8alkyl, heterocycleC1-8alkyl, C1-8alkylcarbonyl, C6-14arylsulfonyl, C1-8alkysulfonyl, or R8R9together with the N atom to which they are attached form a 3,4,5 or 6 membered heterocyclic ring); —OR10(where R10is hydrogen, C1-8alkyl, C6-14aryl, or C6-14arylC1-8alkyl, C2-6alkenyl, C2-6alkynyl, C6-14aryl C2-6alkenyl or C6-14arylC2-6alkynyl); or —SR11(where R11is hydrogen, C1-8alkyl, C6-14aryl, or C6-14arylC1-8alkyl).

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.

Glycine receptor antagonists and the use thereof

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, inducing anesthesia and treating psychosis are disclosed by administering to an animal in need of such treatment a compound having high affinity for the glycine binding site, lacking PCP side effects and which crosses the blood brain barrier of the animal. Also disclosed are novel 1,4-dihydroquinoxaline-2,3-diones, and pharmaceutical compositions thereof. Also disclosed are highly soluble ammonium salts of 1,4-dihydroquinoxaline-2,3-diones.

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.