926663-69-6

Basic information

• Product Name: N-(3-aminophenyl)-3-(trifluoromethyl)benzamide
• Synonyms: N-(3-aminophenyl)-3-(trifluoromethyl)benzamide
• CAS NO: 926663-69-6
• Molecular Formula: C₁₄H₁₁F₃N₂O
• Molecular Weight: 280.25
• Mol File: 926663-69-6.mol

Chemical Properties

• Appearance: /
• CAS DataBase Reference: N-(3-aminophenyl)-3-(trifluoromethyl)benzamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-(3-aminophenyl)-3-(trifluoromethyl)benzamide(926663-69-6)
• EPA Substance Registry System: N-(3-aminophenyl)-3-(trifluoromethyl)benzamide(926663-69-6)

Safety Data

• Hazardous Substances Data: 926663-69-6(Hazardous Substances Data)

Upstream product

• 326903-68-8 N-(3-nitrophenyl)-3-(trifluoromethyl)benzamide 
• 454-92-2 3-(trifluoromethyl)benzoic acid 
• 99-09-2 3-nitro-aniline 
• 2251-65-2 3-(Trifluoromethyl)benzoyl chloride 

Downstream Products

• 1086422-72-1 N-(3-(3-(trifluoromethyl)benzamido)phenyl)-1H-pyrrolo[2,3-b]pyridine-4-carboxamide 
• 1395923-05-3 C₂₉H₂₁F₃N₂O₂ 
• 1395923-33-7 C₂₅H₂₁F₃N₂O₂ 
• 1622869-10-6 C₂₁H₁₅F₃N₂O₂ 

Relevant articles and documents

Discovery and Identification of Small Molecules as Methuosis Inducers with in Vivo Antitumor Activities

Methuosis is a novel nonapoptotic mode of cell death characterized by vacuole accumulation in the cytoplasm. In this article, we describe a series of azaindole-based compounds that cause vacuolization in MDA-MB-231 cells. The most potent vacuole inducer,

Aza-acridine compound and preparation method and application thereof

The invention discloses a method for efficiently preparing an aza-acridine compound. The structural formula of the aza-acridine compound is shown as a formula I; the preparation method comprises the following steps: adding a 2-aminoquinoline-3-methanamide compound and a solvent under an air condition, and heating to reaction temperature; after the reaction is ended, separating and purifying to obtain multisubstituted acridine derivatives shown as the following formula, wherein the reaction temperature is 100 to 200DEG C, and the reaction time is 1 to 24 hours. A synthetic method of the aza-acridine compound, disclosed by the invention, has the advantages of scientificity, reasonability, simple and easily-operated synthesis process and high synthetic yield; a product is easy to purify. The invention also relates to the aza-acridine compound which can be used for inhibiting EGFR (Epidermal Growth Factor Receptor) and SrC, a preparation method of the aza-acridine compound, activity of a drug containing the aza-acridine compound and the application of the drug. The compound is shown in a formula II and can be used for preparing an EGFR and SrC activity inhibitor and a disease treatment medicine activated and mediated by the EGFR and the SrC.

Compositions, methods of use, and methods of treatment

Embodiments of the present disclosure, in one aspect, relate to a beta-lactamase inhibitor, pharmaceutical compositions including a beta-lactamase inhibitor, methods of treatment of a condition (e.g., infection) or disease, methods of treatment using comp

Design, synthesis and evaluation of azaacridine derivatives as dual-target EGFR and Src kinase inhibitors for antitumor treatment

Overexpression of EGFR is often associated with advanced stage disease and poor prognosis. In certain cancers, Src works synergistically with EGFR to promote proliferation, survival, invasion and metastasis. Development of dual-target drugs against EGFR and Src is of therapeutic advantage against these cancers. Based on molecular docking and our previous studies, we rationally designed a new series of azaacridine derivatives as potent EGFR and Src dual inhibitors. Most of the synthesized azaacridines displayed good antiproliferative activity against K562 and A549?cells. The representative compound 13b showed nM IC50 values against K562 and A549?cells, and inhibited EGFR at inhibition rate of 33.53% at 10?μM and Src at inhibition rate of 72.12% at 1?μM. Furthermore, compound 13b could inhibit the expression of EGFR, p-EGFR, Src and p-Src. Moreover, 13b efficiently inhibited the invasion of tumor cells and induced cancer cells apoptosis. Our study suggested that azaacridine scaffold can be developed as novel multi-target kinase inhibitors for cancer therapy.

2-Amino-1-phenyl-pyrrolo[3,2-b]quinoxaline-3-carboxamide derivates

The invention relates to compound characterized by a general formula (1), wherein n of R1n is 0, 1, 2, 3 or 4, in particular n of R1n is 0 or 1, and each R1 independently from any other R1

Pyrrolo[3,2-b ]quinoxaline derivatives as types I1/2 and II Eph tyrosine kinase inhibitors: Structure-based design, synthesis, and in vivo validation

The X-ray crystal structures of the catalytic domain of the EphA3 tyrosine kinase in complex with two type I inhibitors previously discovered in silico (compounds A and B) were used to design type I1/2 and II inhibitors. Chemical synthesis of a

Potent and selective inhibitors of the TASK-1 potassium channel through chemical optimization of a bis-amide scaffold

TASK-1 is a two-pore domain potassium channel that is important to modulating cell excitability, most notably in the context of neuronal pathways. In order to leverage TASK-1 for therapeutic benefit, its physiological role needs better characterization; however, designing selective inhibitors that avoid the closely related TASK-3 channel has been challenging. In this study, a series of bis-amide derived compounds were found to demonstrate improved TASK-1 selectivity over TASK-3 compared to reported inhibitors. Optimization of a marginally selective hit led to analog 35 which displays a TASK-1 IC 50 = 16 nM with 62-fold selectivity over TASK-3 in an orthogonal electrophysiology assay.

COMPOSITIONS, METHODS OF USE, AND METHODS OF TREATMENT

Embodiments of the present disclosure, in one aspect, relate to a beta-lactamase inhibitor, pharmaceutical compositions including a beta-lactamase inhibitor, methods of treatment of a condition (e.g., infection) or disease, methods of treatment using comp

Cyclooxygenase-1-selective inhibitors are attractive candidates for analgesics that do not cause gastric damage. Design and in vitro/in vivo evaluation of a benzamide-type cyclooxygenase-1 selective inhibitor

Although cyclooxygenase-1 (COX-1) inhibition is thought to be a major mechanism of gastric damage by nonsteroidal anti-inflammatory drugs (NSAIDs), some COX-1-selective inhibitors exhibit strong analgesic effects without causing gastric damage. However, it is not clear whether their analgesic effects are attributable to COX-1-inhibitory activity or other bioactivities. Here, we report that N-(5-amino-2-pyridinyl)-4-(trifluoromethyl)benzamide (18f, TFAP), which has a structure clearly different from those of currently available COX-1-selective inhibitors, is a potent COX-1-selective inhibitor (COX-1 IC 50 = 0.80 ± 0.05 μM, COX-2 IC50 = 210 ± 10 μM). This compound causes little gastric damage in rats even at an oral dose of 300 mg/kg, though it has an analgesic effect at as low a dose as 10 mg/kg. Our results show that COX-1-selective inhibitors can be analgesic agents without causing gastric damage.