81709-36-6

Basic information

• Product Name: 2-(4-aminophenyl)-N,N-dimethylacetamide
• Synonyms: 2-(4-aminophenyl)-N,N-dimethylacetamide;2-(4-aminophenyl)-N,N-dimethylacetamide(SALTDATA: FREE)
• CAS NO: 81709-36-6
• Molecular Formula: C₁₀H₁₄N₂O
• Molecular Weight: 178
• Mol File: 81709-36-6.mol
• Article Data: 8

Chemical Properties

• Boiling Point: 346.4°C at 760 mmHg
• Flash Point: 163.3°C
• Appearance: /
• Density: 1.1g/cm³
• Vapor Pressure: 5.76E-05mmHg at 25°C
• Refractive Index: 1.569
• Storage Temp.: 2-8°C
• CAS DataBase Reference: 2-(4-aminophenyl)-N,N-dimethylacetamide(CAS DataBase Reference)
• NIST Chemistry Reference: 2-(4-aminophenyl)-N,N-dimethylacetamide(81709-36-6)
• EPA Substance Registry System: 2-(4-aminophenyl)-N,N-dimethylacetamide(81709-36-6)

Safety Data

• HazardClass: IRRITANT
• Hazardous Substances Data: 81709-36-6(Hazardous Substances Data)

Usage

General Description

2-(4-aminophenyl)-N,N-dimethylacetamide is a chemical compound with the molecular formula C10H14N2O. It is a derivative of acetamide, with a dimethyl substituent and an aminophenyl group attached to the nitrogen atom. 2-(4-aminophenyl)-N,N-dimethylacetamide is commonly used as an intermediate in the synthesis of pharmaceuticals and organic compounds, and it has shown potential as a building block for the development of new drug molecules. It is also known to exhibit antimicrobial and antiviral properties, making it a valuable compound for research in the medical and pharmaceutical fields. Additionally, it is important to handle this chemical with care as it may pose hazards to health and the environment.

InChI:InChI=1/C10H14N2O/c1-12(2)10(13)7-8-3-5-9(11)6-4-8/h3-6H,7,11H2,1-2H3

Upstream product

• 104-03-0 4-nitrobenzeneacetic acid 
• 55536-07-7 4-aminophenyl propionate 
• 50434-36-1 4-nitrophenylacetyl chloride 
• 90405-67-7 N,N-dimethyl-2-(4-nitrophenyl)acetamide 

Downstream Products

• 105105-32-6 N,N-dimethyl-4-N’,N’-dimethylaminobenzeneacetamide 
• 93413-49-1 1-<(4-aminophenyl)<(dimethylamino)carbonyl>methyl>cyclohexanol 
• 93413-48-0 1-<(4-aminophenyl)-2-(dimethylamino)ethyl>cyclohexanol 
• 81709-29-7 2-(4-Hydrazinophenyl)-N,N-dimethylacetamide, hydrochloride 
• 93413-50-4 1-<2-(dimethylamino)-1-(4-nitrophenyl)ethyl>cyclohexanol 
• 5636-52-2 4-[2-(dimethylamino)ethyl]aniline 

Relevant articles and documents

2-Arylamino-6-ethynylpurines are cysteine-targeting irreversible inhibitors of Nek2 kinase

Renewed interest in covalent inhibitors of enzymes implicated in disease states has afforded several agents targeted at protein kinases of relevance to cancers. We now report the design, synthesis and biological evaluation of 6-ethynylpurines that act as covalent inhibitors of Nek2 by capturing a cysteine residue (Cys22) close to the catalytic domain of this protein kinase. Examination of the crystal structure of the non-covalent inhibitor 3-((6-cyclohexylmethoxy-7H-purin-2-yl)amino)benzamide in complex with Nek2 indicated that replacing the alkoxy with an ethynyl group places the terminus of the alkyne close to Cys22 and in a position compatible with the stereoelectronic requirements of a Michael addition. A series of 6-ethynylpurines was prepared and a structure activity relationship (SAR) established for inhibition of Nek2. 6-Ethynyl-N-phenyl-7H-purin-2-amine [IC50 0.15 μM (Nek2)] and 4-((6-ethynyl-7H-purin-2-yl)amino)benzenesulfonamide (IC50 0.14 μM) were selected for determination of the mode of inhibition of Nek2, which was shown to be time-dependent, not reversed by addition of ATP and negated by site directed mutagenesis of Cys22 to alanine. Replacement of the ethynyl group by ethyl or cyano abrogated activity. Variation of substituents on the N-phenyl moiety for 6-ethynylpurines gave further SAR data for Nek2 inhibition. The data showed little correlation of activity with the nature of the substituent, indicating that after sufficient initial competitive binding to Nek2 subsequent covalent modification of Cys22 occurs in all cases. A typical activity profile was that for 2-(3-((6-ethynyl-9H-purin-2-yl)amino)phenyl)acetamide [IC50 0.06 μM (Nek2); GI50 (SKBR3) 2.2 μM] which exhibited >5-10-fold selectivity for Nek2 over other kinases; it also showed > 50% growth inhibition at 10 μM concentration against selected breast and leukaemia cell lines. X-ray crystallographic analysis confirmed that binding of the compound to the Nek2 ATP-binding site resulted in covalent modification of Cys22. Further studies confirmed that 2-(3-((6-ethynyl-9H-purin-2-yl)amino)phenyl)acetamide has the attributes of a drug-like compound with good aqueous solubility, no inhibition of hERG at 25 μM and a good stability profile in human liver microsomes. It is concluded that 6-ethynylpurines are promising agents for cancer treatment by virtue of their selective inhibition of Nek2. This journal is

ANTITUMOR-EFFECT ENHANCER USING PYRAZOLO[3,4-D]PYRIMIDINE COMPOUND

To provide a method for treating cancer using a pyrazolo[3,4-d]pyrimidine compound or a salt thereof. The present invention provides an antitumor agent comprising a pyrazolo[3,4-d]pyrimidine compound of formula (I) wherein X, Y, Z1, Z2/su

Selective Allosteric Antagonists for the G Protein-Coupled Receptor GPRC6A Based on the 2-Phenylindole Privileged Structure Scaffold

G protein-coupled receptors (GPCRs) represent a biological target class of fundamental importance in drug therapy. The GPRC6A receptor is a newly deorphanized class C GPCR that we recently reported for the first allosteric antagonists based on the 2-arylindole privileged structure scaffold (e.g., 1-3). Herein, we present the first structure-activity relationship study for the 2-arylindole antagonist 3, comprising the design, synthesis, and pharmacological evaluation of a focused library of 3-substituted 2-arylindoles. In a FRET-based inositol monophosphate (IP1) assay we identified compounds 7, 13e, and 34b as antagonists at the GPRC6A receptor in the low micromolar range and show that 7 and 34b display >9-fold selectivity for the GPRC6A receptor over related GPCRs, making 7 and 34b the most potent and selective antagonists for the GPRC6A receptor reported to date.