528533-16-6

Basic information

• Product Name: N-(benzo[d][1,3]dioxol-5-yl)-2-phenylacetamide
• Synonyms: N-(benzo[d][1,3]dioxol-5-yl)-2-phenylacetamide
• CAS NO: 528533-16-6
• Molecular Weight: 255.273
• Mol File: 528533-16-6.mol
• Article Data: 3

Chemical Properties

• CAS DataBase Reference: N-(benzo[d][1,3]dioxol-5-yl)-2-phenylacetamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-(benzo[d][1,3]dioxol-5-yl)-2-phenylacetamide(528533-16-6)
• EPA Substance Registry System: N-(benzo[d][1,3]dioxol-5-yl)-2-phenylacetamide(528533-16-6)

Safety Data

• Hazardous Substances Data: 528533-16-6(Hazardous Substances Data)

Upstream product

• 103-82-2 phenylacetic acid 
• 80824-83-5 methyl N-(1,3-benzodioxol-5-yl)-carbamodithioate 
• 126266-77-1 3,5-methylenedioxy-α-phenylacetophenone 
• 60-29-7 diethyl ether 
• 10026-13-8 phosphorus pentachloride 
• 7478-12-8 3,4-methylenedioxy-deoxybenzoin-(E)-oxime 
• 14268-66-7 benzo[1,3]dioxolo-5-ylamine 
• 103-80-0 phenylacetyl chloride 

Relevant articles and documents

Zinc mediated facile amide formation : Application to alkyl, aryl, heterocycle, carbohydrate and amino acids

Synthesis of alkyl, aryl, heterocyclic, carbohydrate and amino acid amides using activated zinc is described. The recovery and reuse of the zinc makes the procedure more economic.

Tyrphostins. 5. Potent inhibitors of platelet-derived growth factor receptor tyrosine kinase: Structure-activity relationships in quinoxalines, quinolines, and indole tyrphostins

A series of 3-indoleacrylonitrile tyrphostins, 2-chloro-3- phenylquinolines, and 3-arylquinoxalines were prepared and tested for inhibition of platelet-derived growth factor receptor tyrosine kinase (PDGF- RTK) activity. The potency of the inhibitors was found to be quinoxalines > quinolines > indoles. Lipophilic groups (methyl, methoxy) in the 6 and 7 positions and phenyl at the 3 position of quinoxalines and quinolines were essential for potency, in contrast to the hydrophilic catechol group in tyrphostins active against EGFR kinase inhibition at different sites. The inhibitors showed selectivity for PDGF and were not active against EGF receptor and HER-2/c-ErbB-2 receptor.