65180-12-3

Usage

InChI:InChI=1/C8H5ClN2O/c9-5-2-1-3-6-8(5)11-7(12)4-10-6/h1-4H,(H,11,12)

Upstream product

• 769-11-9 2-chloro-6-nitroaniline 
• 563-96-2 2,2-dihydroxyacetic acid 
• 347162-14-5 N-(3-chloro-2-nitrophenyl)glycine 
• 59483-54-4 3-chloro-2-nitro-aniline 

Downstream Products

• 347162-29-2 2-[4-(8-chloro-quinoxalin-2-yloxy)-phenoxy]-propionic acid methyl ester 
• 120258-69-7 2,8-dichloroquinoxaline 

Relevant academic research and scientific papers

Regioselective one-step process for synthesizing 2-hydroxyquinoxaline

A regioselective one-step process for the synthesis of 2-hydroxyquinoxaline of Formula (1) or tautomers thereof: comprising reacting 1,2-phenylenediamine of Formula (2): with an excess amount of glyoxylic acid, glyoxylic acid monohydrate, or a 2,2-dialkoxyacetic acid of Formula (3): at a low temperature; wherein R1 and R2 are as defined in the specification.

Design, synthesis, and biological evaluation of analogues of the antitumor agent, 2-{4-[(7-chloro-2-quinoxalinyl)oxy]phenoxy}propionic acid (XK469)

2-{4-[(7-Chloro-2-quinoxalinyl)oxy]phenoxy}propionic acid (XK469) is among the most highly and broadly active antitumor agents to have been evaluated in our laboratories and is currently scheduled to enter clinical trials in 2001. The mechanism or mechanisms of action of XK469 remain to be elaborated. Accordingly, an effort was initiated to establish a pharmacophore hypothesis to delineate the requirements of the active site, via a comprehensive program of synthesis of analogues of XK469 and evaluation of the effects of structural modification(s) on solid tumor activity. The strategy formulated chose to dissect the two-dimensional parent structure into three regions - I, ring A of quinoxaline; II, the hydroquinone connector linkage; and III, the lactic acid moiety - to determine the resultant in vitro and in vivo effects of chemical alterations in each region. Neither the A-ring unsubstituted nor the B-ring 3-chloro-regioisomer of XK469 showed antitumor activity. The modulating antitumor effect(s) of substituents of differing electronegativities, located at the several sites comprising the A-ring of region I, were next ascertained. Thus, a halogen substituent, located at the 7-position of a 2-{4-[(2-quinoxalinyl)oxy]phenoxy}propionic acid, generated the most highly and broadly active antitumor agents. A methyl, methoxy, or an azido substituent at this site generated a much less active structure, whereas 5-, 6-, 8-chloro-, 6-, 7-nitro, and 7-amino derivatives all proved to be essentially inactive. When the connector linkage (region II) of 1 was changed from that of a hydroquinone to either a resorcinol or a catechol derivative, all antitumor activity was lost. Of the carboxylic acid derivatives of XK469 (region III), i.e., CONH2, CONHCH3, CON(CH3)2, CONHOH, CONHNH2, CN, or CN4H (tetrazole), only the monomethyl- and N,N-dimethylamides proved to be active.

O-Alkyl-O-[8-chloro-quinoxal-2-yl]-thionoalkanephosphonic acid esters

O-Alkyl-O-[8-chloro-quinoxal-2-yl]-thionoalkanephosphonic acid esters of the formula STR1 in which R and R1 each independently is alkyl with 1 to 6 carbon atoms, which possess arthropodicidal, especially insecticidal and acaricidal, properties.