58658-15-4Relevant academic research and scientific papers
NOVEL HDMX INHIBITORS AND THEIR USE FOR CANCER TREATMENT
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Paragraph 0033; 0035; 0036, (2015/11/30)
The present invention provides for novel acridine-like class of compounds that have demonstrated efficiency in treating cancer. The compounds of the present invention have demonstrated efficacy in binding to and antagonizing the activity of the p53 repres
Synthesis and?SAR study of?acridine, 2-methylquinoline and?2-phenylquinazoline analogues as?anti-prion agents
Cope,Mutter,Heal,Pascoe,Brown,Pratt,Chen
, p. 1124 - 1143 (2007/10/03)
Transmissible spongiform encephalopathies (TSEs) are thought to arise from aggregation of a protease resistant protein denoted PrPSc, which is a misfolded isoform of the normal cellular prion protein PrPC. Using virtual high-throughp
Antitumor polycyclic acridines. 7. Synthesis and biological properties of DNA affinic tetra- and pentacyclic acridines
Stanslas, Johnson,Hagan, Damien J.,Ellis, Michael J.,Turner, Claire,Carmichael, James,Ward, Wynne,Hammonds, Timothy R.,Stevens, Malcolm F. G.
, p. 1563 - 1572 (2007/10/03)
New synthetic routes to a series of tetra- and pentacyclic acridines related in structure to marine natural products are reported. The novel water-soluble agent dihydroindolizino[7,6,5-kl]acridinium chloride 14 has inhibitory activity in a panel of non-small-cell lung and breast tumor cell lines exceeding that of m-AMSA. The salt inhibited the release of minicircle products of kDNA confirming that disorganization of topoisomerase II partly underlies the activity of the compound. COMPARE analysis of the NCI mean graph profile of compound 14 at the GI50 level corroborates this conclusion with Pearson correlation coefficients (> 0.6) to clinical agents of the topoisomerase II class: however, this correlation was not seen at the LC50 level. The inhibitory action of 14 on Saccharomyces cerevisiae transfected with human topoisomerase II isoforms showed a 3-fold selectivity against the IIα isoform over the IIβ isoform. Unlike m-AMSA, 14 is not susceptible to P-glycoprotein-mediated drug efflux and retains activity in lung cells with derived resistance to the topoisomerase II inhibitor etoposide.
