Disease relevance of ICN 4793

• The mechanism of toxicity of 3-deazaguanosine was studied in a number of human tumor cell lines by determination of the effects of various purine compounds on the growth of the cells in the presence of the drug and by studies of the effects of 3-deazaguanosine on the metabolism of radiolabeled precursors in these cells [1].

High impact information on ICN 4793

• When various inhibitors of IMP dehydrogenase (mycophenolic acid, 3-deazaguanosine, and 2-beta-D-ribofuranosylthiazole-4-carboxamide) were evaluated for their effects upon HL-60 cells, each agent was found to induce the cells to mature morphologically and functionally [2].
• The growth inhibitory activity of 3-deazaguanosine toward a mutant line (TGR-3) of Chinese hamster ovary cells deficient in hypoxanthine-guanine phosphoribosyltransferase (EC 2.4.2.8) was substantially reversed by the simultaneous addition of nicotinamide riboside [3].
• Phosphorylation of 3-deazaguanosine by nicotinamide riboside kinase in Chinese hamster ovary cells [3].
• Actions of 3-deazaguanine and 3-deazaguanosine on variant lines of Chinese hamster ovary cells [4].
• Nicotinamide ribonucleoside kinase (NRK) phosphorylates at least two nucleoside analogs of potential clinical interest, tiazofurin and 3-deazaguanosine [5].

Associations of ICN 4793 with other chemical compounds

• Metabolic studies indicated decreased synthesis of DNA, variable inhibition of de novo purine synthesis, and complete inhibition of the enzyme guanosine monophosphate reductase by 3-deazaguanosine [1].

Analytical, diagnostic and therapeutic context of ICN 4793

• A 3-deazaguanosine phosphorylating activity was separated from other cellular kinases by DEAE-cellulose chromatography [3].
• 3-Deazaguanosine 5'-triphosphate, prepared enzymically from authentic 3-deazaguanosine 5'-monophosphate, co-eluted with the major metabolite peak during HPLC analysis [6].

References