الفهرس 
Overview of cancer incidence and mortalityOnly 14 pages are availabe for public view
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Abstract
Tumor initiation and maintenance are dependent on metabolic reprogramming of cancer cell where the tumor cells use altered metabolic pattern compared to normal tissues. Isocitrate dehydrogenase (IDH) is a vital metabolic enzyme in the Krebs cycle. The mutant IDH2 acquire a neo-enzymatic activity that reduces α-ketoglutarate (α-KG) by NADPH to the oncometabolite, D-2-hydroxyglutarate (2-HG). Enasidenib is the only FDA approved inhibitor of mutant IDH2 for the treatment of adult patients with relapsed or refractory acute myeloid leukemia. Three series of s-triazine derivatives were designed, taking Tumor initiation and maintenance are dependent on metabolic reprogramming of cancer cell where the tumor cells use altered metabolic pattern compared to normal tissues. Isocitrate dehydrogenase (IDH) is a vital metabolic enzyme in the Krebs cycle. The mutant IDH2 acquire a neo-enzymatic activity that reduces α-ketoglutarate (α-KG) by NADPH to the oncometabolite, D-2-hydroxyglutarate (2-HG). Enasidenib is the only FDA approved inhibitor of mutant IDH2 for the treatment of adult patients with relapsed or refractory acute myeloid leukemia. Three series of s-triazine derivatives were designed, taking enasidenib as a lead compound by applying a new symmetric dual tail approach. Herein, we reported design and synthesis of three series comprising 28 novel s-triazines as inhibitors of mutant IDH2R140Q. Chemical structures of the target inhibitors were confirmed via 1H and 13C NMR, NOESY, elemental analysis and EI-MS. The synthesized compounds were submitted to the US National Cancer Institute ”NCI” for assessment of anticancer activity against a panel of sixty cancer cell lines, where five analogues (6a, 6c, 6d, 7g and 7l) were subjected to five-dose experiment. Structure activity relationships for each series were deduced depending on the mean GI % values.