Cyt387 may cause antitumor activity

T chemotherapy Cyt387 The second compares E7389 choice of doctor to chemotherapy in patients previously treated with anthracycline and a taxane. Intense focus on molecular targeted agents with a better amplifier Ndnis biochemical and molecular mediators of mitosis erm glicht Discovery of new drugs that combines these mediators targeted. New means by which these agents interfere with mitosis, the precision Pr, They go with the target cells into mitosis, whereby the potential of some of the difficulties encountered with microtubule-targeted agents and associated widening of the scope of the cancer treatment. Because these drugs are effective microtubules, k They can m Possibly the avoidance of problems with Neurotoxizit t, w While their specificity t Better may cause antitumor activity. They also serve as valuable tools in reinforcing Serve ndnis of cell division, as more players mitotic and r Them are discovered. Inhibitors of Aurora kinases Polo Kinase1 as kinesin spindle protein and E protein Centromeric in clinical development. Aurora Kinase Inhibitors Aurora kinases in humans are a family of 3 members of the serine-threonine kinases: Aurora Malotilate A, Aurora B and C. Aurora A is Haupts chlich centrosomal and localized to the mitotic spindle. It works in early mitosis, when it required centrosome separation and mitotic inhibition of Aurora A assembly.83 then causes highly defective morphology of the spindle, and ultimately terminal t Mitotic and apoptosis. overexpression leads to tumorigenesis and levels of expression in several different tumor types.
84 were Aurora B kinase is found to the centromere and K rpermitte Pin w During the last stages of mitosis recruited and for chromosome required biorientation The station with spindle and cytokinesis embroidered. 85 The inhibition by small molecule inhibitors of the kinase Aurora B, because it is necessary to induce the spindle checkpoint raises the mitotic spindle checkpoint, causing premature mitotic exit without cytokinesis end which resulted in the DNA of cells, 4N cells further characterized by the 88 cycle.86 proceed with the continuous inhibition of Aurora B, cytokinesis occurs in several stages of the cell cycle, to polyploid what die and m may receive apoptosis. Interestingly enough, when combined with other anti-mitotic agents, including normal Aurora A. combined inhibitors, inhibitors of Aurora B have a dominant phenotype.
84 In contrast, much less is known about the function of Aurora C, although recent studies have begun to shed light on its r Vergie s 83 VX 680 VX 680, the first Aurora kinase inhibitor to enter clinical trials. It Aurora A, B and C inhibits in vitro, 3 FMS-related tyrosine kinase BCR and ABL wild-type and T315I mutant.84 In Phase I studies, the dose-limiting toxicity of t Neutropenia.89 Phase II started in patients with refractory rer Leuk mie myelo-treatment with Philadelphia chromosome-positive chronic or acute leukemia mie lymphoblastic