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1 natural product hemiasterlin and is a potent antimitotic agent.
2 ed hydroxyphenstatin, a potent antitumor and antimitotic agent.
3  continued to safely grow in the presence of antimitotic agents.
4 ch is not observed following treatments with antimitotic agents.
5 ermeability relative to many clinically used antimitotic agents.
6 de a molecular marker to predict response to antimitotic agents.
7 ase in caspase-3/7 activation in response to antimitotic agents.
8 s and cancers that are resistant to standard antimitotic agents.
9 n of a series of triazole-based compounds as antimitotic agents.
10 d a great deal of interest as a new class of antimitotic agents.
11 uld affect the sensitivity of tumor cells to antimitotic agents.
12 es with greater efficacy than currently used antimitotic agents.
13 agents that differed in this respect was the antimitotic agents.
14 poptosis in neuroblastoma cells treated with antimitotic agents.
15 r mitotic extension exhibited sensitivity to antimitotic agents.
16 ld enhance traditional and second-generation antimitotic agents.
17 lin binding of the Vinca alkaloids and other antimitotic agents, (2) proximity to stretches of amino
18                   By suppressing APC(Cdc20), antimitotic agents activate the spindle-assembly checkpo
19 fanilamide (GB-II-5), is a potent, selective antimitotic agent against kinetoplastid parasites.
20 ponents of the tubulysin family of picomolar antimitotic agents and previously led to a tubulysin tet
21  agent in those tumors resistant to existing antimitotic agents and those dependent on Hedgehog pathw
22 yins A and B and eleutherobin (coral-derived antimitotic agents) and of compound 1, an analogue of sa
23                              Taxol and other antimitotic agents are frontline chemotherapy agents but
24 (TP53, best known as p53) in the presence of antimitotic agents, as determined by cytofluorometric an
25 and phomopsin A have been found to be potent antimitotic agents, causing cell death at picomolar or l
26   Topical treatments of grafted HSE with the antimitotic agent colchicine select for keratinocyte pro
27 nd-specific reversibility characteristics of antimitotic agents contribute to interactions between ce
28 hesis of the potent microtubule-stabilizing, antimitotic agent (+)-discodermolide is described.
29                       The interaction of the antimitotic agent estramustine with bovine microtubule p
30    Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing ac
31    Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing ac
32 B-II-5, compound 3), a new antikinetoplastid antimitotic agent, have been synthesized and evaluated.
33 TI-286, a synthetic analogue of the peptidic antimitotic agent hemiasterlin, to tubulin is proposed.
34 ifiable, compound-specific characteristic of antimitotic agents in general.
35 inhibition was specifically synergistic with antimitotic agents in killing cancer cells that had unde
36                   Alternatively, exposure to antimitotic agents just after neural tube closure could
37  remarkably also reverse tumor resistance to antimitotic agents mediated via the P-glycoprotein efflu
38 ocking proliferation of these cells with the antimitotic agent mitomycin C.
39 AP1 monoclonal antibody linked to the potent antimitotic agent monomethyl auristatin E.
40 D30 monoclonal antibody cAC10, linked to the antimitotic agents monomethyl auristatin E (MMAE) or F (
41 neration synthesis of the exceedingly potent antimitotic agent N(14)-desacetoxytubulysin H (1) as wel
42 riety of stimuli, including the DNA-cleaving antimitotic agent, neocarzinostatin (NCS).
43 one and in combination with DNA-damaging and antimitotic agents on human cancer cells.
44 was also inhibited by bullatacin and various antimitotic agents (podophyllotoxin, vinblastine, and co
45                Combinations of EM with other antimitotic agents such as docetaxel are synergistic in
46 dentify putative biomarkers of resistance to antimitotic agents such as paclitaxel and monomethyl-aur
47 ally distinct from those of well-established antimitotic agents such as taxol.
48         Chemotherapy of prostate cancer with antimitotic agents such as vinblastine and doxorubicin i
49   The induction of genetic variability using antimitotic agents, such as colchicine, has been widely
50 ctiveness of this drug exceeds that of other antimitotic agents, suggesting it may have an additional
51 nblastine, or dolastatin 10 (another peptide antimitotic agent that depolymerizes microtubules) but w
52                            Vinblastine is an antimitotic agent that has been used extensively in canc
53 Compounds of this series are promising novel antimitotic agents that have the potential for treating
54                                              Antimitotic agents that interfere with microtubule forma
55   Paclitaxel (Taxol) and the epothilones are antimitotic agents that promote the assembly of mammalia
56  potency against GC3/c1, LYC5 cells, and the antimitotic agent vincristine.
57 model, suggesting that 3b is a promising new antimitotic agent with clinical potential.
58 model, suggesting that 4l is a promising new antimitotic agent with clinical potential.
59 lb/c mice, suggesting that 3c could be a new antimitotic agent with clinical potential.
60           Here, we identify DL78 as a potent antimitotic agent with selective anticancer activity thr
61  sulfonamides are a novel promising class of antimitotic agents with clinical development potential.