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1 results from the phase II clinical benchmark ispinesib.
2 her as a single agent or in combination with Ispinesib.
3 to define the mechanism of KSP inhibition by ispinesib.
4 ligand ispinesib to generate the degrader F1-ispinesib.
5  mRNA as a target selectively degraded by F1-Ispinesib.
6                                              Ispinesib, a KIF11-inhibitor, effectively inhibited tumo
7    This series also binds in the presence of Ispinesib, a known anticancer KSP inhibitor in phase I/I
8 c kinesin KIF11, which can be inhibited with ispinesib, a potent molecularly-targeted drug.
9                           Our data show that ispinesib alters the ability of KSP to bind to microtubu
10 sin Eg5 against the potent second-generation ispinesib analogue SB743921 (1), a phase I/II clinical c
11 -metabolizing enzymes and hERG compared with ispinesib and SB-743921, which is important given the li
12 s comparable to the Phase II drug candidates ispinesib and SB-743921.
13 83 and MLN8237), Wee1 kinase (MK-1775), KSP (ispinesib), and tubulin (taxanes, vinca alkaloids), are
14 AT9283, GSK-690693, and gedatolisib, whereas ispinesib, AT7519, and KW-2478 were weaker substrates.
15 us binding implying existence of a novel non-Ispinesib binding pocket within KSP.
16                     Mutations that attenuate Ispinesib binding to KSP in vitro have been identified,
17 ormational changes that occur in response to ispinesib binding.
18 graphy to identify a new structure of an Eg5-ispinesib complex and have combined this with transient
19                                     Thereby, ispinesib distribution is heterogeneous with concentrati
20                 Our results demonstrate that ispinesib-induced structural changes in L5 from Eg5 lead
21 though, achieving durable brain exposures of ispinesib is critical for adequate tumor cell engagement
22                                We discovered ispinesib is efficacious against two embryonal brain tum
23 Our results demonstrate that the delivery of ispinesib is restricted by P-gp and Bcrp efflux at BBB.
24                                              Ispinesib is the first potent, highly specific small-mol
25 itor), AT9283, (Janus kinase 2/3 inhibitor), ispinesib (kinesin spindle protein inhibitor), gedatolis
26 e development and, in the clinical candidate ispinesib, moderate hERG and CYP inhibition.
27 he wild-type KSP motor domain as well as two ispinesib mutants (D130V and A133D) identified to confer
28  consistent with the physiological effect of ispinesib on cells, which is to prevent KSP-driven mitot
29      In human aortic smooth muscle cells, F1-ispinesib phenocopied siRNA-mediated COL15A1 knockdown,
30         One triphenylbutanamine analogue and ispinesib possess very good bioavailability (51% and 45%
31 nstrate direct binding of these compounds to Ispinesib-resistant mutants (D130V, A133D, and A133D + D
32 ormation and corresponding models of the two ispinesib-resistant mutants.
33 e could be a productive strategy for eluding Ispinesib-resistant tumors.
34 crp inhibitor-improves brain accumulation of ispinesib, resulting in remarkably reduced tumor growth
35                                              Ispinesib (SB-715992), a potent and selective inhibitor
36 ng profile was conjugated to the LC3B ligand ispinesib to generate the degrader F1-ispinesib.
37                              A comparison of ispinesib to monastrol, another small-molecule inhibitor
38 nd A133D) identified to confer resistance to ispinesib treatment.
39  ATP-uncompetitive inhibitors, monastrol and ispinesib, we report here the results of thermal denatur
40 mber of small molecule inhibitors, including ispinesib, which is being used in clinical trials in pat