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1  cells in response to treatment with STI571 (Gleevec).
2 he target of the breakthrough drug imatinib (Gleevec).
3 ng the well-establish cancer drug, imatinib (Gleevec).
4 g a therapeutic intervention using imatinib (Gleevec).
5  inhibitor imatinib (also known as STI571 or Gleevec).
6  the targeted therapeutic imatinib mesylate (Gleevec).
7 y to be inhibited by the inhibitor imatinib (Gleevec).
8 ng antibody to PDGF or by imatinib mesylate (Gleevec).
9 g with the tyrosine kinase inhibitor STI571 (Gleevec).
10  kinase inhibitor imatinib mesylate (STI571, Gleevec).
11 ne or in cooperation with imatinib mesylate (Gleevec).
12  binding affinity that is similar to that of Gleevec.
13 er than the corresponding pyridine moiety in Gleevec.
14 uccess of the first small-molecule inhibitor Gleevec.
15 were incubated with the Abl kinase inhibitor Gleevec.
16 hibited in Int3 transgenic mammary tumors by Gleevec.
17 or selectivity of the successful cancer drug Gleevec.
18 cer therapeutic agents such as Herceptin and Gleevec.
19                                    Imatinib (Gleevec), a non-receptor tyrosine kinase inhibitor (nRTK
20                                      STI571 (Gleevec), a novel anti-leukemia drug targeting BCR/ABL k
21                           Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and pl
22 Imatinib mesylate (also known as STI-571 and Gleevec), a tyrosine kinase inhibitor, has shown encoura
23 that disrupting c-Abl activity using STI571 (Gleevec, a c-Abl inhibitor) or stable c-Abl knockdown ab
24                                      STI571 (Gleevec, a c-Abl tyrosine kinase inhibitor) and stable c
25 del of chronic myeloid leukemia treated with Gleevec, a specific inhibitor of aberrant Bcr-Abl protei
26                                              Gleevec, a well-known cancer therapeutic agent, is an ef
27                                              Gleevec, a well-known therapeutic agent against chronic
28 l molecule tyrosine kinase inhibitor STI571 (Gleevec) abrogates cell growth.
29                                              Gleevec affinity is gained during the evolutionary traje
30  we studied the action of imatinib (STI-571, Gleevec) against murine cells and leukemias expressing B
31 echanisms for the anti-cancer drug Imatinib (Gleevec) against wild-type and the N368S mutant of Abl k
32                          Here we report that Gleevec also achieves its Abeta-lowering effects through
33 nd is blocked by imatinib mesylate (STI-571; Gleevec), an Abl family kinase inhibitor used to treat c
34 tyrosine kinases, and is blocked by STI-571 (Gleevec), an Abl-family kinase inhibitor used to treat c
35 the automated modular synthesis of Imatinib (Gleevec), an archetypical clinically approved kinase inh
36 it has been reported that imatinib mesylate (Gleevec), an inhibitor of Bcr-Abl kinase useful in the t
37 d successfully in the development of STI571 (gleevec), an inhibitor of bcr-abl tyrosine kinase that h
38  SCF-neutralizing antibodies or by imatinib (Gleevec), an inhibitor of c-kit.
39 administration of STI571 (imatinib mesylate, Gleevec), an inhibitor of phosphorylation of the platele
40  abnormalities was reduced by treatment with Gleevec, an inhibitor of PDGF signaling.
41 ibitors, imatinib (also known as STI-571 and Gleevec) and PD173955 (Parke-Davis).
42 targets of marketed oncology drugs Imatinib (Gleevec) and Sorafenib (Nexavar), respectively, and BIRB
43   Finally, the Syk-bound cis-conformation of Gleevec bears a striking resemblance to the rigid struct
44  observed differential binding affinities of Gleevec between the two Src-family kinases.
45 nding suggests the existence of two distinct Gleevec binding modes: an extended, trans-conformation c
46                                              Gleevec binds Syk in a novel, compact cis-conformation t
47 ighly selective Abl inhibitors, PD173955 and Gleevec, blocks HK-induced phosphorylation of IkappaB-be
48 milar nonbinding interactions with the bound-Gleevec, but the former pays less entropic penalty for t
49          Cotreatment with SAHA and imatinib (Gleevec) caused more down-regulation of the levels and a
50 molecule kinase inhibitor imatinib mesylate (Gleevec), complete remissions are rare and the majority
51 f its kinase activity with a small molecule (Gleevec) completely inhibited HCMV viral internalization
52 f c-Kit in complex with STI-571 (Imatinib or Gleevec) demonstrates that inhibitor binding disrupts th
53          Consistent with these observations, Gleevec did not modify the radiosensitivity of the norma
54                     These data indicate that Gleevec enhances radiation-induced tumor cell killing an
55                                     However, Gleevec fails to inhibit closely homologous tyrosine kin
56 yrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caught the attention of
57                           Imatinib mesylate (Gleevec, formerly STI571) is an effective therapy for al
58                                  Relative to Gleevec, G6G forms highly favorable van der Waals disper
59 sses a chemical core very similar to that of Gleevec, G6G is a potent inhibitor of both Abl and c-Src
60 l screening that the blockbuster cancer drug Gleevec has the same binding affinity, yet different dis
61                       Imatinib mesylate (IM, Gleevec) has largely supplanted allogeneic hematopoietic
62 successfully treated with imatinib mesylate (Gleevec); however, complete remissions are rare and pati
63 platelet-derived growth factor receptor with Gleevec (imatinib mesylate) reduced overall contractile
64 uous selection pressure of up to 1.0 micro M Gleevec (imatinib mesylate, STI-571), we have isolated G
65 between the Bcr/Abl kinase inhibitor STI571 (Gleevec, imatinib mesylate) and histone deacetylase inhi
66 ermined the interaction of 2ME2 with STI571 (Gleevec, imatinib mesylate) in STI571 drug-sensitive and
67 bition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and
68  signaling and induced apoptosis of STI-571 (Gleevec, Imatinib)-resistant Bcr-Abl-positive cells.
69 the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic acti
70 by the signal transduction inhibitor STI-571/Gleevec/imatinib (STI-571).
71 actions responsible for the stabilization of Gleevec in the binding pocket of Abl.
72 the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs throug
73 three-step synthesis of imatinib, the API of Gleevec, in good yield without the need of solvent switc
74 stant cell types were >/=5-fold resistant to Gleevec-induced apoptosis.
75                                 In addition, Gleevec induces formation of a specific set of APP C-ter
76 RNAi) and blockage of PDGFRbeta signaling by Gleevec inhibited the growth and lung metastasis of SN12
77                                              Gleevec is a potent inhibitor of Abl tyrosine kinase but
78                                              Gleevec is a relatively specific inhibitor of c-Abl, a t
79                                              Gleevec is a tyrosine kinase inhibitor that targets c-Ki
80                           Imatinib mesylate (Gleevec) is a small-molecule inhibitor of the fusion pro
81                           Imatinib mesylate (Gleevec) is effective therapy against Philadelphia chrom
82 e Abl kinase inhibitor, STI-571 (marketed as Gleevec), is toxic to CML cells in culture, causes regre
83  the Kit tyrosine kinase inhibitor imatinib (Gleevec) leads to deficits in pro T and pro B cell devel
84 evious study showed that the anticancer drug Gleevec lowers Abeta levels through indirect inhibition
85 ssion or mutations in Bcr-Abl, resistance to Gleevec may also develop due to a loss of Bcr-Abl expres
86 antileukemia drug STI571 [imatinib mesylate (Gleevec); Novartis], which potently and selectively bloc
87    However, the advent of imatinib mesylate (Gleevec, Novartis Pharmaceuticals, Basel, Switzerland),
88 tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis) ultimately led to the discovery of th
89          Although imatinib mesylate (STI571, Gleevec, Novartis, Basal, Switzerland) produces high rat
90 argeted therapy, such as the use of STI-571 (Gleevec; Novartis Pharmaceuticals, East Hanover, NJ) for
91 as therapeutic targets of imatinib mesylate (Gleevec; Novartis, Basel, Switzerland).
92 Our data demonstrate an inhibitory effect of Gleevec on Int3-induced transformation of HC11 cells and
93 f this study was to determine the effects of Gleevec on Rad51 levels and the radiosensitivity of two
94            Thrombin-injected mice were given Gleevec or PDGF-AA neutralizing antibody.
95                          A PDGFR antagonist (Gleevec) or agonist (PDGF-AA) was administered following
96  the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site
97                                        These Gleevec phenotypes require an intracellular acidic pH an
98 c and new onset diabetic mice with imatinib (Gleevec) prevented and reversed T1D.
99 d Y823D were inhibited by imatinib mesylate (Gleevec, previously STI571) whereas D816V and D816H were
100  the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL
101 reactivity and functional-group tolerance, a Gleevec(R) analogue, using a monofluorostilbene as an am
102       When glioma cells were pretreated with Gleevec, radiation-induced Rad51 expression and nuclear
103 s responsible for the binding specificity of Gleevec remain poorly understood.
104 ble Hsp90beta expression conferred imatinib (Gleevec) resistance.
105  compared with their sensitive counterparts, Gleevec-resistant cell types were >/=5-fold resistant to
106                                          All Gleevec-resistant cell types were sensitive to 17-allyla
107 matinib mesylate, STI-571), we have isolated Gleevec-resistant K562 R (+Bcr-Abl), K562 R (-Bcr-Abl),
108 ingly, pretreatment of the glioma cells with Gleevec resulted in an enhancement in their radiosensiti
109  energy to elucidate the factors controlling Gleevec's binding specificity.
110 kinase inhibitors (BIRB796, Tarceva, NU6102, Gleevec, SB203580, balanol, H89, PP1).
111 ther, this effect is directly dependent on a Gleevec sensitive molecular pathway.
112 observed with unphosphorylated Abl, the more Gleevec-sensitive form of Abl.
113 receiving a PDGF-AA-neutralizing antibody or Gleevec showed minimized thrombin injection-induced BBB
114           This work reveals the mechanism of Gleevec specificity while offering insights into how ene
115                     We also demonstrate that Gleevec (STI-571, Imatinib) inhibits the isolated kinase
116                           Imatinib mesylate (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase
117  These reports describe the potential use of Gleevec (STI571) for dermatofibrosarcoma protuberans and
118                                              Gleevec (STI571) inhibits the Abl kinase and has shown g
119                  The ABL inhibitor Imatinib (Gleevec, STI571) has remarkable efficacy for treating ch
120                           Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr
121                           Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectivel
122                           Imatinib mesylate (Gleevec, STI571), a selective inhibitor of a restricted
123 54825 and another PDGFR inhibitor, imatinib (Gleevec, STI571), in VSMCs indicated that BMS-354825 is
124                           Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of A
125 tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown
126 tyrosine kinase inhibitor imatinib mesylate (Gleevec) targeting the ABL protein tyrosine kinase has r
127 who had progressive leukemia while receiving Gleevec therapy.
128  to imatinib mesylate [also known as STI571 (Gleevec)] therapy.
129  BCR-ABL kinase inhibitor imatinib mesylate (Gleevec), thus showing how a molecular therapeutic targe
130  was used to compute the binding affinity of Gleevec to Abl, c-Kit, Lck, and c-Src.
131 ted the difference in binding specificity of Gleevec to subtle variations in ligand-protein interacti
132 butions affecting the binding specificity of Gleevec to the kinases.
133 resulted in an increase in Rad51 expression; Gleevec treatment alone reduced Rad51 expression.
134 fore, inhibition of Abl by STI571 [imatinib (Gleevec)] treatment or down-regulation of Abl expression
135 trast to the glioma cell lines, radiation or Gleevec treatments had no effect on Rad51 expression or
136 ms treated with the c-Abl inhibitor STI-571 (Gleevec; used in human cancer therapy), two newly synthe
137 mice were treated with continuous release of Gleevec using subcutaneously implanted Alzet pumps.
138 s the most favorable binding environment for Gleevec via optimal protein-ligand interactions and a sm
139 e kinase inhibitor targeting PDGFR activity (Gleevec) was also able to regress late-stage tumors.
140                                   ShRNAi and Gleevec were used to block PDGF-D expression and PDGF re
141 mpetitive small-molecule antagonist STI-571 (Gleevec) were assessed by monitoring the nanowire conduc
142 itors, or use of the c-Abl kinase inhibitor, Gleevec, which blocked cyclin D and cyclin-dependent kin
143                             Correspondingly, Gleevec, which blocks PDGF receptor signaling, and PDGF-
144 eveloped tyrosine kinase inhibitors, such as Gleevec, which inhibit PDGF activity through inhibition
145 and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity.

 
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