ライフサイエンスコーパス: Gleevec

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 were incubated with the Abl kinase inhibitor Gleevec.

15 hibited in Int3 transgenic mammary tumors by Gleevec.

16 or selectivity of the successful cancer drug Gleevec.

17 cer therapeutic agents such as Herceptin and Gleevec.

18 Imatinib (Gleevec), a non-receptor tyrosine kinase inhibitor (nRTK

19 STI571 (Gleevec), a novel anti-leukemia drug targeting BCR/ABL k

20 Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and pl

21 Imatinib mesylate (also known as STI-571 and Gleevec), a tyrosine kinase inhibitor, has shown encoura

22 that disrupting c-Abl activity using STI571 (Gleevec, a c-Abl inhibitor) or stable c-Abl knockdown ab

23 STI571 (Gleevec, a c-Abl tyrosine kinase inhibitor) and stable c

24 del of chronic myeloid leukemia treated with Gleevec, a specific inhibitor of aberrant Bcr-Abl protei

25 Gleevec, a well-known cancer therapeutic agent, is an ef

26 Gleevec, a well-known therapeutic agent against chronic

27 l molecule tyrosine kinase inhibitor STI571 (Gleevec) abrogates cell growth.

28 Gleevec affinity is gained during the evolutionary traje

29 we studied the action of imatinib (STI-571, Gleevec) against murine cells and leukemias expressing B

30 Here we report that Gleevec also achieves its Abeta-lowering effects through

31 nd is blocked by imatinib mesylate (STI-571; Gleevec), an Abl family kinase inhibitor used to treat c

32 tyrosine kinases, and is blocked by STI-571 (Gleevec), an Abl-family kinase inhibitor used to treat c

33 it has been reported that imatinib mesylate (Gleevec), an inhibitor of Bcr-Abl kinase useful in the t

34 d successfully in the development of STI571 (gleevec), an inhibitor of bcr-abl tyrosine kinase that h

35 SCF-neutralizing antibodies or by imatinib (Gleevec), an inhibitor of c-kit.

36 administration of STI571 (imatinib mesylate, Gleevec), an inhibitor of phosphorylation of the platele

37 abnormalities was reduced by treatment with Gleevec, an inhibitor of PDGF signaling.

38 ibitors, imatinib (also known as STI-571 and Gleevec) and PD173955 (Parke-Davis).

39 targets of marketed oncology drugs Imatinib (Gleevec) and Sorafenib (Nexavar), respectively, and BIRB

40 Finally, the Syk-bound cis-conformation of Gleevec bears a striking resemblance to the rigid struct

41 observed differential binding affinities of Gleevec between the two Src-family kinases.

42 nding suggests the existence of two distinct Gleevec binding modes: an extended, trans-conformation c

43 Gleevec binds Syk in a novel, compact cis-conformation t

44 ighly selective Abl inhibitors, PD173955 and Gleevec, blocks HK-induced phosphorylation of IkappaB-be

45 milar nonbinding interactions with the bound-Gleevec, but the former pays less entropic penalty for t

46 Cotreatment with SAHA and imatinib (Gleevec) caused more down-regulation of the levels and a

47 molecule kinase inhibitor imatinib mesylate (Gleevec), complete remissions are rare and the majority

48 f its kinase activity with a small molecule (Gleevec) completely inhibited HCMV viral internalization

49 f c-Kit in complex with STI-571 (Imatinib or Gleevec) demonstrates that inhibitor binding disrupts th

50 Consistent with these observations, Gleevec did not modify the radiosensitivity of the norma

51 These data indicate that Gleevec enhances radiation-induced tumor cell killing an

52 However, Gleevec fails to inhibit closely homologous tyrosine kin

53 yrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caught the attention of

54 Imatinib mesylate (Gleevec, formerly STI571) is an effective therapy for al

55 Relative to Gleevec, G6G forms highly favorable van der Waals disper

56 sses a chemical core very similar to that of Gleevec, G6G is a potent inhibitor of both Abl and c-Src

57 Imatinib mesylate (IM, Gleevec) has largely supplanted allogeneic hematopoietic

58 successfully treated with imatinib mesylate (Gleevec); however, complete remissions are rare and pati

59 platelet-derived growth factor receptor with Gleevec (imatinib mesylate) reduced overall contractile

60 uous selection pressure of up to 1.0 micro M Gleevec (imatinib mesylate, STI-571), we have isolated G

61 between the Bcr/Abl kinase inhibitor STI571 (Gleevec, imatinib mesylate) and histone deacetylase inhi

62 ermined the interaction of 2ME2 with STI571 (Gleevec, imatinib mesylate) in STI571 drug-sensitive and

63 bition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and

64 signaling and induced apoptosis of STI-571 (Gleevec, Imatinib)-resistant Bcr-Abl-positive cells.

65 the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic acti

66 by the signal transduction inhibitor STI-571/Gleevec/imatinib (STI-571).

67 actions responsible for the stabilization of Gleevec in the binding pocket of Abl.

68 the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs throug

69 three-step synthesis of imatinib, the API of Gleevec, in good yield without the need of solvent switc

70 stant cell types were >/=5-fold resistant to Gleevec-induced apoptosis.

71 In addition, Gleevec induces formation of a specific set of APP C-ter

72 RNAi) and blockage of PDGFRbeta signaling by Gleevec inhibited the growth and lung metastasis of SN12

73 Gleevec is a potent inhibitor of Abl tyrosine kinase but

74 Gleevec is a relatively specific inhibitor of c-Abl, a t

75 Gleevec is a tyrosine kinase inhibitor that targets c-Ki

76 Imatinib mesylate (Gleevec) is a small-molecule inhibitor of the fusion pro

77 Imatinib mesylate (Gleevec) is effective therapy against Philadelphia chrom

78 e Abl kinase inhibitor, STI-571 (marketed as Gleevec), is toxic to CML cells in culture, causes regre

79 the Kit tyrosine kinase inhibitor imatinib (Gleevec) leads to deficits in pro T and pro B cell devel

80 evious study showed that the anticancer drug Gleevec lowers Abeta levels through indirect inhibition

81 ssion or mutations in Bcr-Abl, resistance to Gleevec may also develop due to a loss of Bcr-Abl expres

82 antileukemia drug STI571 [imatinib mesylate (Gleevec); Novartis], which potently and selectively bloc

83 However, the advent of imatinib mesylate (Gleevec, Novartis Pharmaceuticals, Basel, Switzerland),

84 tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis) ultimately led to the discovery of th

85 Although imatinib mesylate (STI571, Gleevec, Novartis, Basal, Switzerland) produces high rat

86 argeted therapy, such as the use of STI-571 (Gleevec; Novartis Pharmaceuticals, East Hanover, NJ) for

87 as therapeutic targets of imatinib mesylate (Gleevec; Novartis, Basel, Switzerland).

88 Our data demonstrate an inhibitory effect of Gleevec on Int3-induced transformation of HC11 cells and

89 f this study was to determine the effects of Gleevec on Rad51 levels and the radiosensitivity of two

90 Thrombin-injected mice were given Gleevec or PDGF-AA neutralizing antibody.

91 A PDGFR antagonist (Gleevec) or agonist (PDGF-AA) was administered following

92 the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site

93 These Gleevec phenotypes require an intracellular acidic pH an

94 c and new onset diabetic mice with imatinib (Gleevec) prevented and reversed T1D.

95 d Y823D were inhibited by imatinib mesylate (Gleevec, previously STI571) whereas D816V and D816H were

96 the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL

97 reactivity and functional-group tolerance, a Gleevec(R) analogue, using a monofluorostilbene as an am

98 When glioma cells were pretreated with Gleevec, radiation-induced Rad51 expression and nuclear

99 s responsible for the binding specificity of Gleevec remain poorly understood.

100 ble Hsp90beta expression conferred imatinib (Gleevec) resistance.

101 compared with their sensitive counterparts, Gleevec-resistant cell types were >/=5-fold resistant to

102 All Gleevec-resistant cell types were sensitive to 17-allyla

103 matinib mesylate, STI-571), we have isolated Gleevec-resistant K562 R (+Bcr-Abl), K562 R (-Bcr-Abl),

104 ingly, pretreatment of the glioma cells with Gleevec resulted in an enhancement in their radiosensiti

105 energy to elucidate the factors controlling Gleevec's binding specificity.

106 kinase inhibitors (BIRB796, Tarceva, NU6102, Gleevec, SB203580, balanol, H89, PP1).

107 ther, this effect is directly dependent on a Gleevec sensitive molecular pathway.

108 observed with unphosphorylated Abl, the more Gleevec-sensitive form of Abl.

109 receiving a PDGF-AA-neutralizing antibody or Gleevec showed minimized thrombin injection-induced BBB

110 This work reveals the mechanism of Gleevec specificity while offering insights into how ene

111 We also demonstrate that Gleevec (STI-571, Imatinib) inhibits the isolated kinase

112 Imatinib mesylate (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase

113 These reports describe the potential use of Gleevec (STI571) for dermatofibrosarcoma protuberans and

114 Gleevec (STI571) inhibits the Abl kinase and has shown g

115 The ABL inhibitor Imatinib (Gleevec, STI571) has remarkable efficacy for treating ch

116 Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr

117 Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectivel

118 Imatinib mesylate (Gleevec, STI571), a selective inhibitor of a restricted

119 54825 and another PDGFR inhibitor, imatinib (Gleevec, STI571), in VSMCs indicated that BMS-354825 is

120 Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of A

121 tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown

122 tyrosine kinase inhibitor imatinib mesylate (Gleevec) targeting the ABL protein tyrosine kinase has r

123 who had progressive leukemia while receiving Gleevec therapy.

124 to imatinib mesylate [also known as STI571 (Gleevec)] therapy.

125 BCR-ABL kinase inhibitor imatinib mesylate (Gleevec), thus showing how a molecular therapeutic targe

126 was used to compute the binding affinity of Gleevec to Abl, c-Kit, Lck, and c-Src.

127 ted the difference in binding specificity of Gleevec to subtle variations in ligand-protein interacti

128 butions affecting the binding specificity of Gleevec to the kinases.

129 resulted in an increase in Rad51 expression; Gleevec treatment alone reduced Rad51 expression.

130 fore, inhibition of Abl by STI571 [imatinib (Gleevec)] treatment or down-regulation of Abl expression

131 trast to the glioma cell lines, radiation or Gleevec treatments had no effect on Rad51 expression or

132 ms treated with the c-Abl inhibitor STI-571 (Gleevec; used in human cancer therapy), two newly synthe

133 mice were treated with continuous release of Gleevec using subcutaneously implanted Alzet pumps.

134 s the most favorable binding environment for Gleevec via optimal protein-ligand interactions and a sm

135 e kinase inhibitor targeting PDGFR activity (Gleevec) was also able to regress late-stage tumors.

136 ShRNAi and Gleevec were used to block PDGF-D expression and PDGF re

137 mpetitive small-molecule antagonist STI-571 (Gleevec) were assessed by monitoring the nanowire conduc

138 itors, or use of the c-Abl kinase inhibitor, Gleevec, which blocked cyclin D and cyclin-dependent kin

139 Correspondingly, Gleevec, which blocks PDGF receptor signaling, and PDGF-

140 eveloped tyrosine kinase inhibitors, such as Gleevec, which inhibit PDGF activity through inhibition

141 and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity.