ライフサイエンスコーパス: farnesyltransferase inhibitor

1 were as pronounced as those resulting from a farnesyltransferase inhibitor.

2 , and fail to accumulate when treated with a farnesyltransferase inhibitor.

3 nsformation, and sensitizes tumor cells to a farnesyltransferase inhibitor.

4 aggerated by cotreatment of the cells with a farnesyltransferase inhibitor.

5 nse to growth factors, genotoxic stress, and farnesyltransferase inhibitors.

6 ed as a target for the antitumor activity of farnesyltransferase inhibitors.

7 r growth and that RhoB-F is not a target for farnesyltransferase inhibitors.

8 were abolished by CYP450, lipoxygenase, and farnesyltransferase inhibitors.

9 ibitor LY294002, the Rheb inhibitor FTI-277 (farnesyltransferase inhibitor-277), and the mTOR inhibit

10 a potential target for novel approaches (eg, farnesyltransferase inhibitors) aimed at regulating pulm

11 nyltransferase I inhibitor, GGTI-298, or the farnesyltransferase inhibitor, alpha-hydroxyfarnesylphos

12 17F, and inhibition of Ras by manumycin A, a farnesyltransferase inhibitor, ameliorated erythroid col

13 m axons; BLBP expression was not affected by farnesyltransferase inhibitor, an inhibitor of H-Ras.

14 e proapoptotic and antineoplastic effects of farnesyltransferase inhibitors, and we show here that Rh

15 Farnesyltransferase inhibitors are compounds that were d

16 r the transduction of extracellular signals, farnesyltransferase inhibitors are discussed as chemothe

17 a target for pharmaceutical development, and farnesyltransferase inhibitors are in clinical trials as

18 fort has been expended on the development of farnesyltransferase inhibitors as novel anticancer agent

19 of Ras proteins, recent studies suggest that farnesyltransferase inhibitors block the farnesylation o

20 Inhibition of Ras by the farnesyltransferase inhibitor BZA-5B inhibited prostagla

21 EGF stimulation, and this was blocked by the farnesyltransferase inhibitor BZA-5B.

22 These results demonstrate that a farnesyltransferase inhibitor can induce regression of v

23 These results indicate that treatment with farnesyltransferase inhibitors can alter the oxygenation

24 on a farnesylated protein, as treatment with farnesyltransferase inhibitors caused apoptosis.

25 All previously reported CAAX-based farnesyltransferase inhibitors contain a thiol functiona

26 Farnesyltransferase inhibitors could therefore be of use

27 riments with a C-terminal-truncated Ras or a farnesyltransferase inhibitor demonstrate that the CAAX

28 ine the efficacy and safety of tipifarnib, a farnesyltransferase inhibitor, dosed at the respective m

29 nknown, the FTase substrates responsible for farnesyltransferase inhibitor efficacy are not yet under

30 and growth in nude mice are inhibited by the farnesyltransferase inhibitor FTI-276 in H- and N-Ras tr

31 Third, treatment with the farnesyltransferase inhibitor FTI-277 blocked Ras, but n

32 his study, we investigated the effect of the farnesyltransferase inhibitor FTI-277 on TGFbeta-regulat

33 ltransferase inhibitor GGTI-298, but not the farnesyltransferase inhibitor FTI-277, induced apoptosis

34 Ras farnesyltransferase inhibitor (FTI) exhibit antiprolifer

35 Farnesyltransferase inhibitor (FTI) induces apoptosis of

36 We have investigated farnesyltransferase inhibitor (FTI) L-744,832 in an in v

37 Ras-transformed cells in the presence of the farnesyltransferase inhibitor (FTI) LB42722 leads to up-

38 1478; these responses were also abrogated by farnesyltransferase inhibitor (FTI) or PD98059, inhibito

39 R115777 (tipifarnib) is the first farnesyltransferase inhibitor (FTI) that showed clinical

40 We have used a selective and potent farnesyltransferase inhibitor (FTI) to probe a mechanism

41 Farnesyltransferase inhibitor (FTI) treatment with R1157

42 Previously, the protein farnesyltransferase inhibitor (FTI), L-744, 832, has bee

43 Exposure to a farnesyltransferase inhibitor (FTI), PD169541, caused a

44 eed, when RD fibroblasts were treated with a farnesyltransferase inhibitor (FTI), prelamin A was part

45 phenotypes can be ameliorated with a protein farnesyltransferase inhibitor (FTI), suggesting that pro

46 ell line, MDA-MB-468, by combining it with a farnesyltransferase inhibitor (FTI), which has been show

47 clei can be reduced by treating cells with a farnesyltransferase inhibitor (FTI).

48 this study, we hypothesized that the use of farnesyltransferase inhibitor (FTI, L-744,832) may direc

49 alpha-synuclein toxicity by treatment with a farnesyltransferase inhibitor (FTI-277) reduces alpha-sy

50 Farnesyltransferase inhibitors (FTI) are a class of ther

51 Protein farnesyltransferase inhibitors (FTI) mislocalize progeri

52 Farnesyltransferase inhibitors (FTI), such as R115777, h

53 H-Ras activity by intra-NAc infusion of the farnesyltransferase inhibitor, FTI-276, produced a robus

54 The protein farnesyltransferase inhibitor, FTI-277, had no effect on

55 demonstrate that the novel antitumor agents farnesyltransferase inhibitors (FTIs) and geranylgeranyl

56 Farnesyltransferase inhibitors (FTIs) are a novel class

57 Farnesyltransferase inhibitors (FTIs) are a novel class

58 Farnesyltransferase inhibitors (FTIs) are in clinical tr

59 Farnesyltransferase inhibitors (FTIs) are in clinical tr

60 Farnesyltransferase inhibitors (FTIs) are small-molecule

61 Farnesyltransferase inhibitors (FTIs) block Ras farnesyl

62 Farnesyltransferase inhibitors (FTIs) exhibit the remark

63 Treatment with farnesyltransferase inhibitors (FTIs) has been shown to

64 A series of macrocyclic 3-aminopyrrolidinone farnesyltransferase inhibitors (FTIs) has been synthesiz

65 t to mediate the antitransforming effects of farnesyltransferase inhibitors (FTIs) in H-Ras-transform

66 Despite the success of protein farnesyltransferase inhibitors (FTIs) in the treatment o

67 Pre-clinical studies have demonstrated that farnesyltransferase inhibitors (FTIs) induce growth arre

68 Protein farnesyltransferase inhibitors (FTIs) inhibit Ras transf

69 Farnesyltransferase inhibitors (FTIs) interfere with thi

70 The clinical interest in farnesyltransferase inhibitors (FTIs) makes it important

71 investigated in more detail the influence of farnesyltransferase inhibitors (FTIs) on CD20 expression

72 Farnesyltransferase inhibitors (FTIs) possess antitumor

73 Farnesyltransferase inhibitors (FTIs) represent a new cl

74 Farnesyltransferase inhibitors (FTIs) represent a novel

75 fected HeLa, HEK 293, and NIH 3T3 cells with farnesyltransferase inhibitors (FTIs) restored normal nu

76 Previous studies have shown that farnesyltransferase inhibitors (FTIs) reverse this cellu

77 MS-225975 are tetrahydrobenzodiazepine-based farnesyltransferase inhibitors (FTIs) that have nearly i

78 ecent results have shown that the ability of farnesyltransferase inhibitors (FTIs) to inhibit maligna

79 Farnesyltransferase inhibitors (FTIs) usually cause grow

80 took only 5 years from 1993, when the first farnesyltransferase inhibitors (FTIs) were reported, to

81 Even though farnesyltransferase inhibitors (FTIs), a novel class of

82 icated HDAC6 as a new protein target for the farnesyltransferase inhibitors (FTIs), although HDAC6 la

83 New classes of anticancer drugs, such as the farnesyltransferase inhibitors (FTIs), show therapeutic

84 s no method available to predict response to farnesyltransferase inhibitors (FTIs).

85 trials of a number of independently derived farnesyltransferase inhibitors (FTIs).

86 he chemopreventive efficacy of two different farnesyltransferase inhibitors (FTIs): one is a peptidom

87 diphenyleneiodonium (DPI, 10 microm), by the farnesyltransferase inhibitor H-Ampamb-Phe-Met-OH (2 mic

88 Most unexpectedly, other classes of farnesyltransferase inhibitors had no inhibitory effect.

89 Farnesyltransferase inhibitors have ameliorated disease

90 Farnesyltransferase inhibitors have recently shown clini

91 and eIF4E and a direct therapeutic target of farnesyltransferase inhibitors in cancer.

92 inhibitor resistance and clinical trials of farnesyltransferase inhibitors in combination with other

93 Intriguingly, farnesyltransferase inhibitors increase the binding of W

94 Together, these findings suggest that farnesyltransferase inhibitors interrupt the cytoprotect

95 The mechanism of cytotoxicity of farnesyltransferase inhibitors is incompletely understoo

96 action: see text] The total synthesis of the farnesyltransferase inhibitor kurasoin A has been achiev

97 Since we have previously shown that the farnesyltransferase inhibitor l-744, 832 inhibits cell p

98 ave previously shown that the peptidomimetic farnesyltransferase inhibitor L-744,832 (FTI) inhibits p

99 We tested the antineoplastic effect of the farnesyltransferase inhibitor L-744,832 in mammary and l

100 The farnesyltransferase inhibitor L-744,832 selectively bloc

101 grafts in nude mice after treatment with the farnesyltransferase inhibitor L744,832.

102 ns between the Chk1 inhibitor UCN-01 and the farnesyltransferase inhibitor L744832 were examined in h

103 ion phase I and pharmacokinetic study of the farnesyltransferase inhibitor lonafarnib (SCH66336) was

104 clinical trial demonstrated that the protein farnesyltransferase inhibitor lonafarnib ameliorates som

105 Twenty-five patients with HGPS received the farnesyltransferase inhibitor lonafarnib for a minimum o

106 re used to evaluate the effect of the potent farnesyltransferase inhibitor, manumycin, on insulin ant

107 renylation-dependent as determined using the farnesyltransferase inhibitor methyl {N-[2-phenyl-4-N [2

108 To better understand how the farnesyltransferase inhibitors might be used in the trea

109 The farnesyltransferase inhibitor mislocalized progerin away

110 blasts, and we then examined the effect of a farnesyltransferase inhibitor on nuclear blebbing.

111 is migratory phenotype is not inhibited by a farnesyltransferase inhibitor or dominant-negative (dn)

112 Ras or Rac1, as well as by treatment with a farnesyltransferase inhibitor or with diphenylene iodoni

113 e phenotypes are largely rescued with either farnesyltransferase inhibitors or a farnesylation-incomp

114 ptor type II solution, 1 mM gliotoxin (a Ras farnesyltransferase inhibitor), or vehicle alone (the co

115 ase, Y361L, exhibits increased resistance to farnesyltransferase inhibitors, particularly a tricyclic

116 Here we show that FTI-277, another farnesyltransferase inhibitor, prevented the production

117 aluation of analogues of previously reported farnesyltransferase inhibitors, pyridyl benzyl ether 3 a

118 f patients with advanced MM treated with the farnesyltransferase inhibitor R115777 (Zarnestra) in a p

119 on of these events by pharmacologic (eg, the farnesyltransferase inhibitor R115777 or the MEK1/2 inhi

120 Farnesyltransferase inhibitors represent a new class of

121 Preclinical studies of farnesyltransferase inhibitor resistance and clinical tr

122 nesyltransferase gene ERA1 or application of farnesyltransferase inhibitors resulted in ABA hypersens

123 The farnesyltransferase inhibitor SCH66336 exhibits antitumo

124 s tumors with K-ras mutations implies that a farnesyltransferase inhibitor-sensitive protein other th

125 sferase, the effects of two types of protein farnesyltransferase inhibitors, several chaetomellic aci

126 ndicate that RAS-inactivating drugs, such as farnesyltransferase inhibitors should be examined in hum

127 Treatment with a farnesyltransferase inhibitor significantly improved nuc

128 owth; dominant negative RhoB or manumycin, a farnesyltransferase inhibitor that targets the vascular

129 or farnesylation, it may be a target for the farnesyltransferase inhibitors that block Ras processing

130 Clinical trials of two farnesyltransferase inhibitors--the tricyclic SCH66336 a

131 Farnesyltransferase inhibitors thus represent an attract

132 The farnesyltransferase inhibitor tipifarnib exhibits modest

133 In this phase 2 study, we tested the oral farnesyltransferase inhibitor tipifarnib in 158 older ad

134 A phase 2 study of the oral farnesyltransferase inhibitor tipifarnib was conducted i

135 ceptor signaling pathway with 4 courses of a farnesyltransferase inhibitor, tipifarnib.

136 ere that RhoB alteration is also crucial for farnesyltransferase inhibitors to sensitize neoplastic c

137 sible that Rheb function may be inhibited by farnesyltransferase inhibitors treatment and, consequent

138 nitril es have been synthesized as selective farnesyltransferase inhibitors using structure-based des

139 lly relevant to the long-term use of protein farnesyltransferase inhibitors, which lead to an accumul

140 Manumycin A is a potent and selective farnesyltransferase inhibitor with antitumor activity.

141 ations provided 5h, a non-thiol, non-peptide farnesyltransferase inhibitor with excellent bioavailabi

142 Combinations of farnesyltransferase inhibitors with cytotoxic chemothera