ライフサイエンスコーパス: CCI-779

1 ith 15 to 25 mg lenalidomide and 15 to 20 mg CCI-779.

2 termined to be 25 mg lenalidomide with 15 mg CCI-779.

3 al protection in cells exposed to micromolar CCI-779.

4 thasone was combined with the mTOR inhibitor CCI-779.

5 s target in xenografted human ALL exposed to CCI-779.

6 mors regressed in response to treatment with CCI-779.

7 by the mTOR-specific blockers rapamycin and CCI-779.

8 activity and relatively mild side effects of CCI-779.

9 ycin (mTOR) inhibitors such as rapamycin and CCI-779.

10 graft model following in vivo treatment with CCI-779.

11 ich tumors will be sensitive or resistant to CCI-779.

12 FRAP/mTOR by using the rapamycin derivative CCI-779.

13 In this study, two doses of temsirolimus (CCI-779), a novel inhibitor of the mammalian target of r

14 hesis, we challenged myeloma cell lines with CCI-779, a newly developed analogue of rapamycin and an

15 on bone marrow stroma and were treated with CCI-779, a second generation MTI.

16 treated Pten conditional knockout mice with CCI-779, a specific mTor inhibitor.

17 generated from the same patient samples with CCI-779 after establishment of disease.

18 addition, exposure of abl and C4-2B cells to CCI-779 also decreased UBE2C-dependent cell invasion.

19 Interestingly, CCI-779 also produced growth inhibition of xenografts de

20 ed whether temsirolimus (previously known as CCI-779), an inhibitor of the mammalian target of rapamy

21 ed that the G(1)-S cell-cycle inhibitor-779 (CCI-779), an mTOR inhibitor, inhibited UBE2C mRNA and pr

22 Both rapamycin and CCI-779, an ester analog of rapamycin with improved phar

23 egative PC-3 prostate cancer xenografts with CCI-779, an ester of rapamycin in clinical development c

24 CCI-779, an mTOR inhibitor, arrested growth of a phospha

25 es greater after simultaneous treatment with CCI-779 and cisplatin than after cisplatin alone.

26 Combination treatment with CCI-779 and HCQ suppressed melanoma growth and induced c

27 tor hydroxychloroquine (HCQ) synergizes with CCI-779 and led to melanoma cell death via apoptosis.

28 ectly related to the antitumor activities of CCI-779 and other rapalogues in human cancer patients.

29 Rapamycin and its derivatives, CCI-779 and RAD001 (designated rapamycins), specifically

30 Rapamycin and several analogs, such as CCI-779 and RAD001, are currently undergoing clinical ev

31 Biochemical assays indicated that CCI-779 and rapamycin directly inhibited mTOR kinase act

32 he rapamycin derivatives (RDs) temsirolimus (CCI-779) and everolimus (RAD001) in acute myeloid leukem

33 o specific allosteric inhibitors (rapamycin, CCI-779, and RAD001) of the pivotal cell growth regulato

34 r cell types, and its derivatives RAD001 and CCI-779 are currently in phase I and phase II clinical t

35 RAD001 and CCI-779 are in phase I and II trials, respectively, as a

36 trial using targeted molecular therapy with CCI-779 as a single agent for mTOR-activated residual ce

37 In cell culture studies, CCI-779 at the commonly used nanomolar concentrations ge

38 DA-approved rapamycin analogue temsirolimus (CCI-779) blocks ANDV protein expression and virion relea

39 Thus, rapamycin and CCI-779, by interacting with downstream intermediates in

40 cromolar but not nanomolar concentrations of CCI-779 caused a marked decline in global protein synthe

41 In those animals that formed tumors, CCI-779 caused a significant decrease in the tumor volum

42 ective pharmacologic inhibitor, Ku0063794 or CCI-779, caused the up-regulation of nuclear phospho-Mst

43 block cell-cycle G(1) to S-phase transition, CCI-779 causes a cell-cycle G(2)-M accumulation and an i

44 ally relevant low micromolar concentrations, CCI-779 completely suppressed proliferation of a broad p

45 Growth arrest caused by CCI-779 correlates with a block in translation of mRNA e

46 malian target of rapamycin (mTOR) inhibitor, CCI-779, curtailed the growth of a subcutaneous challeng

47 In vivo, CCI-779 delayed DAOY xenograft growth by 160% after 1 we

48 nor efficacy was significantly influenced by CCI-779 dose level.

49 CCI-779, given as 10 intraperitoneal injections, induced

50 CCI-779 has completed several phase I clinical evaluatio

51 tion of lenalidomide with the mTOR inhibitor CCI-779 has displayed synergy in vitro and represents a

52 Huntington disease, and the rapamycin analog CCI-779 improved performance on four different behaviora

53 ignificance of this pathway was tested using CCI-779 in a mouse xenograft model.

54 this potential, we used the rapamycin analog CCI-779 in a myeloma xenograft model.

55 We also assessed the effect of CCI-779 in a NOD/SCID xenograft model.

56 suppressant agent rapamycin and its analogue CCI-779 in human brain tumor cell lines in vitro and in

57 into possible therapeutic uses of rapamycin/CCI-779 in the treatment of neurodegenerative diseases (

58 which contributes to antitumor activities of CCI-779 in UBE2C overexpressed AR-positive CRPC.

59 ayed an 11-fold resistance to the micromolar CCI-779 in vitro (IC(50), 20 +/- 3.4 micromol/L) and con

60 es kidney cancer cells to the mTOR inhibitor CCI-779 in vitro and in mouse models.

61 s(LA1) mice, was resistant to treatment with CCI-779 in vitro.

62 particular the mTOR inhibitor temsirolimus (CCI-779), induce autophagy, which can promote tumor surv

63 activation were particularly sensitive to a CCI-779-induced antitumor response.

64 However, CCI-779 inhibited expression of c-myc in CCI-sensitive P

65 CCI-779 inhibited growth of established tumors in nude m

66 The molecular mechanisms for CCI-779 inhibition of UBE2C gene expression involved a d

67 These findings suggest that high-dose CCI-779 inhibits mTOR signaling through an FKBP12-indepe

68 studies suggest that the rapamycin analogue CCI-779 is an important new agent to investigate in the

69 biomechanical fluidic environment of the BM, CCI-779 is equally effective in inhibiting BM endothelia

70 Temsirolimus (CCI-779) is a small-molecule inhibitor of the mammalian

71 r cells with WYE-132 or the rapamycin analog CCI-779 led to a rapid loss of the phosphorylation at Se

72 Although CCI-779-mediated inhibition of the p70 mTOR substrate wa

73 own promise in early clinical trials such as CCI-779, pegylated interferon, thalidomide, and anti-VEG

74 Similar and significant changes for CCI-779 pharmacokinetics were also observed with increas

75 Blood samples were collected to determine CCI-779 pharmacokinetics.

76 CCI-779 produced an objective response rate of 7% (one c

77 ice by treatment with the rapamycin analogue CCI-779 reduced the size and number of early epithelial

78 The most frequently occurring CCI-779-related adverse events of all grades were maculo

79 Interestingly, a CCI-779-resistant mTOR mutant (mTOR-SI) displayed an 11-

80 ssion of a constitutively active AKT gene in CCI-779-resistant myeloma cells containing wild-type PTE

81 target of rapamycin inhibitors rapamycin and CCI-779 resulted in inhibition of IL-6-induced myeloma c

82 inetic analysis indicated increased doses of CCI-779 resulted in statistically significant changes in

83 inical interactions between lenalidomide and CCI-779 seemed to occur, with in vitro data indicating l

84 nd quiescent AKT did not convert them to the CCI-779-sensitive phenotype.

85 Conversely, expression of wild-type PTEN in CCI-779-sensitive, PTEN-deficient myeloma cells did not

86 se down-regulation is required for rapamycin/CCI-779 sensitivity.

87 Animals treated with CCI-779 showed a decrease in peripheral-blood blasts and

88 In patients with advanced RCC, CCI-779 showed antitumor activity and encouraging surviv

89 Treatment with CCI-779 significantly decreased abl cell proliferation i

90 The Kaplan-Meier curve showed that CCI-779 significantly increased survival (P < 0.0001).

91 CCI-779 suppressed phosphorylation of mTOR downstream pr

92 mmalian target of rapamycin (mTOR) inhibitor CCI-779 (temsirolimus) is a recently Food and Drug Admin

93 atter cells was remarkably more sensitive to CCI-779 than the growth of control U266 cells.

94 The mTOR inhibitors rapamycin and CCI-779, the PI3-kinase inhibitor LY294002, and the MEK

95 r to be due to differences in the ability of CCI-779 to inhibit mTOR and induce dephosphorylation of

96 Akt in PTEN(+/+) cells also was reversed by CCI-779 treatment, indicating that FRAP/mTOR functions d

97 Differential sensitivity to CCI-779 was not explained by differences in biochemical

98 ndomly assigned to receive 25, 75, or 250 mg CCI-779 weekly as a 30-minute intravenous infusion.

99 Effective doses of CCI-779 were associated with modest toxicity, inducing o

100 iferase allowed us to monitor the effects of CCI-779 with bioluminescence imaging in the MRD model.

101 to cytoreduction and G(1) arrest induced by CCI-779 with ID(50) concentrations of <1 nM.

102 on regimen was 25 mg lenalidomide with 15 mg CCI-779, with toxicities of fatigue, neutropenia, and el

103 Compared with the rapalog temsirolimus/CCI-779, WYE-132 elicited a substantially stronger inhib