ライフサイエンスコーパス: cediranib

1 rebound growth after the discontinuation of cediranib.

2 cules as potential biomarkers of response to cediranib.

3 stoma with a VEGF-targeted kinase inhibitor, cediranib.

4 llagen IV levels, all after a single dose of cediranib.

5 small-molecule inhibitors of VEGFR, such as cediranib.

6 4 to receive the combination of olaparib and cediranib.

7 y approximately 10% in patients treated with cediranib.

8 In all, 860 patients received cediranib 20 mg (n = 502) or placebo (n = 358).

9 In all, 1,422 patients received mFOLFOX6/cediranib 20 mg (n = 709) or mFOLFOX6/bevacizumab (n = 7

10 of-phase II analysis concluded that mFOLFOX6/cediranib 20 mg met predefined criteria for continuation

11 ebo only maintenance (arm B; concurrent), or cediranib 20 mg once-daily alongside chemotherapy then c

12 placebo only maintenance (arm A; reference), cediranib 20 mg once-daily alongside chemotherapy then p

13 20 mg once-daily alongside chemotherapy then cediranib 20 mg once-daily maintenance (arm C; maintenan

14 ation; subsequent patients received mFOLFOX6/cediranib 20 mg or mFOLFOX6/bevacizumab (randomly assign

15 t patients were randomly assigned 2:1 to the cediranib 20 mg or placebo arms.

16 ) through a minimisation approach to receive cediranib 20 mg or placebo orally once daily until disea

17 CONCLUSION Addition of cediranib 20 mg to FOLFOX/CAPOX resulted in a modest PFS

18 4 weeks with olaparib 300 mg twice a day, or cediranib 20 mg, 5 days on/2 days off.

19 ceive (1) cediranib (30 mg) monotherapy; (2) cediranib (20 mg) plus lomustine (110 mg/m(2)); (3) lomu

20 ) over the next 46 hours every 2 weeks] with cediranib (20 or 30 mg per day) or bevacizumab (5 mg/kg

21 initially randomly assigned 1:1:1 to receive cediranib (20 or 30 mg per day) or placebo plus FOLFOX/C

22 d, before and after daily administration of cediranib (3 and 6 mg/kg, 3 and 6 mg/kg/h for 1 h, i.v.)

23 mbination at the recommended phase 2 dose of cediranib 30 mg daily and olaparib capsules 200 mg twice

24 were randomly assigned 2:2:1 to receive (1) cediranib (30 mg) monotherapy; (2) cediranib (20 mg) plu

25 126 (200 mg/kg), or the antiangiogenic agent cediranib (6 mg/kg, daily).

26 rebound after an initial decrease following cediranib (a pan-VEGFR tyrosine kinase inhibitor) admini

27 red dexamethasone, the standard of care, and cediranib, a novel anti-edema agent, are associated with

28 shed light on mechanisms of nGBM response to cediranib, a pan-VEGF receptor tyrosine kinase inhibitor

29 patients who were undergoing treatment with cediranib, a pan-VEGF receptor tyrosine kinase inhibitor

30 We describe here the effects of cediranib, a receptor tyrosine kinase inhibitor, in a mo

31 31 rGBM patients treated with daily doses of cediranib, acquiring serial chemical shift imaging data

32 Cediranib activity, in terms of PFS and OS, was comparab

33 The cediranib AE profile was consistent with those from prev

34 ) was not significantly different for either cediranib alone (hazard ratio [HR] = 1.05; 95% CI, 0.74

35 imed to assess the effect of the addition of cediranib (an oral inhibitor of VEGF receptor 1, 2, and

36 Cediranib, an inhibitor of VEGFR1-3 and c-kit, inhibited

37 ) was conducted to determine the efficacy of cediranib, an oral pan-vascular endothelial growth facto

38 Cediranib, an oral pan-VEGF receptor tyrosine kinase inh

39 oma patients enrolled in a phase II trial of cediranib, an oral pan-VEGF receptor tyrosine kinase inh

40 and OS were 9.9 and 22.8 months for mFOLFOX6/cediranib and 10.3 and 21.3 months for mFOLFOX6/bevacizu

41 Dual therapy using cediranib and MEDI3617 (an anti-Ang-2-neutralizing antib

42 trongly suggest a direct metabolic effect of cediranib and might also reflect an antitumor response t

43 The efficacy of cediranib and the predictive value of these candidate bi

44 R-targeted therapy (sorafenib, pazopanib, or cediranib), and four patients had received two such ther

45 cantly more common, during chemotherapy with cediranib, and diarrhoea, hypothyroidism and voice chang

46 The antitumor activity of cyclophosphamide, cediranib, and ZD6126 was consistently associated with a

47 us olaparib and durvalumab plus intermittent cediranib are tolerable and active.

48 Exposure to durvalumab increased cediranib area under the curve and maximum plasma concen

49 se events with more than 5% incidence in the cediranib arm included diarrhea, neutropenia, and hypert

50 Cediranib (AZD2171) is a potent inhibitor of tyrosine ki

51 HORIZON II [Cediranib (AZD2171, RECENTIN) in Addition to Chemotherap

52 e first reported anti-PD-L1 plus olaparib or cediranib combination therapy.

53 (PD-L1) inhibitor, durvalumab, olaparib, or cediranib combinations are tolerable and active in recur

54 usion occurs only in a subset of patients in cediranib-containing regimens, and is associated with im

55 Treatment with cediranib decreased metastatic tumor burden in the brain

56 Cediranib did not improve the progression-free survival

57 s primary end point of PFS prolongation with cediranib either as monotherapy or in combination with l

58 The recommended monotherapy dose of cediranib for children with extracranial solid tumors is

59 luable patients who received durvalumab plus cediranib, for a 50% response rate and a 75% disease con

60 nib, was developed to enhance the release of cediranib from the device.

61 Durvalumab plus intermittent cediranib grade 3 and 4 AEs were hypertension (one of si

62 progression-free survival was longer in the cediranib group (median 8.1 months [80% CI 7.4-8.8]) tha

63 vival was 8.0 months (95% CI 6.5-9.3) in the cediranib group and 7.4 months (5.7-8.5) in the placebo

64 Although patients in the cediranib group had more adverse events, we recorded no

65 of grade 2-3 hypertension was higher in the cediranib group than in the control group (11 [34%] vs f

66 diarrhoea (five [16%] of 32 patients in the cediranib group vs one [3%] of 35 patients in the placeb

67 in the placebo group and 19 patients in the cediranib group.

68 Patients who received cediranib had more grade 3-4 toxic effects than did pati

69 Cediranib has activity in recurrent EOC, tubal cancer, a

70 Cediranib has significant efficacy when added to carbopl

71 herapy for metastatic ASPS, we observed that cediranib has substantial single-agent activity, produci

72 inhibitors such as sunitinib, sorafenib and cediranib have shown disease stabilization in patients w

73 95% CI, 0.74 to 1.50; two-sided P = .90) or cediranib in combination with lomustine (HR = 0.76; 95%

74 We assessed efficacy and safety of cediranib in combination with platinum-based chemotherap

75 d oxaliplatin (FOLFOX/CAPOX) with or without cediranib in patients with previously untreated metastat

76 We performed a phase II study of cediranib in patients with recurrent glioblastoma.

77 f both dexamethasone and solid dispersion of cediranib in polyvinylpyrrolidone (AZD/PVP) from these d

78 Systemically, cediranib increased plasma VEGF and placenta growth fact

79 Treatment with cyclophosphamide or cediranib induced a 54% or 20% reduction in tumor volume

80 The cediranib intermittent schedule (n = 6) was examined bec

81 Cediranib is a highly potent inhibitor of vascular endot

82 Cediranib is a potent tyrosine kinase inhibitor of VEGFR

83 Cediranib is a potent, oral small-molecule inhibitor of

84 a poly(ADP-ribose) polymerase inhibitor and cediranib is an anti-angiogenic agent with activity agai

85 Cediranib is an oral antiangiogenic vascular endothelial

86 Cediranib is an oral tyrosine kinase inhibitor (TKI) of

87 y as after one day of anti-VEGF therapy with cediranib is predictive of response in patients with rec

88 the effects of delivering dexamethasone and cediranib locally in the brain in an intracranial 9L gli

89 n in (18)F-FMISO uptake after treatment with cediranib may be mistakenly interpreted as a global decr

90 Cediranib monotherapy for recurrent glioblastoma is asso

91 ients were enrolled and randomly assigned to cediranib (n=34) or placebo (n=35).

92 t tumor biopsies and evaluated the effect of cediranib on tumor proliferation and angiogenesis using

93 with either olaparib tablets twice daily or cediranib on two schedules.

94 up to eight cycles]) with either 20 mg oral cediranib or placebo once a day until disease progressio

95 Because of the lack of improvement in OS, cediranib plus an oxaliplatin-based regimen cannot be re

96 and two other cediranib studies (HORIZON I [Cediranib Plus FOLFOX6 Versus Bevacizumab Plus FOLFOX6 i

97 tastatic Colorectal Cancer] and HORIZON III [Cediranib Plus FOLFOX6 Versus Bevacizumab Plus FOLFOX6 i

98 14.7-not reached) for the women treated with cediranib plus olaparib compared with 9.0 months (95% CI

99 erapy, including fatigue (12 patients in the cediranib plus olaparib group vs five patients in the ol

100 Cediranib plus olaparib seems to improve PFS in women wi

101 The cediranib safety profile was consistent with previous st

102 tients with recurrent glioblastoma, although cediranib showed evidence of clinical activity on some s

103 We show by intravital microscopy that cediranib significantly decreased tumor vessel permeabil

104 However, by controlling edema, cediranib significantly increased survival of mice in th

105 In an early analysis of this and two other cediranib studies (HORIZON I [Cediranib Plus FOLFOX6 Ver

106 mor blood perfusion increased in response to cediranib survived 6 to 9 months longer than those whose

107 imed to assess the effect of the addition of cediranib to carboplatin and paclitaxel chemotherapy in

108 The addition of cediranib to FOLFOX/CAPOX resulted in PFS prolongation (

109 Surprisingly, in cediranib-treated GBM, cellular density in the central a

110 Finally, cediranib-treated GBMs showed high levels of PDGF-C (pla

111 Cediranib-treated patients completed fewer chemotherapy

112 aily for 2 d [5 rats] or 7 d [4 rats]) and a cediranib-treated test group (3 mg/kg daily for 2 or 7 d

113 (PROs) were significantly less favorable in cediranib-treated versus bevacizumab-treated patients (P

114 Short-duration cediranib treatment given at the time of tumor cell diss

115 Moreover, cediranib treatment induced normalization of perivascula

116 Cediranib treatment resulted in significant reduction of

117 After cediranib treatment, endothelial proliferation and glome

118 of a change in growth pattern of rGBMs after cediranib treatment, unlike that after chemoradiation.

119 or biomarkers of perfusion and hypoxia after cediranib treatment.

120 1.12; P = .5707; median OS, 19.7 months for cediranib v 18.9 months for placebo).

121 0.98; P = .0121; median PFS, 8.6 months for cediranib v 8.3 months for placebo) but had no impact on

122 pan-VEGF receptor tyrosine kinase inhibitor cediranib versus 7 patients who received no therapy or c

123 Local deliveries of dexamethasone and cediranib via these devices used only 2.36% and 0.21% of

124 The MTD of cediranib was 12 mg/m(2)/d (adult fixed dose equivalent,

125 APF6 after cediranib was 25.8%.

126 Tumor response to cediranib was also associated with a decrease in the dyn

127 mic administration of both dexamethasone and cediranib was equally efficacious in alleviating edema b

128 Poor compliance with cediranib was noted during maintenance treatment with to

129 /PVP, which exhibited similar bioactivity as cediranib, was developed to enhance the release of cedir

130 latinase-associated lipocalin activity after cediranib were associated with radiographic response or

131 Adverse events (AEs) associated with cediranib were manageable.

132 The hypertensive effects of cediranib were unaffected by losartan (10 mg/kg/h), bose

133 The hypertensive effects of cediranib were unaffected by losartan (10 mg/kg/h), bose

134 Cediranib, when given orally with chemotherapy and conti

135 for patients with metastatic ASPS comparing cediranib with another VEGFR inhibitor, sunitinib.

136 s in prospective phase II clinical trials of cediranib with chemoradiation vs. chemoradiation alone i