ライフサイエンスコーパス: vandetanib

1 tor (gefitinib, vandetanib) and RET protein (vandetanib).

2 T1A4, 1A7 and 1A9 by axitinib; and UGT1A9 by vandetanib).

3 eta were blocked by the RET-receptor blocker vandetanib.

4 , patients could elect to receive open-label vandetanib.

5 here was a higher incidence of some AEs with vandetanib.

6 3), 110 (n = 6), and 145 mg/m(2) (n = 6) of vandetanib.

7 ase (n = 127), median PFS was 18.7 weeks for vandetanib 100 mg plus docetaxel (n = 42; hazard ratio v

8 e primary objective was to determine whether vandetanib 100 mg plus docetaxel 75 mg/m(2) intravenousl

9 The primary objective was achieved, with vandetanib 100 mg plus docetaxel demonstrating a signifi

10 se encouraging data, phase III evaluation of vandetanib 100 mg plus docetaxel in second-line NSCLC ha

11 d non-small-cell lung cancer (NSCLC), adding vandetanib 100 mg to docetaxel significantly improved pr

12 rd-party interactive voice system to receive vandetanib (100 mg/day) plus docetaxel (75 mg/m(2) intra

13 on-free survival (PFS) in patients receiving vandetanib (100 or 300 mg/d) plus docetaxel (75 mg/m2 in

14 i.v.), pazopanib (30 and100 mg/kg, i.p.), or vandetanib (12.5 and 25 mg/kg, i.p.).

15 etastatic) were randomly assigned to receive vandetanib (231) or placebo (100).

16 , until disease progression, and either oral vandetanib 300 mg per day once daily or matching placebo

17 = 0.64; one-sided P = .037); 17.0 weeks for vandetanib 300 mg plus docetaxel (n = 44; hazard ratio v

18 eived initial treatment with once-daily oral vandetanib 300 mg.

19 Vandetanib 300 mg/d is currently being evaluated as a mo

20 randomly assigned in a 2:1 ratio to receive vandetanib 300 mg/d or placebo.

21 rty patients received initial treatment with vandetanib 300 mg/d.

22 ; rash was more frequent with erlotinib than vandetanib (38% v 28%, respectively).

23 eated with bevacizumab (10 mg/kg/wk i.v.) or vandetanib (50 mg/kg/d orally) to block the VEGF pathway

24 ctor accelerates cancer cell invasion, while vandetanib, a multitarget kinase inhibitor, dose-depende

25 Vandetanib, a once-daily oral inhibitor of RET kinase, v

26 bel, phase II study assessed the efficacy of vandetanib, a selective oral inhibitor of RET, vascular

27 in a randomized phase II study who received vandetanib, a VEGFR and epidermal growth factor receptor

28 Single-agent vandetanib activity was minimal.

29 10; P = .721); median PFS was 2.6 months for vandetanib and 2.0 months for erlotinib.

30 Vandetanib and cabozantinib have shown benefits on progr

31 nged during transfection-targeted therapies (vandetanib and cabozantinib) in MTC have led to approval

32 od and Drug Administration recently approved vandetanib and cabozantinib, the tyrosine kinase inhibit

33 Vandetanib and chemotherapy treatment led to distinct pa

34 epidermal growth factor receptor (gefitinib, vandetanib) and RET protein (vandetanib).

35 ic and demonstrate that axitinib, pazopanib, vandetanib, and everolimus are also teratogens in these

36 at drugs targeting only VEGFRs (Apatinib and Vandetanib) are not effective, whereas drugs that target

37 ere more commonly seen in the docetaxel plus vandetanib arm and included rash/photosensitivity (11% v

38 n PFS was 2.56 months for the docetaxel plus vandetanib arm versus 1.58 months for the docetaxel plus

39 ased and sVEGFR-2 decreased by day 43 in the vandetanib arm, whereas a distinct pattern was observed

40 had the option to cross over to single-agent vandetanib at progression.

41 dministration of the VEGFR2 kinase inhibitor Vandetanib attenuates OA progression.

42 ts (any grade) occurred more frequently with vandetanib compared with placebo, including diarrhea (56

43 CONCLUSION In this study, vandetanib demonstrated durable objective partial respon

44 rimary efficacy objective was achieved, with vandetanib demonstrating a significant prolongation of P

45 Patients receiving vandetanib experienced adverse events that were manageab

46 131 patients had died: 70 (97%) of 72 in the vandetanib group and 61 (87%) of 70 in the placebo group

47 re randomly assigned to treatment (72 to the vandetanib group and 70 to the placebo group).

48 l was 8.83 months (95% CI 7.11-11.58) in the vandetanib group and 8.95 months (6.55-11.74) in the pla

49 p<0.0001); median PFS was 4.0 months in the vandetanib group versus 3.2 months in placebo group.

50 , p=0.024); median PFS was 4.6 months in the vandetanib group versus 4.2 months in the placebo group.

51 neutropenia (35 [49%] of 72 patients in the vandetanib group vs 22 [31%] of 70 in the placebo group)

52 was febrile neutropenia (46/689 [7%] in the vandetanib group vs 38/690 [6%] in the placebo group).

53 1:1 to receive vandetanib plus gemcitabine (vandetanib group) or placebo plus gemcitabine (placebo g

54 Vandetanib has been shown to improve progression-free su

55 Vandetanib has emerged as one of the more promising smal

56 The recommended phase II dose of vandetanib in children is 145 mg/m(2) per day.

57 Vandetanib in combination with docetaxel was assessed in

58 The Vandetanib in Pancreatic Cancer (ViP) trial was a phase

59 ficant interpatient variability, exposure to vandetanib increased with higher dosage levels.

60 Vandetanib is a novel tyrosine kinase inhibitor of VEGFR

61 Vandetanib is a once-daily oral inhibitor of vascular en

62 Vandetanib is a once-daily oral inhibitor of vascular en

63 Vandetanib is a once-daily oral inhibitor of vascular en

64 Vandetanib is a once-daily oral inhibitor of vascular en

65 Vandetanib is a once-daily, oral inhibitor of vascular e

66 PURPOSE OF REVIEW: Vandetanib is a small molecule tyrosine kinase inhibitor

67 Vandetanib is an oral once-daily tyrosine kinase inhibit

68 In general, vandetanib is well tolerated, but QTc prolongation remai

69 These results demonstrate that vandetanib may provide an effective therapeutic option i

70 The vandetanib monotherapy arm (n = 73) was discontinued aft

71 ied study end point, whereas those receiving vandetanib monotherapy had shorter PFS.

72 The antitumor activity of vandetanib monotherapy or vandetanib with paclitaxel and

73 IL-8 with VCP, MMP-9 with CP, and VEGF with vandetanib monotherapy were associated with increased pr

74 tients initially randomly assigned to either vandetanib or gefitinib.

75 37 patients who crossed over to single-agent vandetanib, ORR was 3% and OS was 5.2 months.

76 1391 patients received vandetanib plus docetaxel (n=694 [197 women]) or placebo

77 Vandetanib plus docetaxel led to a significant improveme

78 9 [9%] vs 48/690 [7%]) were more common with vandetanib plus docetaxel than with placebo plus docetax

79 A similar improvement in PFS with vandetanib plus docetaxel versus placebo plus docetaxel

80 The activity of vandetanib plus docetaxel was assessed in patients with

81 The toxicity of vandetanib plus docetaxel was greater than that for vend

82 tients were randomly assigned 1:1 to receive vandetanib plus gemcitabine (vandetanib group) or placeb

83 In part A, vandetanib prolonged PFS compared with gefitinib (hazard

84 knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breas

85 Vandetanib selectively targets RET, vascular endothelial

86 ents with previously treated advanced NSCLC, vandetanib showed antitumor activity but did not demonst

87 ease, novel chemotherapeutic agents, such as vandetanib, targeting rearranged during transfection, va

88 ence of grade >/= 3 AEs was also higher with vandetanib than erlotinib (50% v 40%, respectively).

89 e events (AEs; any grade) more frequent with vandetanib than erlotinib included diarrhea (50% v 38%,

90 angiogenesis (sorafenib, CA4P, axitinib and vandetanib), the epidermal growth factor receptor (gefit

91 d population of advanced UC, the addition of vandetanib to docetaxel did not result in a significant

92 The addition of vandetanib to docetaxel provides a significant improveme

93 INTERPRETATION: The addition of vandetanib to gemcitabine monotherapy did not improve ov

94 improvement in PFS for patients treated with vandetanib versus erlotinib (hazard ratio [HR], 0.98; 95

95 his phase III study assessed the efficacy of vandetanib versus erlotinib in unselected patients with

96 ority in progression-free survival (PFS) for vandetanib versus erlotinib.

97 < .2) and to demonstrate noninferiority for vandetanib versus PC.

98 s primary objective of PFS prolongation with vandetanib versus placebo (hazard ratio [HR], 0.46; 95%

99 ents were randomly assigned 2:1:1 to receive vandetanib, VPC, or PC.

100 Vandetanib was administered concurrently with radiothera

101 se in intercellular adhesion molecule 1 with vandetanib was associated with decreased risk.

102 t phase II study, the efficacy and safety of vandetanib was compared with that of gefitinib, an inhib

103 Statistically significant advantages for vandetanib were also seen for objective response rate (P

104 four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized by using hepatic microsom

105 We investigated the clinical efficacy of vandetanib when used in combination with gemcitabine in

106 itumor activity of vandetanib monotherapy or vandetanib with paclitaxel and carboplatin (VPC) was com