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1 tor (gefitinib, vandetanib) and RET protein (vandetanib).
2 T1A4, 1A7 and 1A9 by axitinib; and UGT1A9 by vandetanib).
3 t how TKIs bind to RET is unknown except for vandetanib.
4  RET mutants against the TKIs nintedanib and vandetanib.
5 eta were blocked by the RET-receptor blocker vandetanib.
6  consistent with the known safety profile of vandetanib.
7 , patients could elect to receive open-label vandetanib.
8 here was a higher incidence of some AEs with vandetanib.
9  3), 110 (n = 6), and 145 mg/m(2) (n = 6) of vandetanib.
10 ase (n = 127), median PFS was 18.7 weeks for vandetanib 100 mg plus docetaxel (n = 42; hazard ratio v
11 e primary objective was to determine whether vandetanib 100 mg plus docetaxel 75 mg/m(2) intravenousl
12     The primary objective was achieved, with vandetanib 100 mg plus docetaxel demonstrating a signifi
13 se encouraging data, phase III evaluation of vandetanib 100 mg plus docetaxel in second-line NSCLC ha
14 d non-small-cell lung cancer (NSCLC), adding vandetanib 100 mg to docetaxel significantly improved pr
15 rd-party interactive voice system to receive vandetanib (100 mg/day) plus docetaxel (75 mg/m(2) intra
16 on-free survival (PFS) in patients receiving vandetanib (100 or 300 mg/d) plus docetaxel (75 mg/m2 in
17 i.v.), pazopanib (30 and100 mg/kg, i.p.), or vandetanib (12.5 and 25 mg/kg, i.p.).
18 etastatic) were randomly assigned to receive vandetanib (231) or placebo (100).
19 , until disease progression, and either oral vandetanib 300 mg per day once daily or matching placebo
20  = 0.64; one-sided P = .037); 17.0 weeks for vandetanib 300 mg plus docetaxel (n = 44; hazard ratio v
21 eived initial treatment with once-daily oral vandetanib 300 mg.
22                                              Vandetanib 300 mg/d is currently being evaluated as a mo
23  randomly assigned in a 2:1 ratio to receive vandetanib 300 mg/d or placebo.
24 rty patients received initial treatment with vandetanib 300 mg/d.
25 ; rash was more frequent with erlotinib than vandetanib (38% v 28%, respectively).
26 eated with bevacizumab (10 mg/kg/wk i.v.) or vandetanib (50 mg/kg/d orally) to block the VEGF pathway
27 ctor accelerates cancer cell invasion, while vandetanib, a multitarget kinase inhibitor, dose-depende
28                                              Vandetanib, a once-daily oral inhibitor of RET kinase, v
29 bel, phase II study assessed the efficacy of vandetanib, a selective oral inhibitor of RET, vascular
30  in a randomized phase II study who received vandetanib, a VEGFR and epidermal growth factor receptor
31                                 Single-agent vandetanib activity was minimal.
32 10; P = .721); median PFS was 2.6 months for vandetanib and 2.0 months for erlotinib.
33                                              Vandetanib and cabozantinib have shown benefits on progr
34 nged during transfection-targeted therapies (vandetanib and cabozantinib) in MTC have led to approval
35 od and Drug Administration recently approved vandetanib and cabozantinib, the tyrosine kinase inhibit
36                                              Vandetanib and chemotherapy treatment led to distinct pa
37 ent with a combination of kinase inhibitors (vandetanib and dasatinib) showed enhanced sensitivity co
38 epidermal growth factor receptor (gefitinib, vandetanib) and RET protein (vandetanib).
39 onses to other hERG blockers, such as E4031, vandetanib, and clarithromycin.
40 ic and demonstrate that axitinib, pazopanib, vandetanib, and everolimus are also teratogens in these
41 at drugs targeting only VEGFRs (Apatinib and Vandetanib) are not effective, whereas drugs that target
42 ere more commonly seen in the docetaxel plus vandetanib arm and included rash/photosensitivity (11% v
43 n PFS was 2.56 months for the docetaxel plus vandetanib arm versus 1.58 months for the docetaxel plus
44 ased and sVEGFR-2 decreased by day 43 in the vandetanib arm, whereas a distinct pattern was observed
45 g CATNIP, we predicted the kinase inhibitor, vandetanib, as a possible treatment for Type 2 Diabetes.
46 had the option to cross over to single-agent vandetanib at progression.
47 dministration of the VEGFR2 kinase inhibitor Vandetanib attenuates OA progression.
48 ression, including ALKBH2-benzaldehyde, AKT3-vandetanib, BCR-imatinib, CDK1 and 20-palbociclib, CASP1
49 y thyroid cancer who had previously received vandetanib, cabozantinib, or both, the percentage who ha
50 ts (any grade) occurred more frequently with vandetanib compared with placebo, including diarrhea (56
51            High deposition of beads and high vandetanib concentration in tumor led to stronger antitu
52 isons of RET-nintedanib, RET(G810A), and RET-vandetanib crystal structures suggested that the solvent
53                                              Vandetanib demonstrated clinical benefit-specifically, i
54                    CONCLUSION In this study, vandetanib demonstrated durable objective partial respon
55 rimary efficacy objective was achieved, with vandetanib demonstrating a significant prolongation of P
56 he pharmacokinetics, safety, and efficacy of vandetanib-eluting radiopaque bead (VERB) chemoembolizat
57                                   Conclusion Vandetanib-eluting radiopaque bead chemoembolization sho
58                           Patients receiving vandetanib experienced adverse events that were manageab
59 131 patients had died: 70 (97%) of 72 in the vandetanib group and 61 (87%) of 70 in the placebo group
60 re randomly assigned to treatment (72 to the vandetanib group and 70 to the placebo group).
61 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
62  p<0.0001); median PFS was 4.0 months in the vandetanib group versus 3.2 months in placebo group.
63 , p=0.024); median PFS was 4.6 months in the vandetanib group versus 4.2 months in the placebo group.
64  neutropenia (35 [49%] of 72 patients in the vandetanib group vs 22 [31%] of 70 in the placebo group)
65  was febrile neutropenia (46/689 [7%] in the vandetanib group vs 38/690 [6%] in the placebo group).
66  1:1 to receive vandetanib plus gemcitabine (vandetanib group) or placebo plus gemcitabine (placebo g
67                                              Vandetanib has been shown to improve progression-free su
68                                              Vandetanib has emerged as one of the more promising smal
69 inhibitor activity, such as cabozantinib and vandetanib, have been explored in the clinic for tumors
70             The recommended phase II dose of vandetanib in children is 145 mg/m(2) per day.
71                                              Vandetanib in combination with docetaxel was assessed in
72                                          The Vandetanib in Pancreatic Cancer (ViP) trial was a phase
73 r (MTC) to assess the efficacy and safety of vandetanib in patients with progressive and symptomatic
74 ficant interpatient variability, exposure to vandetanib increased with higher dosage levels.
75                                              Vandetanib is a novel tyrosine kinase inhibitor of VEGFR
76                                              Vandetanib is a once-daily oral inhibitor of vascular en
77                                              Vandetanib is a once-daily oral inhibitor of vascular en
78                                              Vandetanib is a once-daily oral inhibitor of vascular en
79                                              Vandetanib is a once-daily oral inhibitor of vascular en
80                                              Vandetanib is a once-daily, oral inhibitor of vascular e
81                           PURPOSE OF REVIEW: Vandetanib is a small molecule tyrosine kinase inhibitor
82                                              Vandetanib is an oral once-daily tyrosine kinase inhibit
83                                  In general, vandetanib is well tolerated, but QTc prolongation remai
84               These results demonstrate that vandetanib may provide an effective therapeutic option i
85 on beads loaded with the antiangiogenic drug vandetanib may provide improved anticancer efficacy.
86                                          The vandetanib monotherapy arm (n = 73) was discontinued aft
87 ied study end point, whereas those receiving vandetanib monotherapy had shorter PFS.
88                    The antitumor activity of vandetanib monotherapy or vandetanib with paclitaxel and
89  IL-8 with VCP, MMP-9 with CP, and VEGF with vandetanib monotherapy were associated with increased pr
90 nd 44.0 months in patients with cabozantinib/vandetanib-naive and pretreated MTC, the median progress
91 e was 82.5% among patients with cabozantinib/vandetanib-naive MTC and 95.8% among patients with treat
92 % and 87.3% among patients with cabozantinib/vandetanib-naive MTC and treatment-naive TC, respectivel
93 lary thyroid cancer with or without previous vandetanib or cabozantinib treatment, as well as those w
94 ary thyroid cancer with and without previous vandetanib or cabozantinib treatment.
95 yroid cancer who had not previously received vandetanib or cabozantinib, the percentage who had a res
96 tients initially randomly assigned to either vandetanib or gefitinib.
97 37 patients who crossed over to single-agent vandetanib, ORR was 3% and OS was 5.2 months.
98      We conducted a post hoc analysis of the vandetanib phase III trial involving patients with advan
99                                              Vandetanib plasma concentration and tumor growth at US w
100                                      Results Vandetanib plasma concentration was lower with VERBs tha
101                       1391 patients received vandetanib plus docetaxel (n=694 [197 women]) or placebo
102                                              Vandetanib plus docetaxel led to a significant improveme
103 9 [9%] vs 48/690 [7%]) were more common with vandetanib plus docetaxel than with placebo plus docetax
104            A similar improvement in PFS with vandetanib plus docetaxel versus placebo plus docetaxel
105                              The activity of vandetanib plus docetaxel was assessed in patients with
106                              The toxicity of vandetanib plus docetaxel was greater than that for vend
107 tients were randomly assigned 1:1 to receive vandetanib plus gemcitabine (vandetanib group) or placeb
108                                   In part A, vandetanib prolonged PFS compared with gefitinib (hazard
109  knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breas
110    Nintedanib is a RET TKI that inhibits the vandetanib-resistant RET(G810A) mutant.
111                         We also identified a vandetanib-resistant RET(L881V) mutation previously foun
112 d blocks water access to two oxygen atoms of vandetanib, resulting in an energetic penalty for buryin
113                                              Vandetanib selectively targets RET, vascular endothelial
114 ents with previously treated advanced NSCLC, vandetanib showed antitumor activity but did not demonst
115 iopaque beads (ROBs), or with intra-arterial vandetanib suspension (VS) or were not treated.
116 ease, novel chemotherapeutic agents, such as vandetanib, targeting rearranged during transfection, va
117 ence of grade >/= 3 AEs was also higher with vandetanib than erlotinib (50% v 40%, respectively).
118 e events (AEs; any grade) more frequent with vandetanib than erlotinib included diarrhea (50% v 38%,
119  angiogenesis (sorafenib, CA4P, axitinib and vandetanib), the epidermal growth factor receptor (gefit
120 mor viability at histologic examination, and vandetanib tissue concentration.
121 d population of advanced UC, the addition of vandetanib to docetaxel did not result in a significant
122                              The addition of vandetanib to docetaxel provides a significant improveme
123              INTERPRETATION: The addition of vandetanib to gemcitabine monotherapy did not improve ov
124 improvement in PFS for patients treated with vandetanib versus erlotinib (hazard ratio [HR], 0.98; 95
125 his phase III study assessed the efficacy of vandetanib versus erlotinib in unselected patients with
126 ority in progression-free survival (PFS) for vandetanib versus erlotinib.
127  < .2) and to demonstrate noninferiority for vandetanib versus PC.
128 s primary objective of PFS prolongation with vandetanib versus placebo (hazard ratio [HR], 0.46; 95%
129 ents were randomly assigned 2:1:1 to receive vandetanib, VPC, or PC.
130                                              Vandetanib was administered concurrently with radiothera
131 se in intercellular adhesion molecule 1 with vandetanib was associated with decreased risk.
132 t phase II study, the efficacy and safety of vandetanib was compared with that of gefitinib, an inhib
133     Statistically significant advantages for vandetanib were also seen for objective response rate (P
134 four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized by using hepatic microsom
135     We investigated the clinical efficacy of vandetanib when used in combination with gemcitabine in
136 itumor activity of vandetanib monotherapy or vandetanib with paclitaxel and carboplatin (VPC) was com
137 was developed from an antitumor drug ZD6474 (Vandetanib) with combined hybrid binding effects, yielde

 
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