PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29517106-7 2018 Vandetanib (25 mg/kg/day) significantly inhibited tumor growth and VEGF-A expression and microvessel density in 8305C tumor tissues. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 67-73 30555244-0 2018 Vandetanib (ZD6474) induces antiangiogenesis through mTOR-HIF-1 alpha-VEGF signaling axis in breast cancer cells. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 70-74 30555244-0 2018 Vandetanib (ZD6474) induces antiangiogenesis through mTOR-HIF-1 alpha-VEGF signaling axis in breast cancer cells. vandetanib 12-18 vascular endothelial growth factor A Homo sapiens 70-74 30555244-9 2018 Vandetanib can reduce both mRNA and protein level of mTOR, HIF-1 alpha, and VEGF. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 76-80 30555244-12 2018 Conclusion: In short, our study showed that vandetanib can control angiogenesis of breast cancer in culture via mTOR, HIF-1 alpha, and VEGF signaling pathway. vandetanib 44-54 vascular endothelial growth factor A Homo sapiens 135-139 31258881-3 2019 We found that administration of the angiogenesis inhibitor vandetanib completely abolished miR-9-induced angiogenesis and promoted autophagy in HUVECs, but induced the release of vascular endothelial growth factor (VEGF)-enriched exosomes. vandetanib 59-69 vascular endothelial growth factor A Homo sapiens 179-213 31258881-3 2019 We found that administration of the angiogenesis inhibitor vandetanib completely abolished miR-9-induced angiogenesis and promoted autophagy in HUVECs, but induced the release of vascular endothelial growth factor (VEGF)-enriched exosomes. vandetanib 59-69 vascular endothelial growth factor A Homo sapiens 215-219 25684635-4 2015 KEY RESULTS: VEGF(165)a produced a concentration-dependent activation of the NFAT-luciferase reporter gene in living cells that was inhibited in a non-competitive fashion by four different RTKIs (cediranib, pazopanib, sorafenib and vandetanib). vandetanib 232-242 vascular endothelial growth factor A Homo sapiens 13-17 28413487-0 2017 Vandetanib and ADAM inhibitors synergistically attenuate the pathological migration of EBV-infected retinal pigment epithelial cells by regulating the VEGF-mediated MAPK pathway. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 151-155 28413487-2 2017 Vandetanib is an oral anticancer drug that selectively inhibits the activities of VEGF receptor and epidermal growth factor receptor tyrosine kinase; however, the effects of vandetanib on VEGF in retinal pigment epithelial (RPE) cells have not yet been studied. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 82-86 28413487-2 2017 Vandetanib is an oral anticancer drug that selectively inhibits the activities of VEGF receptor and epidermal growth factor receptor tyrosine kinase; however, the effects of vandetanib on VEGF in retinal pigment epithelial (RPE) cells have not yet been studied. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 188-192 28413487-5 2017 The migratory activity of ARPE19/EBV induced by VEGF was efficiently blocked by vandetanib. vandetanib 80-90 vascular endothelial growth factor A Homo sapiens 48-52 26715573-1 2016 BACKGROUND: Vandetanib is a multitargeted tyrosine kinase inhibitor that affects vascular endothelial growth factor receptor (VEGF), epidermal growth factor (EGF), and rearranged during transfection (RET) mediated receptors which are important for growth and invasion of biliary and pancreatic cancers. vandetanib 12-22 vascular endothelial growth factor A Homo sapiens 81-124 26715573-1 2016 BACKGROUND: Vandetanib is a multitargeted tyrosine kinase inhibitor that affects vascular endothelial growth factor receptor (VEGF), epidermal growth factor (EGF), and rearranged during transfection (RET) mediated receptors which are important for growth and invasion of biliary and pancreatic cancers. vandetanib 12-22 vascular endothelial growth factor A Homo sapiens 126-130 26832420-2 2016 Oral tyrosine kinase inhibitors (TKI) targeting the VEGF receptor, including sunitinib, sorafenib, axitinib, regorafenib, pazopanib, and vandetanib reduce tumor growth and metastasis. vandetanib 137-147 vascular endothelial growth factor A Homo sapiens 52-56 26677336-3 2015 Novel antiangiogenic agents, such as sunitinib, sorafenib, pazopanib, or vandetanib that target additional proangiogenic signaling pathways beyond VEGF, have also been approved for the treatment of various malignant diseases. vandetanib 73-83 vascular endothelial growth factor A Homo sapiens 147-151 27983649-3 2016 Meanwhile, several of the above compounds demonstrated better bioactivity than vandetanib in VEGF gene expression inhibition. vandetanib 79-89 vascular endothelial growth factor A Homo sapiens 93-97 27429741-4 2016 Vandetanib and cabozantinib, both multi-kinase inhibitors with RET activity, are approved for use in medullary thyroid carcinoma, but additional pharmacological activities, most notably inhibition of vascular endothelial growth factor - VEGFR2 (KDR), lead to dose-limiting toxicity. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 200-234 22415301-8 2012 This loop is functionally impeded by the VEGF receptor inhibitor vandetanib, and our results may contribute to the further development of inhibitors of tumor-angiogenesis. vandetanib 65-75 vascular endothelial growth factor A Homo sapiens 41-45 23856028-2 2013 For MTC therapy, the Food and Drug Administration recently approved vandetanib and cabozantinib, multi-kinase inhibitors targeting RET and other tyrosine kinase receptors of vascular endothelial growth factor, epidermal growth factor, or hepatocyte growth factor. vandetanib 68-78 vascular endothelial growth factor A Homo sapiens 174-208 24913066-4 2014 We report the final results of a single-arm phase II clinical trial of the VEGF receptor inhibitor, vandetanib, combined with intrapleural catheter placement in patients with non-small-cell lung cancer and recurrent malignant pleural effusion, to determine whether vandetanib reduces time to pleurodesis. vandetanib 100-110 vascular endothelial growth factor A Homo sapiens 75-79 24913066-4 2014 We report the final results of a single-arm phase II clinical trial of the VEGF receptor inhibitor, vandetanib, combined with intrapleural catheter placement in patients with non-small-cell lung cancer and recurrent malignant pleural effusion, to determine whether vandetanib reduces time to pleurodesis. vandetanib 265-275 vascular endothelial growth factor A Homo sapiens 75-79 24671507-9 2014 Treatment with vandetanib was associated with a reduction in soluble VEGFR-2 levels after two cycles but an increase in plasma VEGF levels. vandetanib 15-25 vascular endothelial growth factor A Homo sapiens 69-73 24924416-3 2014 We assessed whether vandetanib, an inhibitor of VEGF, epidermal growth factor receptor and RET signalling, improved uNTx response when added to fulvestrant (F) in breast cancer patients with bone metastases. vandetanib 20-30 vascular endothelial growth factor A Homo sapiens 48-52 24089699-0 2013 Specific binding of modified ZD6474 (Vandetanib) monomer and its dimer with VEGF receptor-2. vandetanib 29-35 vascular endothelial growth factor A Homo sapiens 76-80 24089699-0 2013 Specific binding of modified ZD6474 (Vandetanib) monomer and its dimer with VEGF receptor-2. vandetanib 37-47 vascular endothelial growth factor A Homo sapiens 76-80 23766359-2 2013 Vandetanib, a VEGF and EGF receptor inhibitor, blocks RET tyrosine kinase activity and is active in adults with hereditary MTC. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 14-45 21404105-1 2012 BACKGROUND: Vandetanib is a tyrosine kinase inhibitor of both the vascular endothelial growth factor (VEGFR) and epidermal growth factor (EGFR) receptors. vandetanib 12-22 vascular endothelial growth factor A Homo sapiens 66-100 21404105-1 2012 BACKGROUND: Vandetanib is a tyrosine kinase inhibitor of both the vascular endothelial growth factor (VEGFR) and epidermal growth factor (EGFR) receptors. vandetanib 12-22 vascular endothelial growth factor A Homo sapiens 102-107 20811684-9 2010 In comparison, mesenchymal cells demonstrated decreased vimentin expression with the treatment of vandetanib in the presence of EGF and VEGF. vandetanib 98-108 vascular endothelial growth factor A Homo sapiens 136-140 22245891-10 2012 Vandetanib induced a significant increase in circulating VEGF and decrease in circulating VEGFR levels. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 57-61 21390182-10 2011 The expression of VEGF in tumor tissues was upregulated by vandetanib and metronomic S-1 with vandetanib, whereas the expression of thrombospondin-1 was upregulated by metronomic S-1 and metronomic S-1 with vandetanib. vandetanib 59-69 vascular endothelial growth factor A Homo sapiens 18-22 21390182-10 2011 The expression of VEGF in tumor tissues was upregulated by vandetanib and metronomic S-1 with vandetanib, whereas the expression of thrombospondin-1 was upregulated by metronomic S-1 and metronomic S-1 with vandetanib. vandetanib 94-104 vascular endothelial growth factor A Homo sapiens 18-22 21390182-10 2011 The expression of VEGF in tumor tissues was upregulated by vandetanib and metronomic S-1 with vandetanib, whereas the expression of thrombospondin-1 was upregulated by metronomic S-1 and metronomic S-1 with vandetanib. vandetanib 94-104 vascular endothelial growth factor A Homo sapiens 18-22 21106730-6 2011 To overcome tumor resistance, L19mTNFalpha scFv was combined with vandetanib, a tyrosine kinase inhibitor of VEGF receptor, epidermal growth factor receptor, and RET signaling. vandetanib 66-76 vascular endothelial growth factor A Homo sapiens 109-113 21095630-13 2012 The presence of EGFR augmented RT-stimulated VEGF release; this effect was inhibited by vandetanib. vandetanib 88-98 vascular endothelial growth factor A Homo sapiens 45-49 22701615-9 2012 Vandetanib and cetuximab treatment induced a sustained increase in plasma PlGF and a transient decrease in plasma sVEGFR1, but no changes in plasma VEGF and sVEGFR2. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 115-119 21770481-1 2011 Vandetanib is an orally active antagonist of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2), epidermal growth factor receptor (EGFR or HER1 or ErbB1) and RET kinase, and is now available in the US for the treatment of metastatic medullary thyroid cancer (MTC). vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 45-79 21770481-1 2011 Vandetanib is an orally active antagonist of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2), epidermal growth factor receptor (EGFR or HER1 or ErbB1) and RET kinase, and is now available in the US for the treatment of metastatic medullary thyroid cancer (MTC). vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 81-85 19949019-8 2010 For example, increases in IL-8 with VCP, MMP-9 with CP, and VEGF with vandetanib monotherapy were associated with increased progression risk, and increase in intercellular adhesion molecule 1 with vandetanib was associated with decreased risk. vandetanib 70-80 vascular endothelial growth factor A Homo sapiens 60-64 20571071-4 2010 Small molecule tyrosine kinase inhibitors (TKI) targeting the VEGF receptor (i.e., sunitinib, sorafenib, and vandetanib) show activity in phase II clinical studies. vandetanib 109-119 vascular endothelial growth factor A Homo sapiens 62-66 20031962-8 2010 However, clinical development of small molecule multi-kinase inhibitors including those targeting vascular endothelial growth factor receptors, such as vandetanib, sunitinib and sorafenib, has not been very successful. vandetanib 152-162 vascular endothelial growth factor A Homo sapiens 98-132 19002384-1 2009 BACKGROUND: Vandetanib (ZACTIMA) is a once-daily oral inhibitor of vascular endothelial growth factor, epidermal growth factor and RET receptor tyrosine kinases. vandetanib 12-22 vascular endothelial growth factor A Homo sapiens 67-101 19883226-9 2009 The observation that vandetanib causes an early increase in tumor oxygenation has implications for the timing and sequencing of treatment with VEGF signaling inhibitors in combination with radiation. vandetanib 21-31 vascular endothelial growth factor A Homo sapiens 143-147 19519336-9 2009 ZD6474, a small molecule targeting VEGF tyrosine-kinase activity, showing early evidence of antitumour activity and the excellent toxicity profile, seems to be a promising agent for the treatment of advanced NSCLC. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 35-39 19447868-1 2009 PURPOSE: Vandetanib [vascular endothelial growth factor (VEGF) receptor/epidermal growth factor receptor/RET inhibitor] has shown improvements in progression-free survival (PFS) in advanced non-small cell lung cancer in three randomized phase II studies: vandetanib versus gefitinib (study 3), docetaxel +/- vandetanib (study 6), and carboplatin-paclitaxel and/or vandetanib (study 7). vandetanib 308-318 vascular endothelial growth factor A Homo sapiens 21-55 19447868-0 2009 Baseline vascular endothelial growth factor concentration as a potential predictive marker of benefit from vandetanib in non-small cell lung cancer. vandetanib 107-117 vascular endothelial growth factor A Homo sapiens 9-43 19447868-6 2009 RESULTS: Patients with low baseline VEGF had a lower risk of disease progression with vandetanib versus gefitinib [hazard ratio (HR), 0.55; 95% confidence interval (95% CI), 0.35-0.86; P = 0.01] or vandetanib 100 mg/d + docetaxel versus docetaxel (HR, 0.25; 95% CI, 0.09-0.68; P = 0.01). vandetanib 86-96 vascular endothelial growth factor A Homo sapiens 36-40 19447868-1 2009 PURPOSE: Vandetanib [vascular endothelial growth factor (VEGF) receptor/epidermal growth factor receptor/RET inhibitor] has shown improvements in progression-free survival (PFS) in advanced non-small cell lung cancer in three randomized phase II studies: vandetanib versus gefitinib (study 3), docetaxel +/- vandetanib (study 6), and carboplatin-paclitaxel and/or vandetanib (study 7). vandetanib 9-19 vascular endothelial growth factor A Homo sapiens 21-55 19447868-6 2009 RESULTS: Patients with low baseline VEGF had a lower risk of disease progression with vandetanib versus gefitinib [hazard ratio (HR), 0.55; 95% confidence interval (95% CI), 0.35-0.86; P = 0.01] or vandetanib 100 mg/d + docetaxel versus docetaxel (HR, 0.25; 95% CI, 0.09-0.68; P = 0.01). vandetanib 198-208 vascular endothelial growth factor A Homo sapiens 36-40 19447868-1 2009 PURPOSE: Vandetanib [vascular endothelial growth factor (VEGF) receptor/epidermal growth factor receptor/RET inhibitor] has shown improvements in progression-free survival (PFS) in advanced non-small cell lung cancer in three randomized phase II studies: vandetanib versus gefitinib (study 3), docetaxel +/- vandetanib (study 6), and carboplatin-paclitaxel and/or vandetanib (study 7). vandetanib 9-19 vascular endothelial growth factor A Homo sapiens 57-61 19447868-1 2009 PURPOSE: Vandetanib [vascular endothelial growth factor (VEGF) receptor/epidermal growth factor receptor/RET inhibitor] has shown improvements in progression-free survival (PFS) in advanced non-small cell lung cancer in three randomized phase II studies: vandetanib versus gefitinib (study 3), docetaxel +/- vandetanib (study 6), and carboplatin-paclitaxel and/or vandetanib (study 7). vandetanib 255-265 vascular endothelial growth factor A Homo sapiens 21-55 19447868-1 2009 PURPOSE: Vandetanib [vascular endothelial growth factor (VEGF) receptor/epidermal growth factor receptor/RET inhibitor] has shown improvements in progression-free survival (PFS) in advanced non-small cell lung cancer in three randomized phase II studies: vandetanib versus gefitinib (study 3), docetaxel +/- vandetanib (study 6), and carboplatin-paclitaxel and/or vandetanib (study 7). vandetanib 308-318 vascular endothelial growth factor A Homo sapiens 21-55 19447868-7 2009 High VEGF patients had a similar risk of disease progression with vandetanib monotherapy versus gefitinib (HR, 1.03; 95% CI, 0.60-1.75; P = 0.92) or vandetanib 100 mg/d + docetaxel versus docetaxel (HR, 0.95; 95% CI, 0.25-3.61; P = 0.94). vandetanib 66-76 vascular endothelial growth factor A Homo sapiens 5-9 19447868-7 2009 High VEGF patients had a similar risk of disease progression with vandetanib monotherapy versus gefitinib (HR, 1.03; 95% CI, 0.60-1.75; P = 0.92) or vandetanib 100 mg/d + docetaxel versus docetaxel (HR, 0.95; 95% CI, 0.25-3.61; P = 0.94). vandetanib 149-159 vascular endothelial growth factor A Homo sapiens 5-9 19447868-8 2009 In study 7, low VEGF patients had a similar risk of disease progression with vandetanib monotherapy 300 mg/d versus carboplatin-paclitaxel (HR, 0.80; 95% CI, 0.41-1.56; P = 0.51); high VEGF patients progressed more quickly (HR, 1.60; 95% CI, 0.81-3.15; P = 0.17). vandetanib 77-87 vascular endothelial growth factor A Homo sapiens 16-20 19447868-9 2009 CONCLUSIONS: These analyses suggest that low baseline circulating VEGF may be predictive of PFS advantage in patients with advanced non-small cell lung cancer receiving vandetanib versus gefitinib or vandetanib + docetaxel versus docetaxel. vandetanib 169-179 vascular endothelial growth factor A Homo sapiens 66-70 19447868-9 2009 CONCLUSIONS: These analyses suggest that low baseline circulating VEGF may be predictive of PFS advantage in patients with advanced non-small cell lung cancer receiving vandetanib versus gefitinib or vandetanib + docetaxel versus docetaxel. vandetanib 200-210 vascular endothelial growth factor A Homo sapiens 66-70 19447868-10 2009 Moreover, patients with low VEGF levels may have a similar outcome with either vandetanib monotherapy or carboplatin-paclitaxel. vandetanib 79-89 vascular endothelial growth factor A Homo sapiens 28-32 19362942-7 2009 Dual inhibition of EGFR and VEGF pathways has also been accomplished by the novel agents vandetanib and XL647, which are able to target both pathways. vandetanib 89-99 vascular endothelial growth factor A Homo sapiens 28-32 18694994-5 2008 We found that the resistant cell lines exhibit, as common feature, VEGFR-1/Flt-1 overexpression, increased secretion of VEGF and placental growth factor, and augmented migration capabilities and that vandetanib is able to antagonize them. vandetanib 200-210 vascular endothelial growth factor A Homo sapiens 67-71 19747132-9 2009 Vandetanib, a small molecule targeting VEGF tyrosine-kinase activity, due to first indications of antitumor activity and the excellent toxicity profile seems to be a promising agent for the treatment of advanced NSCLC. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 39-43 18695882-10 2008 Interestingly, secretion of VEGF increased significantly in the MS-1-L cell line in the presence of a high dose of vandetanib in vitro. vandetanib 115-125 vascular endothelial growth factor A Homo sapiens 28-32 18379357-10 2008 Baseline plasma VEGF levels appeared to be lower in patients who experienced clinical benefit after vandetanib treatment. vandetanib 100-110 vascular endothelial growth factor A Homo sapiens 16-20 17145834-0 2006 Synergistic antitumor activity of ZD6474, an inhibitor of vascular endothelial growth factor receptor and epidermal growth factor receptor signaling, with gemcitabine and ionizing radiation against pancreatic cancer. vandetanib 34-40 vascular endothelial growth factor A Homo sapiens 58-92 18245671-8 2008 Immunohistochemical analysis showed that ZD6474 treatment led to an increase in endothelial cell apoptosis along with inhibition of VEGF receptor-2 activation on tumor endothelium. vandetanib 41-47 vascular endothelial growth factor A Homo sapiens 132-136 17671152-0 2007 Vascular endothelial growth factor receptor tyrosine kinase inhibitors vandetanib (ZD6474) and AZD2171 in lung cancer. vandetanib 71-81 vascular endothelial growth factor A Homo sapiens 0-34 17671152-0 2007 Vascular endothelial growth factor receptor tyrosine kinase inhibitors vandetanib (ZD6474) and AZD2171 in lung cancer. vandetanib 83-89 vascular endothelial growth factor A Homo sapiens 0-34 17203163-8 2007 These results suggest that ZD6474 has the potential to inhibit two key pathways in tumor growth via inhibition of VEGF-dependent tumor angiogenesis and via inhibition of EGFR-dependent tumor cell proliferation. vandetanib 27-33 vascular endothelial growth factor A Homo sapiens 114-118 17308046-7 2007 In vitro, ZD6474 inhibited EGFR, VEGFR2, mitogen-activated protein kinase and Akt phosphorylation, EGF- and VEGF-induced proliferation, and endothelial cell tube formation and also induced apoptosis. vandetanib 10-16 vascular endothelial growth factor A Homo sapiens 33-37 15928653-1 2005 ZD6474 selectively targets two key pathways in tumour growth by inhibiting vascular endothelial growth factor (VEGF)-dependent tumour angiogenesis and epidermal growth factor (EGF)-dependent tumour cell proliferation and survival. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 75-109 15905307-0 2005 Clinical evaluation of ZD6474, an orally active inhibitor of VEGF and EGF receptor signaling, in patients with solid, malignant tumors. vandetanib 23-29 vascular endothelial growth factor A Homo sapiens 61-65 16640800-2 2006 These include the small-molecule receptor tyrosine kinase (TK) inhibitors ZD6474, sorafenib, sunitinib malate, and AG-013736, all of which inhibit VEGF receptor TK activity. vandetanib 74-80 vascular endothelial growth factor A Homo sapiens 147-151 16332356-2 2006 Recently, it has been demonstrated that an inhibitor of the vascular endothelial growth factor (VEGF) receptor, ZD6474, may directly inhibit the growth of tumor cells. vandetanib 112-118 vascular endothelial growth factor A Homo sapiens 60-94 16332356-2 2006 Recently, it has been demonstrated that an inhibitor of the vascular endothelial growth factor (VEGF) receptor, ZD6474, may directly inhibit the growth of tumor cells. vandetanib 112-118 vascular endothelial growth factor A Homo sapiens 96-100 16377413-4 2006 This article focuses on ZD6474, an inhibitor of EGFR and VEGF receptor signaling in combination with RT. vandetanib 24-30 vascular endothelial growth factor A Homo sapiens 57-61 15928653-1 2005 ZD6474 selectively targets two key pathways in tumour growth by inhibiting vascular endothelial growth factor (VEGF)-dependent tumour angiogenesis and epidermal growth factor (EGF)-dependent tumour cell proliferation and survival. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 111-115 15928657-3 2005 ZD6474 is an orally bioavailable inhibitor of VEGF receptor-2 tyrosine kinase activity that in preclinical studies has been shown to inhibit both VEGF-induced signalling in endothelial cells and tumour-induced angiogenesis. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 46-50 15928657-3 2005 ZD6474 is an orally bioavailable inhibitor of VEGF receptor-2 tyrosine kinase activity that in preclinical studies has been shown to inhibit both VEGF-induced signalling in endothelial cells and tumour-induced angiogenesis. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 146-150 15655420-18 2005 A few VEGF-tyrosine kinase inhibiting small molecules, such as ZD6474, AZD2171 and PTK/ZK, are undergoing clinical trials. vandetanib 63-69 vascular endothelial growth factor A Homo sapiens 6-10 22608542-12 2013 The use of high-dose vandetanib alone may warrant further investigation in patients with docetaxel-resistant AIPC overexpressing VEGFR/EGFR pathways. vandetanib 21-31 vascular endothelial growth factor A Homo sapiens 129-134 15596048-0 2004 Anticancer effects of ZD6474, a VEGF receptor tyrosine kinase inhibitor, in gefitinib ("Iressa")-sensitive and resistant xenograft models. vandetanib 22-28 vascular endothelial growth factor A Homo sapiens 32-36 12684431-0 2003 Antitumor effects of ZD6474, a small molecule vascular endothelial growth factor receptor tyrosine kinase inhibitor, with additional activity against epidermal growth factor receptor tyrosine kinase. vandetanib 21-27 vascular endothelial growth factor A Homo sapiens 46-80 12457433-4 2002 Current efforts have resulted in promising clinical data for several synthetic VEGF receptor kinase inhibitors, of which PTK787/ZK222584 and ZD6474 are proceeding into large size clinical trials. vandetanib 141-147 vascular endothelial growth factor A Homo sapiens 79-83 12183421-4 2002 The activity of ZD6474 versus KDR tyrosine kinase translates into potent inhibition of vascular endothelial growth factor-A (VEGF)-stimulated endothelial cell (human umbilical vein endothelial cell) proliferation in vitro (IC(50) = 60 nM). vandetanib 16-22 vascular endothelial growth factor A Homo sapiens 87-123 12183421-4 2002 The activity of ZD6474 versus KDR tyrosine kinase translates into potent inhibition of vascular endothelial growth factor-A (VEGF)-stimulated endothelial cell (human umbilical vein endothelial cell) proliferation in vitro (IC(50) = 60 nM). vandetanib 16-22 vascular endothelial growth factor A Homo sapiens 125-129 15623642-0 2004 ZD6474, a potent inhibitor of vascular endothelial growth factor signaling, combined with radiotherapy: schedule-dependent enhancement of antitumor activity. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 30-64 15623642-2 2004 ZD6474 (N-(4-bromo-2-fluorophenyl)-6-methoxy-7-[(1-methylpiperidin-4-yl)methoxy]quinazolin-4-amine) is a potent VEGF receptor 2 (KDR) tyrosine kinase inhibitor (TKI) that has additional activity versus the epidermal growth factor receptor. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 112-116 15623642-2 2004 ZD6474 (N-(4-bromo-2-fluorophenyl)-6-methoxy-7-[(1-methylpiperidin-4-yl)methoxy]quinazolin-4-amine) is a potent VEGF receptor 2 (KDR) tyrosine kinase inhibitor (TKI) that has additional activity versus the epidermal growth factor receptor. vandetanib 8-98 vascular endothelial growth factor A Homo sapiens 112-116 15367698-0 2004 ZD6474, a vascular endothelial growth factor receptor tyrosine kinase inhibitor with additional activity against epidermal growth factor receptor tyrosine kinase, inhibits orthotopic growth and angiogenesis of gastric cancer. vandetanib 0-6 vascular endothelial growth factor A Homo sapiens 10-44 33929994-6 2021 Vandetanib also suppressed the hypoxia-induced secretion of VEGF from HCC cells and inhibited proliferation of endothelial cells. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 60-64 33296710-1 2021 Vandetanib (ZD6474, Zactima , Caprelsa ) is a newly developed dual tyrosine kinase inhibitor of vascular endothelial growth factor and epidermal growth factor receptor. vandetanib 0-10 vascular endothelial growth factor A Homo sapiens 96-130 33296710-1 2021 Vandetanib (ZD6474, Zactima , Caprelsa ) is a newly developed dual tyrosine kinase inhibitor of vascular endothelial growth factor and epidermal growth factor receptor. vandetanib 12-18 vascular endothelial growth factor A Homo sapiens 96-130