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1 r endothelial growth factor receptor blocker SU5416.
2 he administration of VEGF receptor inhibitor SU5416.
3  established PH in rats with chronic hypoxia/SU5416.
4 ulmonary hypertension that is exacerbated by SU5416.
5 ension following exposure to chronic hypoxia/SU5416.
6  apoptosis, which was further accentuated by SU5416.
7 phorylation of ERK1/2; this was inhibited by SU5416.
8 /+) mice were exposed to chronic hypoxia and SU5416.
9 db mice but was significantly ameliorated by SU5416.
10 lly increased in diabetes, was unaffected by SU5416.
11 db/db mice but was significantly restored by SU5416.
12 es but was partly increased toward normal by SU5416.
13 2) synthesis may represent novel targets for SU5416.
14 eration of MO7E cells (IC(50) 0.1 microM for SU5416; 0.29 microM for SU6668).
15               PH was induced in male rats by SU5416 (25 mg/kg subcutaneously) injection followed by 4
16  demonstrated that VEGF receptor blockade by SU5416 {3-[(2,4-dimethylpyrrol-5-yl)methylidenyl]-indoli
17                                              SU5416 (5 micro M) inhibited endogenous as well as PMA-m
18 proliferation was inhibited by rapamycin and SU5416 (a vascular endothelial growth factor receptor 2
19                                              SU5416, a novel synthetic compound, is a potent and sele
20 BM); this effect was completely prevented by SU5416, a pan-VEGF receptor inhibitor.
21 eceptor-expressing Jurkat T cell line and by SU5416, a pharmacological KDR inhibitor, in CD4+CD45RO+
22                                              SU5416, a potent inhibitor of the VEGF receptor I (VEGFR
23 phosphorylation was completely suppressed by SU5416, a small-molecule VEGFR2 kinase inhibitor.
24 62 tumors in the liver, 10 were treated with SU5416, a tyrosine kinase inhibitor of vascular endothel
25                                              SU5416, a VEGF receptor tyrosine kinase inhibitor, only
26                                 In addition, SU5416, a VEGFR2 inhibitor, was used to induce emphysema
27 tivation by siRNA transfection or semaxanib (SU5416) abolished VEGFA-induced proliferation of ECs and
28 d initial apoptosis (35.8% at 24 h after the SU5416 addition and 4.8% in control cells) whereas the s
29 icrovascular endothelial cells (HPMVEC) with SU5416 and analyzed these cells utilizing quantitative-P
30 ry hypertension caused by the combination of SU5416 and chronic hypoxia.
31                              Both inhibitors SU5416 and LY294002 attenuated EVs-induced EC migration.
32                             We conclude that SU5416 and SU5614 are potent inhibitors of FLT3.
33                           FLT3 inhibition by SU5416 and SU5614 resulted in reduced proliferation (IC(
34                                         Both SU5416 and SU5614 were capable of inhibiting autophospho
35               Of the six compounds examined, SU5416 and SU6597 demonstrated the best cellular potency
36                                              SU5416 and SU6668 are potent antiangiogenic small-molecu
37 uced by SCF, was inhibited in these cells by SU5416 and SU6668 in a dose-dependent manner (inhibitory
38                            Furthermore, both SU5416 and SU6668 induced apoptosis in a dose- and time-
39                  These studies indicate that SU5416 and SU6668 inhibit biologic functions of c-kit in
40                      In patient blasts, both SU5416 and SU6668 inhibited SCF-induced phosphorylation
41                                              SU5416 and SU6668 respectively inhibited metastases (48.
42      The c-kit kinase inhibitory activity of SU5416 and SU6668 was evaluated in MO7E cells, a human m
43 regimes combining the two kinase inhibitors (SU5416 and SU6668) were more efficacious against all sta
44 was inhibited by the VEGF receptor inhibitor SU5416 at doses that are specific for VEGF receptor 1 (V
45      In contrast, systemic administration of SU5416 at nontoxic doses in mice resulted in inhibition
46 Inhibiting VEGF signaling using anti-VEGF or SU5416 attenuates type 1 diabetes-induced glomerular inj
47 e VEGFR2-specific tyrosine kinase inhibitor, SU5416, blocked this effect.
48 exin-V and BrdU supported our concept, since SU5416 caused initial apoptosis (35.8% at 24 h after the
49 th pulmonary arterial hypertension (PAH-RVH; SU5416+chronic-hypoxia or Monocrotaline) versus pulmonar
50 , in mice treated with TRC105, or TRC105 and SU5416 combined, a strong inhibition in the number of me
51 ting autophosphorylation of ITD and WT FLT3 (SU5416 concentration that inhibits 50% [IC(50)], 100 nM;
52 sion were reduced compared with the normoxia/SU5416 control group.
53  determine whether an angiogenic antagonist, SU5416, could inhibit endogenous and phorbol 12-myristat
54 xygen species by blocking NADPH oxidase with SU5416, COX-2 expression and PGE(2) synthesis were also
55                          Although TRC105 and SU5416 decreased tumor vascular density, tumor volume wa
56 emlin 1 neutralizing mAb reduced the hypoxic/SU5416-dependent increase in pulmonary vascular remodeli
57  Both sFlk-1 and the Flk-1-specifc inhibitor SU5416 eliminated the resistance phenotype in GBM and me
58                                              SU5416 expanded the number of CD34 and/or c-kit positive
59 xamined the development of PAH after hypoxic/SU5416 exposure in Tph1-deficient mice (Tph1(-/-)).
60                              Chronic hypoxic/SU5416 exposure of mice induced upregulation of Gremlin
61                                        After SU5416 exposure, EC Hif-2alpha-knockout mice developed m
62 ain of collagen IV, alpha5(IV) collagen, and SU5416 failed to reverse the known inhibitory effect of
63            In conclusion, our data show that SU5416 generated a selection pressure that killed some E
64                                 Single agent SU5416 had biologic and modest clinical activity in refr
65 lective ILK inhibitor Cpd22 at Days 22-35 of SU5416/hypoxia exposure restored LATS1 signaling and red
66             PH was induced in rats using the SU5416/hypoxia model (Su/Hx), followed by 6-week treatme
67 ental models of PAH (i.e., monocrotaline and Su5416/hypoxia treated rats) palbociclib reverses the el
68                            The model of RVD (SU5416/hypoxia) exhibited a significantly decreased gene
69  of the peptide in monocrotaline-induced and SU5416/hypoxia-induced hypertensive lungs but not in hea
70  small remodeled PAs from rats and mice with SU5416/hypoxia-induced PH showed down-regulation of LATS
71 athic PAH lungs, and rat and mouse models of SU5416/hypoxia-induced pulmonary hypertension (PH) were
72 evere pulmonary vascular leak and hypoxia or SU5416/hypoxia-induced pulmonary hypertension.
73 kt-mTORC1 in small muscular PAs of mice with SU5416/hypoxia-induced pulmonary hypertension.
74 ling and pulmonary hypertension in mice with SU5416/hypoxia-induced pulmonary hypertension.
75 416/hypoxia-treated Sprague-Dawley rats, and SU5416/hypoxia-treated C57BL/6 mice.
76 eated rats, SU5416/hypoxia-treated rats, and SU5416/hypoxia-treated mice.
77 on of TGFBRII-Fc to monocrotaline-treated or SU5416/hypoxia-treated rats with established PH improved
78 ar remodeling in monocrotaline-treated rats, SU5416/hypoxia-treated rats, and SU5416/hypoxia-treated
79 n monocrotaline-treated Sprague-Dawley rats, SU5416/hypoxia-treated Sprague-Dawley rats, and SU5416/h
80 henotyped in response to chronic hypoxia and SU5416/hypoxia.
81 zation in mice exposed to chronic hypoxia or SU5416/hypoxia.
82  demonstrate here that VEGFR-2 blockade with SU5416 in combination with chronic hypobaric hypoxia cau
83 othelial growth factor (VEGF) receptors with SU5416 in mice, a model of apoptosis-dependent emphysema
84 in disease after exposure to chronic hypoxia/SU5416 in mice.
85 way, with the VEGF receptor kinase inhibitor SU5416, increased antiangiogenic effects in vitro and in
86                  The VEGF receptor inhibitor SU5416 induced alveolar septal cell apoptosis but did no
87  monocrotaline-induced rat model and hypoxia/Su5416-induced mouse model, were used in this study.
88  caspase inhibitor Z-Asp-CH(2)-DCB prevented SU5416-induced septal cell apoptosis and emphysema devel
89 ts with nitrite and metformin at the time of SU5416 injection reduced pulmonary pressures and vascula
90                                              SU5416 is a small molecule RTK inhibitor (RTKI) of VEGFR
91 bitor targeting VEGFRs in endothelial cells (SU5416) is effective against early-stage angiogenic lesi
92 tment of rats with the VEGF receptor blocker SU5416 led to enlargement of the air spaces, indicative
93 n fact, inhibiting VEGF-A using anti-VEGF or SU5416 markedly attenuated diabetes-induced glomerular i
94 easures of PAH pathology observed in hypoxia/SU5416 mice.
95 logic processes, VEGF receptor inhibition by SU5416 might become a useful adjunct to anti-albuminuria
96  arterial hypertension in the murine hypoxia/SU5416 model, and that Gremlin 1 is a potential therapeu
97 mic sclerosis-associated PAH and the hypoxia/SU5416 mouse model identified the presence von Willebran
98  molecular signatures in the chronic hypoxia/SU5416 murine model of PAH.
99 1 monoclonal antibody in the chronic hypoxia/SU5416 murine model of pulmonary arterial hypertension.
100 lar breast cancer, the effects of TRC105 and SU5416 on tumor growth and metastasis were explored.
101 e the effects of a VEGF receptor antagonist (SU5416) on human pulmonary microvascular endothelial cel
102 periments, T1D rats were treated with either SU5416 or humanized monoclonal anti-VEGF-A neutralizing
103 y the KDR tyrosine kinase inhibitor compound SU5416 or inhibitors of endosomal acidification.
104 le, tyrosine kinase inhibitor for Flk-1/KDR (SU5416) or tyrosine kinase inhibitor for VEGF, basic fib
105 ificantly attenuated hypoxic PAH and hypoxic+SU5416 PAH in vivo.
106  CYP1B1 is increased in hypoxic PAH, hypoxic+SU5416 PAH, and human PAH and is highly expressed within
107                The selective flk-1 inhibitor SU5416 partially rescued the flt-1-/- mutant phenotype,
108 oxyl 35 castor oil or hyperosmolarity of the SU5416 preparation).
109 ased TCTP expression was also evident in the SU5416 rat model of severe and irreversible PAH, associa
110           Chronic hypoxia or chronic hypoxia/SU5416 rats were treated with the TLR3 agonist polyinosi
111 1 leukemia cells with the ITD-Flt3 inhibitor SU5416 reduced Survivin expression and inhibited cell pr
112  and SU groups received only microspheres or SU5416, respectively.
113             The Flk-1 antagonists sFlk-1 and SU5416 reverted these cell models to apoptosis-prone phe
114 yrosine kinase inhibitors such as SU6668 and SU5416 (semaxanib) demonstrated poor pharmacologic prope
115 g by the Flk-1/KDR receptor kinase inhibitor SU5416 significantly inhibited the growth of VR tumors.
116 d1KO mice, exposure to the VEGFR-2 inhibitor SU5416 significantly reduced liver cyst development, liv
117 icrospheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group.
118 In vitro studies in HPMVEC demonstrated that SU5416 suppressed PGI2S gene expression while potently i
119                  Following administration of SU5416, the pulmonary vascular phenotype was more florid
120 action model), obese ZSF-1 rats treated with SU5416 to stimulate resting pulmonary hypertension (obes
121 r organs, vascularity, and perfusion between SU5416-treated and control tumors.
122 ent membrane thickening was prevented in the SU5416-treated db/db mice, whereas mesangial matrix expa
123                       Viewed by angiography, SU5416-treated rat lungs showed a pruning of the pulmona
124             Similar results were obtained in SU5416-treated rats given human alpha1-antitrypsin intra
125 y hypertension, lungs of chronically hypoxic SU5416-treated rats show significant pulmonary endotheli
126 r of metastases, respectively, were lower in SU5416-treated rats than in control rats (1580 mm3 +/- 8
127 ovascular density was significantly lower in SU5416-treated rats than in control rats (6.4 vessels pe
128 r = 0.25, respectively; P < .01 for both) in SU5416-treated tumors but not control tumors.
129 t functional CT were significantly higher in SU5416-treated tumors than in control tumors (P < .001 f
130                                  Efficacy of SU5416 treatment in the kidney was verified by the inhib
131                                              SU5416 treatment led to a decrease in lung expression of
132 a creatinine did not change with diabetes or SU5416 treatment.
133 2 MDS: 15 [68%] relapsed) received 145 mg/m2 SU5416 twice weekly intravenously.
134 pan-VEGF receptor tyrosine kinase inhibitor, SU5416, twice a week for 8 wk.
135                      The antitumor effect of SU5416 was accompanied by the appearance of pale white t
136               A multicenter phase 2 study of SU5416 was conducted in patients with refractory AML or
137                                              SU5416 was shown to inhibit vascular endothelial growth
138 ling and hemodynamics in response to hypoxia/SU5416 were attenuated in Tph1(-/-) mice and further dec
139 ation of NADPH oxidase was also inhibited by SU5416, whereas an inhibitor of epidermal growth factor

 
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