ライフサイエンスコーパス: SU5416

1 ulmonary hypertension that is exacerbated by SU5416.

2 r endothelial growth factor receptor blocker SU5416.

3 apoptosis, which was further accentuated by SU5416.

4 phorylation of ERK1/2; this was inhibited by SU5416.

5 db mice but was significantly ameliorated by SU5416.

6 lly increased in diabetes, was unaffected by SU5416.

7 db/db mice but was significantly restored by SU5416.

8 es but was partly increased toward normal by SU5416.

9 2) synthesis may represent novel targets for SU5416.

10 eration of MO7E cells (IC(50) 0.1 microM for SU5416; 0.29 microM for SU6668).

11 PH was induced in male rats by SU5416 (25 mg/kg subcutaneously) injection followed by 4

12 demonstrated that VEGF receptor blockade by SU5416 {3-[(2,4-dimethylpyrrol-5-yl)methylidenyl]-indoli

13 SU5416 (5 micro M) inhibited endogenous as well as PMA-m

14 proliferation was inhibited by rapamycin and SU5416 (a vascular endothelial growth factor receptor 2

15 SU5416, a novel synthetic compound, is a potent and sele

16 BM); this effect was completely prevented by SU5416, a pan-VEGF receptor inhibitor.

17 eceptor-expressing Jurkat T cell line and by SU5416, a pharmacological KDR inhibitor, in CD4+CD45RO+

18 SU5416, a potent inhibitor of the VEGF receptor I (VEGFR

19 phosphorylation was completely suppressed by SU5416, a small-molecule VEGFR2 kinase inhibitor.

20 62 tumors in the liver, 10 were treated with SU5416, a tyrosine kinase inhibitor of vascular endothel

21 SU5416, a VEGF receptor tyrosine kinase inhibitor, only

22 tivation by siRNA transfection or semaxanib (SU5416) abolished VEGFA-induced proliferation of ECs and

23 d initial apoptosis (35.8% at 24 h after the SU5416 addition and 4.8% in control cells) whereas the s

24 icrovascular endothelial cells (HPMVEC) with SU5416 and analyzed these cells utilizing quantitative-P

25 ry hypertension caused by the combination of SU5416 and chronic hypoxia.

26 Both inhibitors SU5416 and LY294002 attenuated EVs-induced EC migration.

27 We conclude that SU5416 and SU5614 are potent inhibitors of FLT3.

28 FLT3 inhibition by SU5416 and SU5614 resulted in reduced proliferation (IC(

29 Both SU5416 and SU5614 were capable of inhibiting autophospho

30 Of the six compounds examined, SU5416 and SU6597 demonstrated the best cellular potency

31 SU5416 and SU6668 are potent antiangiogenic small-molecu

32 uced by SCF, was inhibited in these cells by SU5416 and SU6668 in a dose-dependent manner (inhibitory

33 Furthermore, both SU5416 and SU6668 induced apoptosis in a dose- and time-

34 These studies indicate that SU5416 and SU6668 inhibit biologic functions of c-kit in

35 In patient blasts, both SU5416 and SU6668 inhibited SCF-induced phosphorylation

36 SU5416 and SU6668 respectively inhibited metastases (48.

37 The c-kit kinase inhibitory activity of SU5416 and SU6668 was evaluated in MO7E cells, a human m

38 regimes combining the two kinase inhibitors (SU5416 and SU6668) were more efficacious against all sta

39 was inhibited by the VEGF receptor inhibitor SU5416 at doses that are specific for VEGF receptor 1 (V

40 In contrast, systemic administration of SU5416 at nontoxic doses in mice resulted in inhibition

41 e VEGFR2-specific tyrosine kinase inhibitor, SU5416, blocked this effect.

42 exin-V and BrdU supported our concept, since SU5416 caused initial apoptosis (35.8% at 24 h after the

43 th pulmonary arterial hypertension (PAH-RVH; SU5416+chronic-hypoxia or Monocrotaline) versus pulmonar

44 , in mice treated with TRC105, or TRC105 and SU5416 combined, a strong inhibition in the number of me

45 ting autophosphorylation of ITD and WT FLT3 (SU5416 concentration that inhibits 50% [IC(50)], 100 nM;

46 sion were reduced compared with the normoxia/SU5416 control group.

47 determine whether an angiogenic antagonist, SU5416, could inhibit endogenous and phorbol 12-myristat

48 xygen species by blocking NADPH oxidase with SU5416, COX-2 expression and PGE(2) synthesis were also

49 Although TRC105 and SU5416 decreased tumor vascular density, tumor volume wa

50 emlin 1 neutralizing mAb reduced the hypoxic/SU5416-dependent increase in pulmonary vascular remodeli

51 Both sFlk-1 and the Flk-1-specifc inhibitor SU5416 eliminated the resistance phenotype in GBM and me

52 SU5416 expanded the number of CD34 and/or c-kit positive

53 xamined the development of PAH after hypoxic/SU5416 exposure in Tph1-deficient mice (Tph1(-/-)).

54 Chronic hypoxic/SU5416 exposure of mice induced upregulation of Gremlin

55 ain of collagen IV, alpha5(IV) collagen, and SU5416 failed to reverse the known inhibitory effect of

56 In conclusion, our data show that SU5416 generated a selection pressure that killed some E

57 Single agent SU5416 had biologic and modest clinical activity in refr

58 lective ILK inhibitor Cpd22 at Days 22-35 of SU5416/hypoxia exposure restored LATS1 signaling and red

59 The model of RVD (SU5416/hypoxia) exhibited a significantly decreased gene

60 of the peptide in monocrotaline-induced and SU5416/hypoxia-induced hypertensive lungs but not in hea

61 small remodeled PAs from rats and mice with SU5416/hypoxia-induced PH showed down-regulation of LATS

62 athic PAH lungs, and rat and mouse models of SU5416/hypoxia-induced pulmonary hypertension (PH) were

63 416/hypoxia-treated Sprague-Dawley rats, and SU5416/hypoxia-treated C57BL/6 mice.

64 eated rats, SU5416/hypoxia-treated rats, and SU5416/hypoxia-treated mice.

65 on of TGFBRII-Fc to monocrotaline-treated or SU5416/hypoxia-treated rats with established PH improved

66 ar remodeling in monocrotaline-treated rats, SU5416/hypoxia-treated rats, and SU5416/hypoxia-treated

67 n monocrotaline-treated Sprague-Dawley rats, SU5416/hypoxia-treated Sprague-Dawley rats, and SU5416/h

68 zation in mice exposed to chronic hypoxia or SU5416/hypoxia.

69 demonstrate here that VEGFR-2 blockade with SU5416 in combination with chronic hypobaric hypoxia cau

70 othelial growth factor (VEGF) receptors with SU5416 in mice, a model of apoptosis-dependent emphysema

71 in disease after exposure to chronic hypoxia/SU5416 in mice.

72 way, with the VEGF receptor kinase inhibitor SU5416, increased antiangiogenic effects in vitro and in

73 The VEGF receptor inhibitor SU5416 induced alveolar septal cell apoptosis but did no

74 caspase inhibitor Z-Asp-CH(2)-DCB prevented SU5416-induced septal cell apoptosis and emphysema devel

75 ts with nitrite and metformin at the time of SU5416 injection reduced pulmonary pressures and vascula

76 SU5416 is a small molecule RTK inhibitor (RTKI) of VEGFR

77 bitor targeting VEGFRs in endothelial cells (SU5416) is effective against early-stage angiogenic lesi

78 tment of rats with the VEGF receptor blocker SU5416 led to enlargement of the air spaces, indicative

79 easures of PAH pathology observed in hypoxia/SU5416 mice.

80 logic processes, VEGF receptor inhibition by SU5416 might become a useful adjunct to anti-albuminuria

81 arterial hypertension in the murine hypoxia/SU5416 model, and that Gremlin 1 is a potential therapeu

82 mic sclerosis-associated PAH and the hypoxia/SU5416 mouse model identified the presence von Willebran

83 molecular signatures in the chronic hypoxia/SU5416 murine model of PAH.

84 1 monoclonal antibody in the chronic hypoxia/SU5416 murine model of pulmonary arterial hypertension.

85 lar breast cancer, the effects of TRC105 and SU5416 on tumor growth and metastasis were explored.

86 e the effects of a VEGF receptor antagonist (SU5416) on human pulmonary microvascular endothelial cel

87 y the KDR tyrosine kinase inhibitor compound SU5416 or inhibitors of endosomal acidification.

88 le, tyrosine kinase inhibitor for Flk-1/KDR (SU5416) or tyrosine kinase inhibitor for VEGF, basic fib

89 ificantly attenuated hypoxic PAH and hypoxic+SU5416 PAH in vivo.

90 CYP1B1 is increased in hypoxic PAH, hypoxic+SU5416 PAH, and human PAH and is highly expressed within

91 The selective flk-1 inhibitor SU5416 partially rescued the flt-1-/- mutant phenotype,

92 oxyl 35 castor oil or hyperosmolarity of the SU5416 preparation).

93 ased TCTP expression was also evident in the SU5416 rat model of severe and irreversible PAH, associa

94 1 leukemia cells with the ITD-Flt3 inhibitor SU5416 reduced Survivin expression and inhibited cell pr

95 and SU groups received only microspheres or SU5416, respectively.

96 The Flk-1 antagonists sFlk-1 and SU5416 reverted these cell models to apoptosis-prone phe

97 yrosine kinase inhibitors such as SU6668 and SU5416 (semaxanib) demonstrated poor pharmacologic prope

98 g by the Flk-1/KDR receptor kinase inhibitor SU5416 significantly inhibited the growth of VR tumors.

99 d1KO mice, exposure to the VEGFR-2 inhibitor SU5416 significantly reduced liver cyst development, liv

100 icrospheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group.

101 In vitro studies in HPMVEC demonstrated that SU5416 suppressed PGI2S gene expression while potently i

102 Following administration of SU5416, the pulmonary vascular phenotype was more florid

103 r organs, vascularity, and perfusion between SU5416-treated and control tumors.

104 ent membrane thickening was prevented in the SU5416-treated db/db mice, whereas mesangial matrix expa

105 Viewed by angiography, SU5416-treated rat lungs showed a pruning of the pulmona

106 Similar results were obtained in SU5416-treated rats given human alpha1-antitrypsin intra

107 y hypertension, lungs of chronically hypoxic SU5416-treated rats show significant pulmonary endotheli

108 r of metastases, respectively, were lower in SU5416-treated rats than in control rats (1580 mm3 +/- 8

109 ovascular density was significantly lower in SU5416-treated rats than in control rats (6.4 vessels pe

110 r = 0.25, respectively; P < .01 for both) in SU5416-treated tumors but not control tumors.

111 t functional CT were significantly higher in SU5416-treated tumors than in control tumors (P < .001 f

112 Efficacy of SU5416 treatment in the kidney was verified by the inhib

113 SU5416 treatment led to a decrease in lung expression of

114 a creatinine did not change with diabetes or SU5416 treatment.

115 2 MDS: 15 [68%] relapsed) received 145 mg/m2 SU5416 twice weekly intravenously.

116 pan-VEGF receptor tyrosine kinase inhibitor, SU5416, twice a week for 8 wk.

117 The antitumor effect of SU5416 was accompanied by the appearance of pale white t

118 A multicenter phase 2 study of SU5416 was conducted in patients with refractory AML or

119 SU5416 was shown to inhibit vascular endothelial growth

120 ling and hemodynamics in response to hypoxia/SU5416 were attenuated in Tph1(-/-) mice and further dec

121 ation of NADPH oxidase was also inhibited by SU5416, whereas an inhibitor of epidermal growth factor