ライフサイエンスコーパス: VEGF trap

1 VEGF-A and blocks its function (a so-called VEGF trap).

2 GFR-2 were highly susceptible to blockade by VEGF Trap.

3 EGF gene and receptor and the fusion protein VEGF trap.

4 t of plasma VEGF bound to VEGF Trap and free VEGF Trap.

5 VEGF antagonist now in clinical trials, the VEGF Trap.

6 even more potently than the VEGF antagonist, VEGF-trap.

7 ombinant adenovirus expressing (1) VEGF, (2) VEGF-trap, (3) VEGF plus VEGF-trap, or (4) control adeno

8 VEGF Trap (5, 25, or 250 mug) was injected intravitreall

9 VEGF-trap (72%), anti-VEGF-C (25%), and sVEGFR-3 (11%) a

10 ect VEGFA inhibition via antibody binding or VEGF trap (a soluble decoy receptor) is associated with

11 eceptors R1 (Flt-1), R2 (Flk-1), R3 (Flt-4), VEGF-Trap (a chimera of R1 and R2), or neutralizing anti

12 types to anti-VEGF therapy with Aflibercept (VEGF Trap), a potent inhibitor of VEGF-A(164).

13 study evaluated the efficacy of aflibercept (VEGF Trap), a recombinantly produced fusion protein that

14 n be effectively reversed by the addition of VEGF Trap, a potent VEGF antagonist.

15 We found that blockade of VEGF action with VEGF Trap, a potent VEGF blocker, completely inhibited n

16 Administration of VEGF Trap, a receptor-based fusion protein that binds an

17 ; a monoclonal anti-human VEGF antibody; and VEGF-Trap, a composite decoy receptor based on VEGFR-1 a

18 ockade of VEGF, using the recently described VEGF-Trap, abolishes mature, preexisting vasculature in

19 y, pharmacokinetics, and pharmacodynamics of VEGF Trap administered intravenously (IV) every 2 weeks.

20 Vascular endothelial growth factor (VEGF) Trap (aflibercept) is an angiogenesis inhibitor co

21 eatment of 4-, 8-, and 16-week-old mice with VEGF-Trap, an inhibitor of VEGF, the number of capillari

22 included measurement of plasma VEGF bound to VEGF Trap and free VEGF Trap.

23 In contrast, VEGF trap and VEGFR2 blockers mimicked the effect of HT.

24 e of tubulogenesis was markedly inhibited by VEGF-Trap and to a lesser extent by soluble VEGFR-1.

25 pegaptanib sodium, ranibizumab, bevacizumab, VEGF trap, and bevasiranib in the treatment of various n

26 unctival vascular endothelial growth factor (VEGF)-trap, anti-VEGF-C, sVEGFR-3, or no treatment, begi

27 cokinetics, the recommended phase II dose of VEGF Trap as a single agent is 4 mg/kg every 2 weeks.

28 Eyes with existing NV that received 5 mug VEGF Trap at P22 exhibited substantial resolution of OIR

29 Systemic administration of VEGF Trap beginning on day 2 and 6 completely prevented

30 duced in eyes injected with 250 or 25 mug of VEGF Trap, but the 5 mug dose did not inhibit retinal re

31 VEGF blockade, as achieved by high doses of VEGF-Trap, can lead to regression of coopted vascular st

32 ry circulation, in the embryos injected with VEGF-Trap caused an accumulation of erythrocytes in the

33 nge of efficacy was observed, with high-dose VEGF-Trap causing the greatest inhibition of tumor growt

34 area were observed in patients who received VEGF Trap compared with increases of 66% (P = 0.004, Man

35 Cotreatment with VEGF-trap completely sequestered free VEGF and abrogated

36 Maximal VEGF-bound VEGF Trap complex levels were reached at doses > or = 2.

37 ation of exogenous and/or endogenous VEGF by VEGF-trap delayed reendothelialization and significantly

38 Based on this assay, VEGF Trap doses currently being assessed in clinical tri

39 This VEGF-Trap effectively suppresses tumor growth and vascul

40 ygen-treated animals, all eyes injected with VEGF Trap exhibited markedly less intravitreal NV than t

41 igned randomly to 1 of 5 treatment regimens: VEGF Trap-Eye 0.5 mg every 4 weeks (0.5q4); 2 mg every 4

42 24 weeks, monthly intravitreal injection of VEGF Trap-Eye 2 mg in eyes with macular edema resulting

43 Eyes were randomized 3:2 to receive VEGF Trap-Eye 2 mg or sham injection monthly for 6 month

44 urred in 0 and 5 (6.8%) of eyes treated with VEGF Trap-Eye and sham-treated eyes, respectively (P = 0

45 In addition, new pharmacologic agents like VEGF Trap-Eye are being developed and investigated; prel

46 nvestigated; preliminary 1-year results with VEGF Trap-Eye are encouraging.

47 y reported, mean improvements in BCVA in the VEGF Trap-Eye groups at week 24 were 8.6, 11.4, 8.5, and

48 Mean reductions in CRT in the VEGF Trap-Eye groups at week 52 were -165.4 mum, -227.4

49 Mean improvements in BCVA in the VEGF Trap-Eye groups at week 52 were 11.0, 13.1, 9.7, an

50 f 15 or more ETDRS letters at week 52 in the VEGF Trap-Eye groups were 40.9%, 45.5%, 23.8%, and 42.2%

51 ere maintained or improved at week 52 in all VEGF Trap-Eye groups.

52 Serious ocular AEs were reported by 3.5% of VEGF Trap-Eye patients and 13.5% of sham patients.

53 At week 24, 56.1% of VEGF Trap-Eye treated eyes gained 15 letters or more fro

54 The VEGF Trap-Eye treated eyes gained a mean of 17.3 letters

55 decreased by 457.2 mum in eyes treated with VEGF Trap-Eye versus 144.8 mum in sham-treated eyes (P<0

56 The most frequent ocular adverse events with VEGF Trap-Eye were conjunctival hemorrhage, eye pain, oc

57 Neutralizing VEGF with aflibercept (VEGF Trap-Eye) safely and effectively protected rabbits

58 lar Degeneration Treatments) study and VIEW (VEGF Trap-Eye: Investigation of Efficacy and Safety in W

59 The VEGF Trap-Eye: Investigation of Efficacy and Safety in W

60 Two similarly designed, phase-3 studies (VEGF Trap-Eye: Investigation of Efficacy and Safety in W

61 ieved in routine clinical practice using the VEGF Trap-Eye: Investigation of Efficacy and Safety in W

62 osing of intravitreal aflibercept injection (VEGF Trap-Eye; Regeneron, Tarrytown, NY, and Bayer Healt

63 phase-3 Vascular Endothelial Growth Factor (VEGF) Trap-Eye: Investigation of Efficacy and Safety in

64 phase 3 Vascular Endothelial Growth Factor (VEGF) Trap-Eye: Investigation of Efficacy and Safety in

65 plexes that are usually rapidly cleared, the VEGF Trap forms inert complexes with tissue- and tumor-d

66 VEGF-Trap further reduced VEGFR-2 expression in tracheal

67 ffect of vascular endothelial growth factor (VEGF) Trap in CNV (group 2).

68 y topotecan with or without ziv-aflibercept (VEGF-trap) in this clinical setting.

69 Maximum plasma concentration of free VEGF Trap increased proportionally with dose.

70 However, intravitreal VEGF trap induced increases in inflammatory molecules wh

71 rotective effect, as judged by prevention of VEGF-Trap-induced reduction in tracheal capillaries in t

72 The VEGF Trap inhibited the formation of NV, but higher dose

73 Most importantly, we found that VEGF-Trap injected at either E6 or E7 prevented the form

74 al capillaries were reduced in 250 or 25 mug VEGF Trap-injected eyes, and deep capillaries were absen

75 how similar protection, thus indicating that VEGF trapping is a potentially viable mechanism for AFSC

76 tment begins at the time of transplantation, VEGF-trap is significantly more effective in improving l

77 VEGF-Trap-mediated blockade may be superior to that achi

78 for 10 days before treatment was initiated, VEGF Trap not only prevented its further progression, bu

79 f a vascular endothelial growth factor trap (VEGF Trap) on retinal vascular development and pathologi

80 her oxygen-exposed animals received 5 mug of VEGF Trap or hFc on P22 after confirmation of retinopath

81 ssing (1) VEGF, (2) VEGF-trap, (3) VEGF plus VEGF-trap, or (4) control adenovirus.

82 stingly, sequestration of endogenous VEGF by VEGF-trap overexpression alone also led to delayed reend

83 GF receptor (VEGFR) ectodomains, recombinant VEGF Trap protein and the VEGFR2-selective antibody DC10

84 molecular trap designed to eliminate VEGF-A (VEGF Trap(R1R2); 12.5 mg/kg) was tested for its ability

85 administration of a potent VEGF antagonist (VEGF-TRAP(R1R2)), thus defining a paraneoplastic syndrom

86 Finally, glaucomatous patients injected with VEGF traps (ranibizumab or aflibercept) due to either AM

87 VEGF Trap (Regeneron Pharmaceuticals, Tarrytown, NY), a

88 of IL-17A, or increasing the activity of the VEGF trap, represents a useful approach to inhibiting CV

89 Multiday treatments with a VEGF trap reverted MV back to normal microvessels.

90 VEGF-trap significantly decreased graft hemangiogenesis

91 o determine whether two agents, AG013736 and VEGF-Trap, that inhibit vascular endothelial growth fact

92 When Ang1 was given in combination with VEGF-Trap, tracheal vessels presented the typical respon

93 Macular volume decreased by 11% in VEGF Trap-treated patients and increased by 10% in place

94 Administering VEGF Trap treatment before or shortly after injection of

95 In addition, VEGF Trap treatment reduced the total lesion volume and

96 Hence the VEGF trap was strengthened.

97 IV VEGF Trap was well tolerated at the dose levels tested.

98 survival compared to control (0%), although VEGF-trap was significantly more effective than both ant

99 al injections of VEGF-A, VEGF-E, PlGF-1, and VEGF trap were also studied.

100 Aflibercept ('VEGF Trap', which neutralizes VEGF-A, VEGF-B and PlGF) s

101 VEGF and a soluble, chimeric VEGF receptor (VEGF-trap), which binds free VEGF with high affinity, in