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1 ikely underlies the antifibrotic activity of verteporfin.
2  was performed using half the normal dose of verteporfin.
3 ked at 6 hours, showing a dose dependence of verteporfin.
4 e photosensitizer, benzoporphyrin derivative verteporfin.
5 e rats were injected intravenously with fVII-verteporfin (0.5 and 1.0 mg/m(2)) or Visudyne (6.0 mg/ m
6 ated with verteporfin PDT, with two doses of verteporfin (3.0 and 6.0 mg/m(2)) and four activating do
7  re nata; PRN) combination (standard-fluence verteporfin 6 mg/m(2) PDT and ranibizumab 0.5 mg) or PRN
8 600 mW/cm2, 83 seconds, 4-mm spot size) with verteporfin (6 mg/m2 intravenous infusion) was performed
9              YAP knockdown or treatment with verteporfin, a drug that was recently identified as a po
10                                              Verteporfin accumulation in vascularized regions of the
11 eporfin PDT also varied as a function of the verteporfin and light energy doses.
12  the CNV varied as a function of the dose of verteporfin and of the activating light energy.
13 ined therapy with inhibitors of YAP (such as verteporfin) and FGF receptors (such as BGJ398) can prov
14 lling by genetic (RNAi) and pharmacological (Verteporfin) approaches suppresses AR-dependent gene exp
15                 The socio-economic impact of verteporfin approval has yet to be determined.
16                          We further identify verteporfin as a small molecule that inhibits TEAD-YAP a
17                  Ranibizumab was superior to verteporfin as intravitreal treatment of predominantly c
18                         PDT was applied with verteporfin at a dose of 6 mg/m(2) body surface area and
19                   Photodynamic therapy using verteporfin at a dose of 6 mg/m(2) body surface area and
20 mice that had been treated with 2.0 mg/kg of verteporfin at post-PDT day 7.
21 of 25 J/cm(2) after intravenous injection of verteporfin at the doses of 3, 6, and 12 mg/m(2).
22                                         fVII-verteporfin binds tightly and specifically to tissue fac
23 /11 in UM development, and the YAP inhibitor verteporfin blocks tumor growth of UM cells containing G
24         However, it has also been shown that Verteporfin can have non-photoactivated effects such as
25                                              Verteporfin did not alter the Akt survival pathway or th
26 se of 1.5 mg/kg, and the pharmacokinetics of verteporfin distribution in the anterior segment or PDT-
27 reas of normal choroid and retina at the two verteporfin doses and four light energy doses.
28 r with the small-molecule YAP/TEAD inhibitor verteporfin, eliminated modulus-dependent lapatinib resi
29 h benzoporphyrin derivative monoacid ring A, verteporfin for injection (BPD; 1-mg/kg injected i.v. fo
30                                   Using fVII-verteporfin for TPT may improve the efficacy and safety
31 e 0.5-mg group, as compared with 5.6% of the verteporfin group (P<0.001 for each comparison).
32 mpared with a decrease of 9.5 letters in the verteporfin group (P<0.001 for each comparison).
33 ters, as compared with 64.3% of those in the verteporfin group (P<0.001 for each comparison).
34           To date, photodynamic therapy with verteporfin has been shown to benefit those patients wit
35                                          The Verteporfin in Ocular Histoplasmosis study evaluated pho
36 r Degeneration with Photodynamic Therapy and Verteporfin in Photodynamic Therapy studies have suggest
37 ular Degeneration with Photodynamic Therapy; Verteporfin in Photodynamic Therapy; VEGF Inhibition Stu
38 wth factor A--with photodynamic therapy with verteporfin in the treatment of predominantly classic ne
39 nd breast cancer cells (MCF7) we showed that Verteporfin-induced HMWC require the presence of light.
40 hermore, pharmacological YAP inhibition with verteporfin inhibited tumor cell proliferation and resto
41 (an inhibitor of forkhead box M1 [FOXM1]) or verteporfin (inhibitor of the interaction between YAP an
42 e optical irradiation was given 15 min after verteporfin injection, the tumor pO(2) decreased slightl
43                                         Peak verteporfin intensities in the CNV were detected at 15 t
44 stration is requiring additional data before verteporfin is approved for treatment of occult subfovea
45              Photodynamic therapy (PDT) with verteporfin (lipid form of benzoporphyrin derivative,ben
46 g the interaction between YAP and TEAD4 with verteporfin, or inhibiting FOXM1 with thiostrepton, redu
47 as of normal choroid and retina treated with verteporfin PDT also varied as a function of the vertepo
48   The combination PRN treatment regimen with verteporfin PDT and ranibizumab was effective in achievi
49                                              Verteporfin PDT for experimental CNV in the rat is a fea
50     Ranibizumab monotherapy or combined with verteporfin PDT improved BCVA at month 12; however, noni
51 e and placebo in the other, alternating with verteporfin PDT in both eyes on a weekly basis for 6 to
52                                              Verteporfin PDT was also performed on areas of normal ch
53  combination of intravitreal ranibizumab and verteporfin PDT were demonstrated compared with PDT alon
54       The CNV lesions were then treated with verteporfin PDT, with two doses of verteporfin (3.0 and
55 therapy (PDT) or sham ocular injections with verteporfin PDT.
56 esting the efficacy of adjunctive therapy to verteporfin PDT.
57 mab (0.3 mg or 0.5 mg), sham injections plus verteporfin photodynamic therapy (ANCHOR), or sham injec
58 vacizumab monotherapy or combination IVB and verteporfin photodynamic therapy (IVB/PDT).
59                                              Verteporfin photodynamic therapy (PDT) is the most effec
60 or 24 months (MARINA), or were randomized to verteporfin photodynamic therapy (PDT; n=143), 0.3-mg ra
61 ); (2) intravitreal anti-VEGF injection; (3) verteporfin photodynamic therapy (vPDT); or (4) laser ph
62 States Food and Drug Administration approved verteporfin photodynamic therapy for the treatment of su
63 f anti-vascular endothelial growth factor or verteporfin photodynamic therapy in combination with sys
64                                 Furthermore, verteporfin reduced YAP/TAZ levels and decreased the tot
65 ormal mouse eyes treated with 2 or 4.0 mg/kg verteporfin returned to the level of the fellow control
66 4.4 letters with verteporfin SF (n = 103) or verteporfin RF (n = 105) plus ranibizumab, respectively,
67                                              Verteporfin RF did not confer clinical benefits over ver
68 the patients randomized to verteporfin SF or verteporfin RF groups, respectively, with a mean of 5.1
69 e at month 12 was +5.3 and +4.4 letters with verteporfin SF (n = 103) or verteporfin RF (n = 105) plu
70 decreased by 151.7 mum and 140.9 mum for the verteporfin SF and RF groups, respectively, and by 172.2
71 2.6% and 83.5% of the patients randomized to verteporfin SF or verteporfin RF groups, respectively, w
72 fin RF did not confer clinical benefits over verteporfin SF.
73                           The mean number of verteporfin/sham PDT treatments was comparable in the 2
74                     This study suggests that verteporfin should be further explored as an adjuvant th
75        The small-molecule inhibitor of YAP1, verteporfin, significantly blocks CSC properties in cell
76 for the clinically approved photosensitizers verteporfin, temoporfin, protoporphyrin IX, and trisulfo
77 t of clinically established photosensitizers verteporfin, temoporfin, S3AlOHPc, or protoporphyrin IX.
78  of ranibizumab (0.3 mg or 0.5 mg) plus sham verteporfin therapy or monthly sham injections plus acti
79 erapy or monthly sham injections plus active verteporfin therapy.
80                   The rats treated with fVII-verteporfin TPT at a dose of 0.5 mg/m(2) showed leakage
81 lesions was significantly reduced using fVII-verteporfin TPT compared with PDT.
82                                              Verteporfin treatment of mice subjected to unilateral ur
83 versely correlated with vascular patency and verteporfin uptake, suggesting interstitial hypertension
84 mellitus, myocardial infarction, stroke, and verteporfin use).
85     Treatment of mice with the YAP inhibitor verteporfin (VP) inhibited activation of genes associate
86                                              Verteporfin (VP) was first used in Photodynamic therapy,
87                                              Verteporfin (VP), a light-activated drug used in photody
88                                              Verteporfin was administered by intravenous injection at
89               The efficacious dose with fVII-verteporfin was approximately 10% of the dose usually us
90 nsit and accumulation of the photosensitizer verteporfin was assessed angiographically in CNV lesions
91                                         When verteporfin was injected 3 h before light irradiation, t
92                                              Verteporfin was injected intravenously at doses of 1.0 (

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