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1 y micromolar responses to the YAP1 inhibitor Verteporfin.
2 itted to half-dose photodynamic therapy with verteporfin.
3    Treatment with standard fluence PDT using verteporfin.
4 ikely underlies the antifibrotic activity of verteporfin.
5  was performed using half the normal dose of verteporfin.
6 ked at 6 hours, showing a dose dependence of verteporfin.
7 e photosensitizer, benzoporphyrin derivative verteporfin.
8 e rats were injected intravenously with fVII-verteporfin (0.5 and 1.0 mg/m(2)) or Visudyne (6.0 mg/ m
9  the residence of subconjunctivally injected verteporfin 12-fold at 24 h after injection compared wit
10 ated with verteporfin PDT, with two doses of verteporfin (3.0 and 6.0 mg/m(2)) and four activating do
11  re nata; PRN) combination (standard-fluence verteporfin 6 mg/m(2) PDT and ranibizumab 0.5 mg) or PRN
12 600 mW/cm2, 83 seconds, 4-mm spot size) with verteporfin (6 mg/m2 intravenous infusion) was performed
13              YAP knockdown or treatment with verteporfin, a drug that was recently identified as a po
14                               Treatment with verteporfin, a nuclear Yap inhibitor, restored apical su
15                                              Verteporfin, a pharmacological inhibitor of the Hippo pa
16         We show that one-time treatment with verteporfin, a YAP inhibitor, immediately after wounding
17  +/- 0.3-3000 nM methylprednisolone +/- 3 uM verteporfin, a YAP/TAZ inhibitor.
18                                              Verteporfin accumulation in vascularized regions of the
19                                              Verteporfin, an inhibitor of YAP, significantly reduced
20 ng mechanotransduction signaling with either verteporfin, an inhibitor of Yes-associated protein (YAP
21                                              Verteporfin, an inhibitor of Yes-associated protein (YAP
22  Inhibition of the YAP/TAZ binding to TEADs (verteporfin and K-975) dampened the effects of CdtB, par
23 eporfin PDT also varied as a function of the verteporfin and light energy doses.
24  the CNV varied as a function of the dose of verteporfin and of the activating light energy.
25 ined therapy with inhibitors of YAP (such as verteporfin) and FGF receptors (such as BGJ398) can prov
26 lling by genetic (RNAi) and pharmacological (Verteporfin) approaches suppresses AR-dependent gene exp
27                 The socio-economic impact of verteporfin approval has yet to be determined.
28                          We further identify verteporfin as a small molecule that inhibits TEAD-YAP a
29                  Ranibizumab was superior to verteporfin as intravitreal treatment of predominantly c
30                         PDT was applied with verteporfin at a dose of 6 mg/m(2) body surface area and
31                   Photodynamic therapy using verteporfin at a dose of 6 mg/m(2) body surface area and
32 mice that had been treated with 2.0 mg/kg of verteporfin at post-PDT day 7.
33 of 25 J/cm(2) after intravenous injection of verteporfin at the doses of 3, 6, and 12 mg/m(2).
34                                              Verteporfin attenuated upregulation of CCN2, but not PTG
35                                         fVII-verteporfin binds tightly and specifically to tissue fac
36 /11 in UM development, and the YAP inhibitor verteporfin blocks tumor growth of UM cells containing G
37         However, it has also been shown that Verteporfin can have non-photoactivated effects such as
38                                              Verteporfin did not alter the Akt survival pathway or th
39 se of 1.5 mg/kg, and the pharmacokinetics of verteporfin distribution in the anterior segment or PDT-
40 reas of normal choroid and retina at the two verteporfin doses and four light energy doses.
41 r with the small-molecule YAP/TEAD inhibitor verteporfin, eliminated modulus-dependent lapatinib resi
42 t photodynamic therapy (PDT) using half-dose verteporfin for acute CSCR led to a significant decrease
43 h benzoporphyrin derivative monoacid ring A, verteporfin for injection (BPD; 1-mg/kg injected i.v. fo
44                                   Using fVII-verteporfin for TPT may improve the efficacy and safety
45                             We observed that verteporfin formed a direct 1:1 complex with C99, with a
46 e 0.5-mg group, as compared with 5.6% of the verteporfin group (P<0.001 for each comparison).
47 mpared with a decrease of 9.5 letters in the verteporfin group (P<0.001 for each comparison).
48 ters, as compared with 64.3% of those in the verteporfin group (P<0.001 for each comparison).
49           To date, photodynamic therapy with verteporfin has been shown to benefit those patients wit
50                                          The Verteporfin in Ocular Histoplasmosis study evaluated pho
51 r Degeneration with Photodynamic Therapy and Verteporfin in Photodynamic Therapy studies have suggest
52 ular Degeneration with Photodynamic Therapy; Verteporfin in Photodynamic Therapy; VEGF Inhibition Stu
53 wth factor A--with photodynamic therapy with verteporfin in the treatment of predominantly classic ne
54 nd breast cancer cells (MCF7) we showed that Verteporfin-induced HMWC require the presence of light.
55 erformed with 6 mg/m(2) body surface area of verteporfin infused intravenously over 10 minutes activa
56               Treatment of HFD-fed mice with verteporfin inhibited KC activation, reduced liver infla
57 hermore, pharmacological YAP inhibition with verteporfin inhibited tumor cell proliferation and resto
58                         Lastly, we show that verteporfin inhibition of YAP1/TEAD1 activity in aged WI
59 (an inhibitor of forkhead box M1 [FOXM1]) or verteporfin (inhibitor of the interaction between YAP an
60 e optical irradiation was given 15 min after verteporfin injection, the tumor pO(2) decreased slightl
61                                         Peak verteporfin intensities in the CNV were detected at 15 t
62                    Photodynamic therapy with verteporfin is an effective outpatient method for small
63 stration is requiring additional data before verteporfin is approved for treatment of occult subfovea
64              Photodynamic therapy (PDT) with verteporfin (lipid form of benzoporphyrin derivative,ben
65             To prolong the residence time of verteporfin on the ocular surface, the cohesive viscoela
66 g the interaction between YAP and TEAD4 with verteporfin, or inhibiting FOXM1 with thiostrepton, redu
67 as of normal choroid and retina treated with verteporfin PDT also varied as a function of the vertepo
68 ed half-dose verteporfin PDT versus 30%-dose verteporfin PDT and found that 94.6% in the half-dose PD
69   The combination PRN treatment regimen with verteporfin PDT and ranibizumab was effective in achievi
70                                              Verteporfin PDT for experimental CNV in the rat is a fea
71     Ranibizumab monotherapy or combined with verteporfin PDT improved BCVA at month 12; however, noni
72 e and placebo in the other, alternating with verteporfin PDT in both eyes on a weekly basis for 6 to
73 PDT-naive macular PCV patients who underwent verteporfin PDT using one of two PDT regimens at a terti
74    A second level I study compared half-dose verteporfin PDT versus 30%-dose verteporfin PDT and foun
75                                              Verteporfin PDT was also performed on areas of normal ch
76  combination of intravitreal ranibizumab and verteporfin PDT were demonstrated compared with PDT alon
77       The CNV lesions were then treated with verteporfin PDT, with two doses of verteporfin (3.0 and
78 were identified, of which 14 received rescue verteporfin PDT.
79 therapy (PDT) or sham ocular injections with verteporfin PDT.
80 esting the efficacy of adjunctive therapy to verteporfin PDT.
81 mab (0.3 mg or 0.5 mg), sham injections plus verteporfin photodynamic therapy (ANCHOR), or sham injec
82 vacizumab monotherapy or combination IVB and verteporfin photodynamic therapy (IVB/PDT).
83 ged with the development of 2 therapies: (1) verteporfin photodynamic therapy (PDT) and (2) anti-vasc
84                                              Verteporfin photodynamic therapy (PDT) is the most effec
85 or 24 months (MARINA), or were randomized to verteporfin photodynamic therapy (PDT; n=143), 0.3-mg ra
86 ); (2) intravitreal anti-VEGF injection; (3) verteporfin photodynamic therapy (vPDT); or (4) laser ph
87 States Food and Drug Administration approved verteporfin photodynamic therapy for the treatment of su
88  PCV was based on the Efficacy and Safety of Verteporfin Photodynamic Therapy in Combination with Ran
89 f anti-vascular endothelial growth factor or verteporfin photodynamic therapy in combination with sys
90  in vivo with the nuclear Yap-TEAD inhibitor verteporfin prolonged MF persistence and converted tissu
91  inhibition of autophagy with mefloquine and verteporfin re-establishes cholangiocyte cilia and cilia
92                      YAP/TAZ inhibition with verteporfin reduced leukocyte accumulation in the aortic
93           Inhibition of YAP activity through verteporfin reduced myofibroblast activation on stiff su
94                                 Furthermore, verteporfin reduced YAP/TAZ levels and decreased the tot
95 ortantly, administration of a YAP1 inhibitor Verteporfin resensitized ZNF367-overexpressing breast ca
96 ormal mouse eyes treated with 2 or 4.0 mg/kg verteporfin returned to the level of the fellow control
97           Pharmacological YAP inhibition via verteporfin reverses fibrotic alveolar type II cell repr
98 4.4 letters with verteporfin SF (n = 103) or verteporfin RF (n = 105) plus ranibizumab, respectively,
99                                              Verteporfin RF did not confer clinical benefits over ver
100 the patients randomized to verteporfin SF or verteporfin RF groups, respectively, with a mean of 5.1
101 e at month 12 was +5.3 and +4.4 letters with verteporfin SF (n = 103) or verteporfin RF (n = 105) plu
102 decreased by 151.7 mum and 140.9 mum for the verteporfin SF and RF groups, respectively, and by 172.2
103 2.6% and 83.5% of the patients randomized to verteporfin SF or verteporfin RF groups, respectively, w
104 fin RF did not confer clinical benefits over verteporfin SF.
105                           The mean number of verteporfin/sham PDT treatments was comparable in the 2
106                     This study suggests that verteporfin should be further explored as an adjuvant th
107  RPTC or administration of the YAP inhibitor verteporfin significantly attenuated diabetic tubulointe
108        The small-molecule inhibitor of YAP1, verteporfin, significantly blocks CSC properties in cell
109                 The small-molecule inhibitor verteporfin suppressed the disease severity in autoimmun
110 for the clinically approved photosensitizers verteporfin, temoporfin, protoporphyrin IX, and trisulfo
111 t of clinically established photosensitizers verteporfin, temoporfin, S3AlOHPc, or protoporphyrin IX.
112 r, we identified a small-molecule inhibitor, verteporfin, that inhibited GLK kinase activity and AhR-
113  of ranibizumab (0.3 mg or 0.5 mg) plus sham verteporfin therapy or monthly sham injections plus acti
114 erapy or monthly sham injections plus active verteporfin therapy.
115 hemical assays showed that direct binding of verteporfin to C99 inhibits gamma-secretase cleavage of
116                   The rats treated with fVII-verteporfin TPT at a dose of 0.5 mg/m(2) showed leakage
117 lesions was significantly reduced using fVII-verteporfin TPT compared with PDT.
118 nd perturbations in fibroblast dynamics with verteporfin treatment and the presence of putative pro-r
119                                              Verteporfin treatment of mice subjected to unilateral ur
120 versely correlated with vascular patency and verteporfin uptake, suggesting interstitial hypertension
121 mellitus, myocardial infarction, stroke, and verteporfin use).
122  is an FDA-approved liposomal formulation of verteporfin used to treat abnormal blood vessels in the
123                     Among all the compounds, verteporfin (VER) was really efficient in enhancing PMN-
124        Previously, we tested the efficacy of Verteporfin (VP) in EMCA cells and observed cytotoxic an
125     Treatment of mice with the YAP inhibitor verteporfin (VP) inhibited activation of genes associate
126                                              Verteporfin (VP) was first used in Photodynamic therapy,
127                                              Verteporfin (VP), a light-activated drug used in photody
128                                              Verteporfin was administered by intravenous injection at
129                       YAP specific inhibitor Verteporfin was also administrated in cardiac fibroblast
130               The efficacious dose with fVII-verteporfin was approximately 10% of the dose usually us
131 nsit and accumulation of the photosensitizer verteporfin was assessed angiographically in CNV lesions
132                                         When verteporfin was injected 3 h before light irradiation, t
133                                              Verteporfin was injected intravenously at doses of 1.0 (
134 ensitivity to the YAP-TEAD complex inhibitor verteporfin, whereas cells with confluency-driven nuclea
135 his screen, we identified the small-molecule verteporfin with these properties.
136 hibitors, and its effects were equivalent to verteporfin (YAP) or SB525334 (Smad) for regulating expr

 
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