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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
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
23 /11 in UM development, and the YAP inhibitor verteporfin blocks tumor growth of UM cells containing G
26 se of 1.5 mg/kg, and the pharmacokinetics of verteporfin distribution in the anterior segment or PDT-
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
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
44 stration is requiring additional data before verteporfin is approved for treatment of occult subfovea
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
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
53 combination of intravitreal ranibizumab and verteporfin PDT were demonstrated compared with PDT alon
57 mab (0.3 mg or 0.5 mg), sham injections plus verteporfin photodynamic therapy (ANCHOR), or sham injec
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
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,
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
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
83 versely correlated with vascular patency and verteporfin uptake, suggesting interstitial hypertension
85 Treatment of mice with the YAP inhibitor verteporfin (VP) inhibited activation of genes associate
90 nsit and accumulation of the photosensitizer verteporfin was assessed angiographically in CNV lesions
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