Catalog No.S1786 Synonyms: CL 318952
Molecular Weight(MW): 718.79
Verteporfin is a small molecule that inhibits TEAD–YAP association and YAP-induced liver overgrowth. It is also a potent second-generation photosensitizing agent derived from porphyrin.
Cited by 8 Publications
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Verteporfin treatment inhibits proliferation and induces apoptosis of Tsc1-null cells in vivo. Mice were administered i.p. with vehicle or verteporfin at a dose of 100 mg/kg every other day for 10 d before sacrifice. Mice were sacrificed at 6 wk of age. Three independent experiments were performed and mice in different treatments were pooled for analysis. Percentage of Ki67 and αSMA double-positive cells in α-SMA+ mesenchymal lesions in the indicated kidneys. Immunofluorescence staining and counting were performed on three sagittal sections from different kidney regions for each mouse.
J Exp Med 2014 211(11), 2249-63. Verteporfin purchased from Selleck.
The indicated cell lines were treated with control (Ctrl) or YAP-targeting siRNAs and growth assessed by XTT proliferation assays at the indicated time points. The mean and +SD are shown for three independent experiments. (Left panel, *, P < 0.05, significantly different from U87Rictor DMSO; Right panel, *, P < 0.05, significantly different from H4Rictor DMSO).
J Biol Chem, 2015, 290(32): 19387-401 . Verteporfin purchased from Selleck.
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|Description||Verteporfin is a small molecule that inhibits TEAD–YAP association and YAP-induced liver overgrowth. It is also a potent second-generation photosensitizing agent derived from porphyrin.|
Verteporfin is about four times more efficient in absorbing light at wavelengths that penetrate tissues best (i.e., around 700 nm) and thus provides a much higher cytotoxic effect than hematoporphyrin (10 times more in human adherent cell lines). Verteporfin is lipophilic and is more readily taken up by malignant or activated cells, compared with normal or resting cells. Verteporfin binds with LDL to form a complex, which is then taken up into proliferating cells (e.g., neovascular endothelial cells) probably via LDL receptors and endocytosis. Verteporfin therapy achieves complete angiographic occlusion of the neovascular compartment by thrombosis of vascular channels, following selective endothelial damage. Verteporfin therapy selectively induces reproducible and isolated choriocapillary occlusion without alteration of overlying photoreceptors or ganglion cells, as shown by light and electron microscopy.  Verteporfin conbined with light rapidly exhibits apoptotic changes reflected by caspase-3 and caspase-9 activation and PARP cleavage in HL-60 cells, changes that are blocked by the general caspase inhibitor ZVAD.fmk. 
|In vivo||Verteporfin can be used for angiographic visualization of choroidal vessels and CNV, which demonstrates that the photosensitizer accumulates rapidly in experimental CNV in monkeys. Verteporfin accumulates rapidly in the established vasculature of the choroid, RPE, and photoreceptors of rabbit eyes. Verteporfin reaches maximal tissue levels within 3 hours of intravenous injection, followed by a rapid decline within 24 hours in mice. Verteporfin is metabolized to a less active form in vivo and is cleared very rapidly, predominantly in the feces and a very small proportion excreted in urine. Verteporfin therapy effectively and selectively prevents fluorescein dye leakage from experimentally induced CNV in monkeys. |
|In vitro||DMSO||100 mg/mL (139.12 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01846273||Completed||Age-related Macular Degeneration|Polypoidal Choroidal Vasculopathy PCV||Novartis Pharmaceuticals|Novartis||August 7 2013||Phase 4|
|NCT02939274||Recruiting||Metastatic Breast Cancer||Rogers Sciences Inc.||October 2016||Phase 2|
|NCT01968486||Completed||Myopia Degenerative||University of Campania Luigi Vanvitelli||June 2012||Phase 1|
|NCT00674323||Completed||Polypoidal Choroidal Vasculopathy||Novartis||April 2008||Phase 4|
|NCT00574093||Completed||Neovascular Age Related Macular Degeneration||Fondazione G.B. Bietti IRCCS||January 2008||Phase 2|
|NCT00433017||Terminated||Macular Degeneration|Choroidal Neovascularization||Novartis||May 2007||Phase 2|Phase 3|
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