Verteporfin (CL 318952)
For research use only.
Catalog No.S1786 Synonyms: Visudyne
CAS No. 129497-78-5
Verteporfin (CL 318952, Visudyne) 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 an autophagy inhibitor. Verteporfin inhibits cell proliferation and induces apoptosis.
Selleck's Verteporfin (CL 318952) has been cited by 80 publications
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|Description||Verteporfin (CL 318952, Visudyne) 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 an autophagy inhibitor. Verteporfin inhibits cell proliferation and induces apoptosis.|
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||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT04590664||Recruiting||Drug: Verteporfin||Glioblastoma|Recurrent Glioblastoma||Emory University|National Cancer Institute (NCI)||January 15 2021||Phase 1|Phase 2|
|NCT01846273||Completed||Drug: Ranibizumab|Drug: Verteporfin PDT|Drug: Sham PDT||Age-related Macular Degeneration|Polypoidal Choroidal Vasculopathy||Novartis Pharmaceuticals|Novartis||August 7 2013||Phase 4|
|NCT00423189||Terminated||Drug: Ranibizumab (Lucentis)|Drug: 0.5mg ranibizumab||Age-Related Macular Degeneration||David M. Brown M.D.|Novartis Pharmaceuticals|Greater Houston Retina Research||January 2007||Phase 4|
|NCT00403442||Terminated||Device: Verteporfin Therapy/ Drug: Bevacizumab||Macular Degeneration||Vitreous -Retina- Macula Consultants of New York|QLT Inc.||September 2006||Phase 1|
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