Verteporfin

Catalog No.S1786 Synonyms: CL 318952

Verteporfin  Chemical Structure

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.

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3 Customer Reviews

  • 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.

  • The levels of YAP, phospho-YAP (S127), and its downstream targeted molecules CTGF and CYR61 were analyzed by Western blotting after UM cells were exposed to verteporfin for 24 hours.

    Am J Cancer Res, 2016, 6(12):2816-2830.. Verteporfin purchased from Selleck.

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Biological Activity

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.
Targets
VDA [1]
(Endothelial cells)
YAP/TEAD interaction [3]
In vitro

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. [1] 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. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HL-60 NXPsU4ptTnWwY4Tpc44h[XO|YYm= NEXNNVd,OTByIH7nM41N NIK2UWtFVVOR NHPSeW1qdmO{ZXHz[ZMhTE6DIH\yZYdu\W62YYTpc44hdGW4ZXzz M1zDZVExPjB5N{Gw
HL-60 M3HNVYN6fG:2b4jpZ4l1gSCjc4PhfS=> NF3MdI1,OTByIH7nM41N M4D6[GROW09? M4KxcIlvcGmkaYTzJINmdGxidnnhZoltcXS7 MXixNFYxPzdzMB?=
Jurkat NUWycXVtSXCxcITvd4l{KGG|c3H5 NFWxTId,OjhyIH7N NHixfIpFVVOR M1LOOYlv\HWlZYOgZUBD[2xvMj3k[ZBmdmSnboSgZZBweHSxc3nz NWG3SWE4OTF{NEW0NVU>
RIF-1 MlS2SpVv[3Srb36gZZN{[Xl? MnXDNUDPxGdxbXy= NHizS4FFVVOR M4\QT4Rm[3KnYYPld{BwgHmpZX6gZ49ve3WvcITpc44> M{G5NVEzPjF3N{G4
RIF-1 NGHFRYlkgXSxdH;4bYNqfHliYYPzZZk> MYixJO69\y:vbB?= NH7J[VJFVVOR MlzY[IVkemWjc3WgeI8hOjBiwsGgOUUh[2WubDDzeZJ3cX[jbB?= M3LaUFEzPjF3N{G4
SVEC4-10 M{DUTGZ2dmO2aX;uJIF{e2G7 MUmyNFAhdmdxbXy= NHHvdYZFVVOR MoXybY5lfWOnczDtbYNzd3S3YoXs[UBl\XCxbInt[ZJqgmG2aX;u MVqxOlQ3PzFyNh?=
SVEC4-10 MU\GeY5kfGmxbjDhd5NigQ>? MnfwNlAxKG6pL33s Mlu1SG1UVw>? MmrobY5lfWOnczDzeJJme3NiYXP0bY4h\mmkZYKg[o9zdWG2aX;u NXrSSGcxOTZ2NkexNFY>
ARPE-19 NXrz[Jc6[3m2b4TvfIlkcXS7IHHzd4F6 NH;ybnZ,OC5zIN88[{9udA>? NUHMepE1TE2VTx?= MUnzbI94eyCjIHTvd4Uu\GWyZX7k[Y51KHSxeHnjbZR6 NX3ZOWxrOTZ7OEe5NFU>
ARPE-19 NYf5eXBxTnWwY4Tpc44h[XO|YYm= MVmwMlAyKM7:Zz;tcC=> NXvIT3pbTE2VTx?= MUnpcoNz\WG|ZYOgWmVITiCjbnSgdoVlfWOnczDQSWRHKGW6cILld5Nqd25? MlO4NVY6QDd7MEW=
Y-79 NUHHR|JbT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MXT+NUDPxGdxbXy= M1u4bWROW09? M1ro[IRm[3KnYYPld{Bz\XSrbn;icIF{fG:vYTDj[YxtKHC{b3zp[oVz[XSrb36= MVexPFU4QTd4NB?=
WERI-Rb1 NFqzOJNIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MnTlglEh|rypL33s NWDZWpJVTE2VTx?= MoHD[IVkemWjc3XzJJJmfGmwb3LsZZN1d22jIHPlcIwheHKxbHnm[ZJifGmxbh?= M33PN|E5PTd7N{[0
RB247C3 MWjHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NUD1cGNihjFizsznM41t NFGzNYxFVVOR Ml\O[IVkemWjc3XzJJJmfGmwb3LsZZN1d22jIHPlcIwheHKxbHnm[ZJifGmxbh?= MWixPFU4QTd4NB?=
RB355 NWD6SFlkT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MUj+NUDPxGdxbXy= M3;GSWROW09? NW[yVIdv\GWlcnXhd4V{KHKndHnuc4Jt[XO2b33hJINmdGxicILvcIln\XKjdHnvci=> Mk\5NVg2Pzl5NkS=
RB383 MoXwS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? MV7+NUDPxGdxbXy= NI\HVXFFVVOR M1nRdYRm[3KnYYPld{Bz\XSrbn;icIF{fG:vYTDj[YxtKHC{b3zp[oVz[XSrb36= M2\3SlE5PTd7N{[0
hFibro MlzYZ5l1d3SxeHnjbZR6KGG|c3H5 MYSwMlUhyrWpL33s MV3EUXNQ MWjk[YNz\WG|ZYOgeoli[mmuaYT5JIJ6KDh4LEWl MVSyN|Q1OTFzNB?=
pTMC M1HxcIN6fG:2b4jpZ4l1gSCjc4PhfS=> NH;TXlcxNjViwsXnM41t MXHEUXNQ MmT5[IVkemWjc3XzJJZq[WKrbHn0fUBjgSB7Mj65KS=> M3HGS|I{PDRzMUG0
hTMC M2e0d4N6fG:2b4jpZ4l1gSCjc4PhfS=> M3;IXlAvPSEEtXevcYw> NW\vTm1zTE2VTx?= NVvCWGxW\GWlcnXhd4V{KH[rYXLpcIl1gSCkeTC4PE46LQ>? NU\SXHU3OjN2NEGxNVQ>
ARPE-19 NE\CW4VkgXSxdH;4bYNqfHliYYPzZZk> NHPD[lgxNjViwsXnM41t NU\EWHVJTE2VTx?= M3vldoRm[3KnYYPld{B3cWGkaXzpeJkh[nliNUWuOUU> NHrlT4UzOzR2MUGxOC=>
Panc-1 NEO5NoZIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NEjx[pYyOCEQvF2= NFXFO29FVVOR NF3I[3BqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> MnPONlQxPjlyNkm=
MIA PaCa-2 MmHzS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? M2T3bVExKM7:TR?= MnfaSG1UVw>? MkXFbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;u MkC1NlQxPjlyNkm=
BxPC-3 NX;sdpU2T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NHfoS|AyOCEQvF2= M{TSVWROW09? M1TteYlvcGmkaYTzJINmdGxicILvcIln\XKjdHnvckBkd22ybHX0[Yx6 MlOzNlQxPjlyNkm=
SU86.86 NH24fFZIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MVOxNEDPxE1? M{PSemROW09? MkDmbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJINwdXCuZYTlcJk> M2HE[VI1ODZ7ME[5
MCF-7 NYnt[Yx2SXW2b4DoZYd6KGG|c3H5 MUWxNEDPxE1? MUDEUXNQ MUDpcohq[mm2czDn[Y1kcXSjYnnu[U1qdmS3Y3XkJIF2fG:yaHHnfS=> NEXFZmczPDB4OUC2PS=>
WERI Ml7XS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NHLaRXN,OTBizsznM41t MmjYSG1UVw>? M1XZXolvcGmkaYTzJIdzd3e2aDDv[kBz\XSrbn;icIF{fG:vYTDj[Yxtew>? MoXRNlQ5OzdzNEK=
WERI M2PGRmZ2dmO2aX;uJIF{e2G7 Mli1glExKM7:Zz;tcC=> NWPBfWIxTE2VTx?= MnG4Zoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44> MkXjNlQ5OzdzNEK=
Y-79 M{fYdWZ2dmO2aX;uJIF{e2G7 MlL3glExKM7:Zz;tcC=> Mny0SG1UVw>? MnW3Zoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44> NVnyW2ZvOjR6M{exOFI>
Y-79 M162fGZ2dmO2aX;uJIF{e2G7 NVrQZ492hjFyIN88[{9udA>? MXXEUXNQ MVPh[oZm[3S|IGnBVE1VTUGGIIDyc5RwNW:wY3;n[Y5mKHCjdHj3ZZk> NVnTPXpCOjR6M{exOFI>
Y-79 M2DyXGZ2dmO2aX;uJIF{e2G7 NXexUZFVhjFyIN88[{9udA>? MXrEUXNQ NE\kRlFld3ewLYLl[5Vt[XSnczDwcJVzcXCxdHXuZ5khdWG{a3XyJG9EXC12 MW[yOFg{PzF2Mh?=

... Click to View More Cell Line Experimental Data

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. [1]

Protocol

Solubility (25°C)

In vitro DMSO 100 mg/mL (139.12 mM)
Water Insoluble
Ethanol Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 718.79
Formula

C41H42N4O8

CAS No. 129497-78-5
Storage powder
in solvent
Synonyms CL 318952

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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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID