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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  • 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.
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 MnmwSpVv[3Srb36gZZN{[Xl? NW\jZXY3hjFyMDDu[{9uVA>? M4jYSmROW09? NU[3dGFJcW6lcnXhd4V{KESQQTDmdoFodWWwdHH0bY9vKGyndnXsdy=> NX3qS5Y5OTB4MEe3NVA>
HL-60 NWW3dWhJ[3m2b4TvfIlkcXS7IHHzd4F6 M2G2Xp4yODBibnevcWw> MnPaSG1UVw>? NVHtcmxFcW6qaXLpeJMh[2WubDD2bYFjcWyrdIm= MnvzNVA3ODd5MUC=
Jurkat NGfabWhCeG:ydH;zbZMh[XO|YYm= MU\+NlgxKG6P MV7EUXNQ NIDwS5FqdmS3Y3XzJIEhSmOuLUKt[IVx\W6mZX70JIFxd3C2b4Ppdy=> NYq5VnVNOTF{NEW0NVU>
RIF-1 NVvSeJJSTnWwY4Tpc44h[XO|YYm= NWOxVZlwOSEQvHevcYw> NVz2V5AyTE2VTx?= MnPS[IVkemWjc3XzJI95gWenbjDjc45{fW2ydHnvci=> M2TnOlEzPjF3N{G4
RIF-1 MV\jfZRwfG:6aXPpeJkh[XO|YYm= NFj6flcyKM7:Zz;tcC=> MUTEUXNQ NHLxZVZl\WO{ZXHz[UB1dyB{MDFCtUA2LSClZXzsJJN2en[rdnHs NF\TcYQyOjZzNUexPC=>
SVEC4-10 NVmzbGR3TnWwY4Tpc44h[XO|YYm= MXWyNFAhdmdxbXy= NUn6WopzTE2VTx?= NETGeZFqdmS3Y3XzJI1q[3KxdIXieYxmKGSncH;sfY1memm8YYTpc44> NUP1bIdMOTZ2NkexNFY>
SVEC4-10 M1HEZWZ2dmO2aX;uJIF{e2G7 MofGNlAxKG6pL33s MX\EUXNQ MlPRbY5lfWOnczDzeJJme3NiYXP0bY4h\mmkZYKg[o9zdWG2aX;u MmTkNVY1PjdzME[=
ARPE-19 NXLSV442[3m2b4TvfIlkcXS7IHHzd4F6 MVn+NE4yKM7:Zz;tcC=> NWDtTZBLTE2VTx?= M1rHOZNpd3e|IHGg[I9{\S2mZYDlcoRmdnRidH;4bYNqfHl? MWCxOlk5PzlyNR?=
ARPE-19 NETuTYhHfW6ldHnvckBie3OjeR?= MYGwMlAyKM7:Zz;tcC=> NYD3VXhyTE2VTx?= NWDpdolicW6lcnXhd4V{KF[HR1[gZY5lKHKnZIXj[ZMhWEWGRjDlfJBz\XO|aX;u NV24dGFDOTZ7OEe5NFU>
Y-79 M3vXNmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MX3+NUDPxGdxbXy= M4HGdGROW09? MoLu[IVkemWjc3XzJJJmfGmwb3LsZZN1d22jIHPlcIwheHKxbHnm[ZJifGmxbh?= NFrxNI0yQDV5OUe2OC=>
WERI-Rb1 M2W2NWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NWLLXWdFhjFizsznM41t MXLEUXNQ NHflcWFl\WO{ZXHz[ZMhemW2aX7vZoxie3SxbXGgZ4VtdCCycn;sbYZmemG2aX;u MmjJNVg2Pzl5NkS=
RB247C3 M4ryZWdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MWH+NUDPxGdxbXy= NUXsUGJvTE2VTx?= M3j6bIRm[3KnYYPld{Bz\XSrbn;icIF{fG:vYTDj[YxtKHC{b3zp[oVz[XSrb36= MYGxPFU4QTd4NB?=
RB355 NVfnO4lYT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NXS0TJFFhjFizsznM41t MkPKSG1UVw>? NEXtZ2hl\WO{ZXHz[ZMhemW2aX7vZoxie3SxbXGgZ4VtdCCycn;sbYZmemG2aX;u MkHhNVg2Pzl5NkS=
RB383 M2[xVGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 Mm\JglEh|rypL33s MWPEUXNQ MVzk[YNz\WG|ZYOgdoV1cW6xYnzhd5RwdWFiY3XscEBxem:uaX\ldoF1cW:w NImw[nkyQDV5OUe2OC=>
hFibro NUTBTYx{[3m2b4TvfIlkcXS7IHHzd4F6 MoW1NE42KML3Zz;tcC=> NXuwR5RZTE2VTx?= M2faN4Rm[3KnYYPld{B3cWGkaXzpeJkh[nliOE[sOUU> MX:yN|Q1OTFzNB?=
pTMC NHvpe41kgXSxdH;4bYNqfHliYYPzZZk> MVewMlUhyrWpL33s NGDVN|dFVVOR NWT0fld1\GWlcnXhd4V{KH[rYXLpcIl1gSCkeTC5Nk46LQ>? Ml\UNlM1PDFzMUS=
hTMC NGLkSoRkgXSxdH;4bYNqfHliYYPzZZk> Mn2yNE42KML3Zz;tcC=> NUnTN4hQTE2VTx?= Mkfi[IVkemWjc3XzJJZq[WKrbHn0fUBjgSB6OD65KS=> NIPxR2QzOzR2MUGxOC=>
ARPE-19 NIXzWZpkgXSxdH;4bYNqfHliYYPzZZk> MWiwMlUhyrWpL33s NWrubmhITE2VTx?= M3TuboRm[3KnYYPld{B3cWGkaXzpeJkh[nliNUWuOUU> MVSyN|Q1OTFzNB?=
Panc-1 NXvwVFN5T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NHLvRWoyOCEQvF2= NIOwc4lFVVOR NHvnUolqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> M4jBSlI1ODZ7ME[5
MIA PaCa-2 MmK0S5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? NUnMW4ZJOTBizszN MVHEUXNQ NHzr[WhqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> NF3Vdm4zPDB4OUC2PS=>
BxPC-3 MXrHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? M{H4XlExKM7:TR?= NF:5W5hFVVOR NXPybGljcW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9vKGOxbYDs[ZRmdHl? NGDPcnkzPDB4OUC2PS=>
SU86.86 MVzHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? NFqwZ4EyOCEQvF2= MX\EUXNQ MmX4bY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;uJINwdXCuZYTlcJk> MlqyNlQxPjlyNkm=
MCF-7 M2nzZmF2fG:yaHHnfUBie3OjeR?= MV:xNEDPxE1? M1z1NmROW09? MlzEbY5pcWKrdIOg[4Vu[2m2YXLpcoUucW6mdXPl[EBifXSxcHjh[5k> NILOd2UzPDB4OUC2PS=>
WERI NYrRb2J{T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MUD+NVAh|rypL33s MoD6SG1UVw>? M4qyOIlvcGmkaYTzJIdzd3e2aDDv[kBz\XSrbn;icIF{fG:vYTDj[Yxtew>? M2rDO|I1QDN5MUSy
WERI MYjGeY5kfGmxbjDhd5NigQ>? NXTRNHhyhjFyIN88[{9udA>? NGnweIFFVVOR M{DZeIJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9v MofiNlQ5OzdzNEK=
Y-79 M3n3dGZ2dmO2aX;uJIF{e2G7 NHPVUWl,OTBizsznM41t M3PJe2ROW09? MljDZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44> M1L2NFI1QDN5MUSy
Y-79 NIjD[G1HfW6ldHnvckBie3OjeR?= MYX+NVAh|rypL33s MnzGSG1UVw>? MY\h[oZm[3S|IGnBVE1VTUGGIIDyc5RwNW:wY3;n[Y5mKHCjdHj3ZZk> NXLPWm1UOjR6M{exOFI>
Y-79 MlzHSpVv[3Srb36gZZN{[Xl? NXTnU3lPhjFyIN88[{9udA>? Mn75SG1UVw>? MoDz[I94di2{ZXf1cIF1\XNicHz1dolxd3SnbnP5JI1iemuncjDPR3QuPA>? NWHpN4R7OjR6M{exOFI>

... 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]


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


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

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01846273 Active, not recruiting Age-related Macular Degeneration; Polypoidal Choroidal Vasculopathy (PCV) Novartis Pharmaceuticals|Novartis August 7, 2013 Phase 4
NCT03033225 Active, not recruiting Pancreatic Cancer Non-Resectable Mayo Clinic January 2017 Phase 2
NCT02939274 Recruiting Metastatic Breast Cancer Rogers Sciences Inc. October 2016 Phase 2
NCT02702700 Recruiting Pleural Effusion, Malignant Centre Hospitalier Universitaire Vaudois January 2016 Phase 1
NCT02495181 Recruiting Polypoidal Choroidal Vasculopathy Association for Innovation and Biomedical Research on Light and Image|European Vision Institute Clinical Research Network January 2016 Phase 4
NCT02457026 Withdrawn Neovascular Age-related Macular Degeneration Duke University|Bausch & Lomb Incorporated January 2016 --

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID