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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  • 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 NUL4SG13TnWwY4Tpc44h[XO|YYm= MWD+NVAxKG6pL33M MYnEUXNQ NWLuS3drcW6lcnXhd4V{KESQQTDmdoFodWWwdHH0bY9vKGyndnXsdy=> NFW4OHoyODZyN{exNC=>
HL-60 M1vTVYN6fG:2b4jpZ4l1gSCjc4PhfS=> NIT5NZp,OTByIH7nM41N NYPsdGZ3TE2VTx?= M1KxbIlvcGmkaYTzJINmdGxidnnhZoltcXS7 NXjpV5V1OTB4MEe3NVA>
Jurkat NFLicoFCeG:ydH;zbZMh[XO|YYm= MWf+NlgxKG6P NX7UUIozTE2VTx?= Mn3PbY5lfWOnczDhJGJkdC1{LXTldIVv\GWwdDDhdI9xfG:|aYO= M17YWlEyOjR3NEG1
RIF-1 NVTHOZZ2TnWwY4Tpc44h[XO|YYm= MWGxJO69\y:vbB?= MoDWSG1UVw>? Ml75[IVkemWjc3XzJI95gWenbjDjc45{fW2ydHnvci=> NFWwVlIyOjZzNUexPC=>
RIF-1 M2nZPIN6fG:2b4jpZ4l1gSCjc4PhfS=> NGnDPYcyKM7:Zz;tcC=> NYPPTJJWTE2VTx?= NFWxeINl\WO{ZXHz[UB1dyB{MDFCtUA2LSClZXzsJJN2en[rdnHs M3jUT|EzPjF3N{G4
SVEC4-10 NX7CcVg4TnWwY4Tpc44h[XO|YYm= NETydmozODBibnevcYw> MUHEUXNQ MVrpcoR2[2W|IH3pZ5JwfHWkdXzlJIRmeG:ueX3ldol7[XSrb36= NEX2VocyPjR4N{GwOi=>
SVEC4-10 NYCyS|JDTnWwY4Tpc44h[XO|YYm= NILj[WYzODBibnevcYw> MVjEUXNQ NXLIO2JGcW6mdXPld{B{fHKnc4OgZYN1cW5iZnni[ZIh\m:{bXH0bY9v NETnPIIyPjR4N{GwOi=>
ARPE-19 MmHNZ5l1d3SxeHnjbZR6KGG|c3H5 MljqglAvOSEQvHevcYw> NXfxNoh2TE2VTx?= M{jidZNpd3e|IHGg[I9{\S2mZYDlcoRmdnRidH;4bYNqfHl? M2XWeFE3QTh5OUC1
ARPE-19 MmT0SpVv[3Srb36gZZN{[Xl? MlzCNE4xOSEQvHevcYw> MVnEUXNQ MUTpcoNz\WG|ZYOgWmVITiCjbnSgdoVlfWOnczDQSWRHKGW6cILld5Nqd25? MWSxOlk5PzlyNR?=
Y-79 NHX4WmdIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NGPIVHF,OSEQvHevcYw> NUHISWp1TE2VTx?= Mmrl[IVkemWjc3XzJJJmfGmwb3LsZZN1d22jIHPlcIwheHKxbHnm[ZJifGmxbh?= NYK4dpkxOTh3N{m3OlQ>
WERI-Rb1 NX7yXWhIT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NF7XT3N,OSEQvHevcYw> NGq0[llFVVOR M1fvcIRm[3KnYYPld{Bz\XSrbn;icIF{fG:vYTDj[YxtKHC{b3zp[oVz[XSrb36= MkOxNVg2Pzl5NkS=
RB247C3 M13lXGdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 NYrSZYdyhjFizsznM41t NEPBbIRFVVOR Mn;3[IVkemWjc3XzJJJmfGmwb3LsZZN1d22jIHPlcIwheHKxbHnm[ZJifGmxbh?= MUKxPFU4QTd4NB?=
RB355 NHH4ZZZIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MVv+NUDPxGdxbXy= NG\3SpRFVVOR M2PiT4Rm[3KnYYPld{Bz\XSrbn;icIF{fG:vYTDj[YxtKHC{b3zp[oVz[XSrb36= MmfZNVg2Pzl5NkS=
RB383 NV;qTXFCT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NILa[XZ,OSEQvHevcYw> M3\ndGROW09? MWrk[YNz\WG|ZYOgdoV1cW6xYnzhd5RwdWFiY3XscEBxem:uaX\ldoF1cW:w NUG1THdvOTh3N{m3OlQ>
hFibro M2Dab4N6fG:2b4jpZ4l1gSCjc4PhfS=> MnvNNE42KML3Zz;tcC=> NWLHbIY3TE2VTx?= NGjNOpJl\WO{ZXHz[ZMhfmmjYnnsbZR6KGK7IEi2MFUm NELHTJkzOzR2MUGxOC=>
pTMC NEXkV5pkgXSxdH;4bYNqfHliYYPzZZk> NULRbmhMOC53INM1[{9udA>? M1niRWROW09? Mm\4[IVkemWjc3XzJJZq[WKrbHn0fUBjgSB7Mj65KS=> NWHYXYVROjN2NEGxNVQ>
hTMC NEXVRVdkgXSxdH;4bYNqfHliYYPzZZk> MoX2NE42KML3Zz;tcC=> Ml;TSG1UVw>? NEDTfGZl\WO{ZXHz[ZMhfmmjYnnsbZR6KGK7IEi4Mlkm MljPNlM1PDFzMUS=
ARPE-19 NIL6fplkgXSxdH;4bYNqfHliYYPzZZk> NXrvfJhvOC53INM1[{9udA>? MkL5SG1UVw>? MmHU[IVkemWjc3XzJJZq[WKrbHn0fUBjgSB3NT61KS=> NWfoWIFrOjN2NEGxNVQ>
Panc-1 MmDsS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? Ml:yNVAh|ryP MnXlSG1UVw>? M2XzdYlvcGmkaYTzJINmdGxicILvcIln\XKjdHnvci=> M1;nbFI1ODZ7ME[5
MIA PaCa-2 NUiy[YhxT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MWexNEDPxE1? MVnEUXNQ M2W4cYlvcGmkaYTzJINmdGxicILvcIln\XKjdHnvci=> NX;wNog5OjRyNkmwOlk>
BxPC-3 NIPiTIRIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MnLWNVAh|ryP Mlv5SG1UVw>? NVnLcWRFcW6qaXLpeJMh[2WubDDwdo9tcW[ncnH0bY9vKGOxbYDs[ZRmdHl? MUKyOFA3QTB4OR?=
SU86.86 NW\Ubo9uT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MoPzNVAh|ryP M2LZcGROW09? M3HYTIlvcGmkaYTzJINmdGxicILvcIln\XKjdHnvckBkd22ybHX0[Yx6 M{OySVI1ODZ7ME[5
MCF-7 M4TqWmF2fG:yaHHnfUBie3OjeR?= MXOxNEDPxE1? M3rJdWROW09? MmDUbY5pcWKrdIOg[4Vu[2m2YXLpcoUucW6mdXPl[EBifXSxcHjh[5k> NXi1eogxOjRyNkmwOlk>
WERI MXfHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? Mn7RglExKM7:Zz;tcC=> MYHEUXNQ M1e0ZolvcGmkaYTzJIdzd3e2aDDv[kBz\XSrbn;icIF{fG:vYTDj[Yxtew>? M{HNUlI1QDN5MUSy
WERI MoWySpVv[3Srb36gZZN{[Xl? M3[0TZ4yOCEQvHevcYw> NELxRllFVVOR MYnicI9kc3NiY3XscEBkgWOuZTDwdo9oemW|c3nvci=> MoLhNlQ5OzdzNEK=
Y-79 M1[wdWZ2dmO2aX;uJIF{e2G7 M3XUW54yOCEQvHevcYw> MYPEUXNQ NEPXd3NjdG:la4OgZ4VtdCCleXPs[UBxem:pcnXzd4lwdg>? NIjVRmkzPDh|N{G0Ni=>
Y-79 M1;jOmZ2dmO2aX;uJIF{e2G7 M3;ZNp4yOCEQvHevcYw> MmS1SG1UVw>? MmXlZYZn\WO2czDZRXAuXEWDRDDwdo91dy2xbnPv[4Vv\SCyYYToe4F6 M3jxdlI1QDN5MUSy
Y-79 M{Xv[WZ2dmO2aX;uJIF{e2G7 NFf6[4V,OTBizsznM41t M{PxZWROW09? MmfI[I94di2{ZXf1cIF1\XNicHz1dolxd3SnbnP5JI1iemuncjDPR3QuPA>? NYnNVosxOjR6M{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]

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
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