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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Cited by 15 Publications

6 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.

  • A representative immunostaining results of p-EGFR, p-ERK, YAP1, and cleavage caspase-3 in tumors of each group of nude mice.

    Theranostics, 2017, 7(5):1114-1132. Verteporfin purchased from Selleck.

  • Colony formation in H520 cells and H1581 cells that were with or without verteporfin

    Cancer Lett, 2018, 423:36-46. Verteporfin purchased from Selleck.

  • The effects of ADR and Verteporfin on the growth of HCC xenograft derived from MHCC-97H cells (n = 5 for each group). Representative images of IHC staining of KI67 and cleaved caspase-3 in tumors. Scale bar: 100 μm.

    EBioMedicine, 2018, 35:142-154. 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 MnX0SpVv[3Srb36gZZN{[Xl? NYPOU21khjFyMDDu[{9uVA>? NEXaSotFVVOR NF\oUYRqdmO{ZXHz[ZMhTE6DIH\yZYdu\W62YYTpc44hdGW4ZXzz MWixNFYxPzdzMB?=
HL-60 M1fnUIN6fG:2b4jpZ4l1gSCjc4PhfS=> MXL+NVAxKG6pL33M MXXEUXNQ NFftcJNqdmirYnn0d{Bk\WyuII\pZYJqdGm2eR?= MWixNFYxPzdzMB?=
Jurkat M{DBNmFxd3C2b4Ppd{Bie3OjeR?= MYT+NlgxKG6P NGXUW2VFVVOR M{Hw[4lv\HWlZYOgZUBD[2xvMj3k[ZBmdmSnboSgZZBweHSxc3nz NGCwR|QyOTJ2NUSxOS=>
RIF-1 NHnPeFFHfW6ldHnvckBie3OjeR?= MkfrNUDPxGdxbXy= MVLEUXNQ NEDmSG1l\WO{ZXHz[ZMhd3i7Z3XuJINwdnO3bYD0bY9v NFvMbYEyOjZzNUexPC=>
RIF-1 M{n1VYN6fG:2b4jpZ4l1gSCjc4PhfS=> M13NfFEh|rypL33s MmSzSG1UVw>? M1LuUoRm[3KnYYPlJJRwKDJyINMxJFUmKGOnbHygd5Vzfmm4YXy= M1j1cVEzPjF3N{G4
SVEC4-10 M1LFRWZ2dmO2aX;uJIF{e2G7 M1u0eFIxOCCwZz;tcC=> M2LxfGROW09? MVLpcoR2[2W|IH3pZ5JwfHWkdXzlJIRmeG:ueX3ldol7[XSrb36= NHj5OnUyPjR4N{GwOi=>
SVEC4-10 MkDsSpVv[3Srb36gZZN{[Xl? NGLsNnozODBibnevcYw> MWLEUXNQ NG\jWZVqdmS3Y3XzJJN1emW|czDhZ5RqdiCoaXLldkBnd3KvYYTpc44> NWT2SmFROTZ2NkexNFY>
ARPE-19 Mmi3Z5l1d3SxeHnjbZR6KGG|c3H5 MXT+NE4yKM7:Zz;tcC=> MneySG1UVw>? MkDhd4hwf3NiYTDkc5NmNWSncHXu[IVvfCC2b4jpZ4l1gQ>? NGDjTmwyPjl6N{mwOS=>
ARPE-19 NX;Ec2JETnWwY4Tpc44h[XO|YYm= MoHaNE4xOSEQvHevcYw> MV3EUXNQ NYL4dZNEcW6lcnXhd4V{KF[HR1[gZY5lKHKnZIXj[ZMhWEWGRjDlfJBz\XO|aX;u MVixOlk5PzlyNR?=
Y-79 NVTSNnduT3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= NIn6bo1,OSEQvHevcYw> MULEUXNQ M4LZXoRm[3KnYYPld{Bz\XSrbn;icIF{fG:vYTDj[YxtKHC{b3zp[oVz[XSrb36= MmTqNVg2Pzl5NkS=
WERI-Rb1 MWnHdo94fGhiaX7obYJqfG:{eTDhd5NigQ>? MXf+NUDPxGdxbXy= NIrWWXBFVVOR MVzk[YNz\WG|ZYOgdoV1cW6xYnzhd5RwdWFiY3XscEBxem:uaX\ldoF1cW:w M3PjdFE5PTd7N{[0
RB247C3 M2fObmdzd3e2aDDpcohq[mm2b4L5JIF{e2G7 M3S2UJ4yKM7:Zz;tcC=> MmS4SG1UVw>? NXHPO5hD\GWlcnXhd4V{KHKndHnuc4Jt[XO2b33hJINmdGxicILvcIln\XKjdHnvci=> NWnqTXg3OTh3N{m3OlQ>
RB355 M{PMe2dzd3e2aDDpcohq[mm2b4L5JIF{e2G7 MVf+NUDPxGdxbXy= Mm[5SG1UVw>? MXPk[YNz\WG|ZYOgdoV1cW6xYnzhd5RwdWFiY3XscEBxem:uaX\ldoF1cW:w NFT5[|YyQDV5OUe2OC=>
RB383 NH;nU2FIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= NG\STHl,OSEQvHevcYw> MWTEUXNQ NVq5e2hr\GWlcnXhd4V{KHKndHnuc4Jt[XO2b33hJINmdGxicILvcIln\XKjdHnvci=> NGrVcHIyQDV5OUe2OC=>
hFibro MojCZ5l1d3SxeHnjbZR6KGG|c3H5 NFnPXmgxNjViwsXnM41t NX\aW|JYTE2VTx?= NHnNZ2hl\WO{ZXHz[ZMhfmmjYnnsbZR6KGK7IEi2MFUm NEi2b5gzOzR2MUGxOC=>
hTMC NYDCfI8x[3m2b4TvfIlkcXS7IHHzd4F6 MX6wMlUhyrWpL33s M1Ppd2ROW09? M4i2TIRm[3KnYYPld{B3cWGkaXzpeJkh[nliOEiuPUU> NFvwRWIzOzR2MUGxOC=>
ARPE-19 NF3YTHlkgXSxdH;4bYNqfHliYYPzZZk> MX:wMlUhyrWpL33s M1fLVmROW09? Ml;B[IVkemWjc3XzJJZq[WKrbHn0fUBjgSB3NT61KS=> MmHVNlM1PDFzMUS=
Panc-1 NHT1PJFIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= MYGxNEDPxE1? MVfEUXNQ Mk\JbY5pcWKrdIOgZ4VtdCCycn;sbYZmemG2aX;u NIPL[XgzPDB4OUC2PS=>
MIA PaCa-2 NFizT5RIem:5dHigbY5pcWKrdH;yfUBie3OjeR?= Mk\nNVAh|ryP M17YT2ROW09? NEjHXZNqdmirYnn0d{Bk\WyuIIDyc4xq\mW{YYTpc44> MmLLNlQxPjlyNkm=
BxPC-3 NXvSU3B5T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MXWxNEDPxE1? NVztc4pxTE2VTx?= M4OwTIlvcGmkaYTzJINmdGxicILvcIln\XKjdHnvckBkd22ybHX0[Yx6 MVmyOFA3QTB4OR?=
SU86.86 NXnjTVB7T3Kxd4ToJIlvcGmkaYTvdpkh[XO|YYm= MXexNEDPxE1? M4S0eWROW09? M{P1V4lvcGmkaYTzJINmdGxicILvcIln\XKjdHnvckBkd22ybHX0[Yx6 MWeyOFA3QTB4OR?=
MCF-7 NEXvRmdCfXSxcHjh[5kh[XO|YYm= NXXEdJJDOTBizszN NILWXGVFVVOR MU\pcohq[mm2czDn[Y1kcXSjYnnu[U1qdmS3Y3XkJIF2fG:yaHHnfS=> MVqyOFA3QTB4OR?=
WERI Ml3FS5Jwf3SqIHnubIljcXSxcomgZZN{[Xl? M{OyOp4yOCEQvHevcYw> MULEUXNQ NFzt[HlqdmirYnn0d{Boem:5dHigc4YhemW2aX7vZoxie3SxbXGgZ4VtdHN? M13YNFI1QDN5MUSy
WERI M3:5WmZ2dmO2aX;uJIF{e2G7 MVn+NVAh|rypL33s MlXPSG1UVw>? M3ns[oJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9v MXmyOFg{PzF2Mh?=
Y-79 NXnkNWx1TnWwY4Tpc44h[XO|YYm= NFvBcIN,OTBizsznM41t M{n6XWROW09? M3LjZoJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9v NYj1O3NZOjR6M{exOFI>
Y-79 MVrGeY5kfGmxbjDhd5NigQ>? MX7+NVAh|rypL33s NHPwT3RFVVOR MYfh[oZm[3S|IGnBVE1VTUGGIIDyc5RwNW:wY3;n[Y5mKHCjdHj3ZZk> NHvpeJEzPDh|N{G0Ni=>
Y-79 M1;oSmZ2dmO2aX;uJIF{e2G7 NWnZfHFMhjFyIN88[{9udA>? NIP0SHNFVVOR Mlqz[I94di2{ZXf1cIF1\XNicHz1dolxd3SnbnP5JI1iemuncjDPR3QuPA>? MUSyOFg{PzF2Mh?=

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
p-S6(S240/244) / p-4EBP1(S65); 

PubMed: 28202507     

KLE, EFE184 and NOU-1 were treated with Verteporfin (0.1 μM, 0.3 μM). After 36h, cell lysates were western blotted with indicated antibodies. Bands are from one of three independent experiments.

c-Myc / Bcl-2; 

PubMed: 29416644     

In CAL27 cell lines, the expression of BCL-2 and C-MYC proteins decreased with the increase of Verteporfin concentration. The presented columns are given as the means ± SD. *p < 0.05, **P < 0.01, ***p < 0.001.

ECAD / Vimentin / Sox2 / CD44 / CD133; 

PubMed: 30467925     

Yes-associated protein 1 (YAP1), E-cadherin, vimentin (epithelial-mesenchymal transition [EMT] pathway), SOX2 CD44 and CD133 (autophagy markers) were detected by western blot in control, verteporfin (1 μmol/L) and verteporfin + 231-taxol (0.5 μmol/L) resistance groups.


PubMed: 28202507     

KLE, EFE184, NOU-1 and SKUT-2 were treated with 3 μM Verteporfin. After 24h, cell lysates were western blotted with indicated antibodies. Bands are from one of three independent experiments.

28202507 29416644 30467925
Growth inhibition assay
Cell viability; 

PubMed: 28042502     

A: Cell viability was determined by MTS assay after the UM cells were exposed to verteporfin for 72 hours. B: After treated with various concentrations of verteporfin for 24 hours, the UM cells (e.g., 92.1, Mel 270, Omm 1, Omm 2.3) were seeded in drug-free soft agar culture for 14 days. Colonies were counted. 


PubMed: 30254296     

Treatment of U343 cells with 5 μM VP between 1-8 h in both 21% and 1% O2 induced morphological changes. Scale bar represents 10 µm. VP: Verteporfin


PubMed: 30254296     

Calreticulin (CRT) significantly increased in VP-treated (5 µM, 2 h) U87 cells in both 21% and 1% O2 indicating likely ER stress.


PubMed: 28404908     

Confocal images of HEC-1-B cells and organoids which were subjected to immunofluorescence detection of A. YAP and B. phospho-YAP after VP treatment. YAP and phospho-YAP are conjugated with goat anti-mouse and goat anti-rabbit Alexa flour secondary antibodies respectively. (A) Upper panel bar=63x and lower panel bar = 20x. (B) Upper panel bar=63x and lower panel bar = 20x.

30254296 28404908
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
in solvent
Synonyms CL 318952

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03067051 Recruiting Recurrent Prostate Cancer SpectraCure AB March 21 2017 Phase 1
NCT03067051 Recruiting Recurrent Prostate Cancer SpectraCure AB March 21 2017 Phase 1
NCT03033225 Recruiting Pancreatic Cancer Non-Resectable Mayo Clinic January 5 2017 Phase 2
NCT03033225 Recruiting Pancreatic Cancer Non-Resectable Mayo Clinic January 5 2017 Phase 2
NCT02939274 Recruiting Metastatic Breast Cancer Rogers Sciences Inc. October 2016 Phase 2
NCT02939274 Recruiting Metastatic Breast Cancer Rogers Sciences Inc. October 2016 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID