Verteporfin

Catalog No.S1786 Batch:S178615

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Technical Data

Formula

C41H42N4O8
Molecular Weight 718.79 CAS No. 129497-78-5
Solubility (25°C)* In vitro DMSO 100 mg/mL (139.12 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml means slightly soluble or 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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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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. Verteporfin is an autophagy inhibitor. Verteporfin inhibits cell proliferation and induces apoptosis.
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]
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 (from reference)

Cell Assay:

[4]
  • Cell lines

    Ki67+ and Sox10+ cells

  • Concentrations

    2 uM

  • Incubation Time

    72 h

  • Method

    Cells were treated with verteporfin (2 µM) for 72 hr for Brdu staining.
Animal Study:

[4]
  • Animal Models

    Atoh1-Ptch mice

  • Dosages

    100 mg/kg

  • Administration

    i.p.

References

  • https://pubmed.ncbi.nlm.nih.gov/11094244/
  • https://pubmed.ncbi.nlm.nih.gov/10607710/
  • https://pubmed.ncbi.nlm.nih.gov/22677547/
  • https://pubmed.ncbi.nlm.nih.gov/29438698/
  • https://pubmed.ncbi.nlm.nih.gov/31474569/

Customer Product Validation

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.

Data from [ J Exp Med , 2014 , 211(11), 2249-63 ]

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

Data from [ , , Theranostics, 2017, 7(5):1114-1132 ]

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

Data from [ , , Cancer Lett, 2018, 423:36-46 ]

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.

Data from [ , , EBioMedicine, 2018, 35:142-154 ]

Selleck's Verteporfin has been cited by 164 publications

Non-canonical Wnt signaling promotes epithelial fluidization in the repairing airway [ Nat Commun, 2025, 16(1):4124] PubMed: 40319020
YAP/TEAD4/SP1-induced VISTA expression as a tumor cell-intrinsic mechanism of immunosuppression in colorectal cancer [ Cell Death Differ, 2025, 10.1038/s41418-025-01446-2] PubMed: 39875519
Targeting the NAT10/XIST/YAP1 Axis-Mediated Vascular Abnormalization Enhances Immune Checkpoint Blockade in Gastric Cancer [ Int J Biol Sci, 2025, 21(11):4997-5014] PubMed: 40860183
A novel clinically relevant antagonistic interplay between prolactin and oncogenic YAP-CCN2 pathways as a differentiation therapeutic target in breast cancer [ Cell Death Dis, 2025, 16(1):221] PubMed: 40157909
YAP1 facilitates the pathogenesis of psoriasis via modulating keratinocyte proliferation and inflammation [ Cell Death Dis, 2025, 16(1):186] PubMed: 40108109
Loss of LATS1 and LATS2 promotes ovarian tumor formation by enhancing AKT activity and PD-L1 expression [ Oncogene, 2025, 10.1038/s41388-025-03387-z] PubMed: 40221530
Targeting yes-associated protein to overcome imatinib resistance in gastrointestinal stromal tumor drug-tolerant persister cells [ Gastric Cancer, 2025, 10.1007/s10120-025-01657-z] PubMed: 40921853
YAP as a therapeutic target to reverse trastuzumab resistance [ Gastric Cancer, 2025, 10.1007/s10120-025-01630-w] PubMed: 40542295
Engineering anti-c-MET scFv-conjugated PLGA nanoparticles for precision verteporfin delivery in lung cancer cells: a formulation study [ Int J Pharm, 2025, 683:126004] PubMed: 40730320
Verteporfin combined with ROCK inhibitor promotes the restoration of corneal endothelial cell dysfunction in rats [ Biochem Pharmacol, 2025, 231:116641] PubMed: 39571917

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.