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Catalog No.GC14482

Verteporfin Chemical Structure

Verteporfin is a potent inhibitor of PD-L1 expression used for treatment in the age-related macular degeneration , port-wine stain birthmarks and cancer.

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10mM (in 1mL DMSO)
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Cell experiment [1]:

Cell lines

RAW 264.7 cells

Preparation Method

RAW 264.7 cells were pretreated with 2 μM verteporfin for 2 h, then stimulated with LPS (1 μg/ml) for 22 h.

Reaction Conditions

2 μM; 2 h


When RAW 264.7 cells were treated with 2 μM verteporfin, GCSF, IL-6, CCL2, MCP-5, CCL5, and TNF-α were significantly inhibited compared with cells treated with LPS alone.

Animal experiment [2]:

Animal models

C57BL/6 mice

Preparation Method

Lewis lung carcinoma cells (LLCs, 5 x 105 in 100 μl phosphate-buffered saline) were inoculated subcutaneously into C57BL/6 mice (male, 8–12 weeks) in both flanks. Five days after inoculation, mice were randomly divided into 4 groups and treated with vehicle, BMN 673 0.33 mg/Kg daily (oral gavage), verteporfin 30 mg/kg daily (intraperitoneal injection) and the combination of BMN 673 with verteporfin for 16 days. Tumors size were measured every 2 days by digital calipers to determine tumor volume using the formula [length/2] × [width2].

Dosage form

30 mg/kg; i.p.


Verteporfin treatment led to marked decreases in PD-L1 expression and increases in CD8 T cells especially in the combinatorial group of vereporfin and BMN 673.


[1]. Wang Y, Wang L, Wise JTF, Shi X, Chen Z. Verteporfin inhibits lipopolysaccharide-induced inflammation by multiple functions in RAW 264.7 cells. Toxicol Appl Pharmacol. 2020 Jan 15;387:114852.

[2]. Liang J, et al. Verteporfin Inhibits PD-L1 through Autophagy and the STAT1-IRF1-TRIM28 Signaling Axis, Exerting Antitumor Efficacy. Cancer Immunol Res. 2020 Jul;8(7):952-965.


Verteporfin is a potent inhibitor of PD-L1 expression used for treatment in the age-related macular degeneration , port-wine stain birthmarks and cancer.[1]

In vitro experiment it shown that at 1μM versus 0.5 μM concentrations of verteporfin, it was sufficient to decrease PD-L1 expression in ATG5 depleted cells.[1] In vitro, at very low concentrations of verteporfin (0.1–0.2 μm) , verteporfin induced significant cell death in GSCs. However, 0.5 μm verteporfin had no effect on the cell death in differentiated GSCs, IMR90, rat NSCs or mouse astrocytes.[2] In vitro efficacy test it indicated treatment with 4, 8 and 12 μM verteporfin decreased significantly the expression levels of YAP, AXL and CYR61 mRNA in MCF-7, BT-474 and BT-549 cells. And verteporfin also downregulated the mRNA expression of CTGF in BT-474 and BT-549 cells.[3] Treatment with 0.5, 1, 2, and 5 μM verteporfin inhibited the viability of HeLa cells and had no obvious effect on H8 cells.[4]

In vivo study it demonstrated that treatment with 2 mg.kg-1 free verteporfin induced severe phototoxic adverse effects leading to the death of 5 out of 8 mice. However, mice were treated 8 mg.kg-1 nanostructured lipid carriers-verteporfin intravenously laser light exposure of tumors significantly inhibited tumor growth without visible toxicity.[5] In vivo, 2 mg/kg verteporfin infusion alone resulted in nitric oxide and malonyldialdehyde level increments in the retina.[6]

[1].Liang J, et al. Verteporfin Inhibits PD-L1 through Autophagy and the STAT1-IRF1-TRIM28 Signaling Axis, Exerting Antitumor Efficacy. Cancer Immunol Res. 2020 Jul;8(7):952-965. Kuramoto K, Yamamoto M, Suzuki S, Sanomachi T, Togashi K, Seino S, Kitanaka C, Okada M.
[2].Kuramoto K, et al. Verteporfin inhibits oxidative phosphorylation and induces cell death specifically in glioma stem cells. FEBS J. 2020 May;287(10):2023-2036.
[3].Wei C, Li X. Verteporfin inhibits cell proliferation and induces apoptosis in different subtypes of breast cancer cell lines without light activation. BMC Cancer. 2020 Oct 29;20(1):1042.
[4].Yin L, Chen G. Verteporfin Promotes the Apoptosis and Inhibits the Proliferation, Migration, and Invasion of Cervical Cancer Cells by Downregulating SULT2B1 Expression. Med Sci Monit. 2020 Oct 20;26:e926780.
[5].Michy T, et al. Verteporfin-Loaded Lipid Nanoparticles Improve Ovarian Cancer Photodynamic Therapy In Vitro and In Vivo. Cancers (Basel). 2019 Nov 8;11(11):1760.
[6].Turkuoglu P, et al. Retinal nitric oxide and malonyldialdehyde levels following photodynamic therapy. Indian J Ophthalmol. 2011 Jan-Feb;59(1):5-8.

Chemical Properties

Cas No. 129497-78-5 SDF
Synonyms CL 318952;Visudyne
Chemical Name N/A
Canonical SMILES O=C([C@H]1[C@](/C(N=C2/C=C(C(C)=C/3C=C)\NC3=C/C4=N/C(C(CCC(O)=O)=C4C)=C\5)=C/C6=C(C)C(CCC(OC)=O)=C5N6)(C)C2=CC=C1C(OC)=O)OC
Formula C41H42N4O8 M.Wt 718.79
Solubility ≥ 18.3mg/mL in DMSO Storage 4°C, protect from light
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

Verteporfin Inhibits PD-L1 through Autophagy and the STAT1-IRF1-TRIM28 Signaling Axis, Exerting Antitumor Efficacy

Cancer Immunol Res2020 Jul;8(7):952-965.PMID: 32265228DOI: 10.1158/2326-6066.CIR-19-0159

Programmed cell death 1 ligand 1 (PD-L1) is a key driver of tumor-mediated immune suppression, and targeting it with antibodies can induce therapeutic responses. Given the costs and associated toxicity of PD-L1 blockade, alternative therapeutic strategies are needed. Using reverse-phase protein arrays to assess drugs in use or likely to enter trials, we performed a candidate drug screen for inhibitors of PD-L1 expression and identified verteporfin as a possible small-molecule inhibitor. Verteporfin suppressed basal and IFN-induced PD-L1 expression in vitro and in vivo through Golgi-related autophagy and disruption of the STAT1-IRF1-TRIM28 signaling cascade, but did not affect the proinflammatory CIITA-MHC II cascade. Within the tumor microenvironment, verteporfin inhibited PD-L1 expression, which associated with enhanced T-lymphocyte infiltration. Inhibition of chromatin-associated enzyme PARP1 induced PD-L1 expression in high endothelial venules (HEV) in tumors and, when combined with verteporfin, enhanced therapeutic efficacy. Thus, verteporfin effectively targets PD-L1 through transcriptional and posttranslational mechanisms, representing an alternative therapeutic strategy for targeting PD-L1.

Photosensitizers and Photodynamic Therapy: Verteporfin

Dev Ophthalmol2016;55:330-6.PMID: 26501167DOI: 10.1159/000434704

Photodynamic therapy (PDT) is a phototherapy in which a photosensitive dye is injected into a peripheral vein and activated by light in order to occlude choroidal vessels or change their permeability. PDT has been largely applied in the treatment of choroidal neovascularization (CNV), especially CNV related to age-related macular degeneration, but was also of benefit in other diseases, including central serous chorioretinopathy and choroidal hemangioma.

EUS-guided verteporfin photodynamic therapy for pancreatic cancer

Gastrointest Endosc2021 Jul;94(1):179-186.PMID: 33647286DOI: 10.1016/j.gie.2021.02.027

Background and aims: Locally advanced pancreatic cancer (LAPC) often causes obstruction. Verteporfin photodynamic therapy (PDT) can feasibly "debulk" the tumor more safely than noncurative surgery and has multiple advantages over older PDT agents. We aimed to assess the feasibility of EUS-guided verteporfin PDT in ablating nonresectable LAPC.
Methods: Adults with LAPC with adequate biliary drainage were prospectively enrolled. Exclusion criteria were significant metastatic disease burden, disease involving >50% duodenal or major artery circumference, and recent treatment with curative intent. CT was obtained between days -28 to 0. On day 0, verteporfin .4 mg/kg was infused 60 to 90 minutes before EUS, during which a diffuser was positioned in the tumor and delivered light at 50 J/cm for 333 seconds. CT was obtained on day 2, with adverse event monitoring occurring on days 1, 2, and 14. The primary outcome was presence of necrosis.
Results: Of 8 patients (62.5% men, mean age 65 ± 7.9 years) included in the study, 5 were staged at T3, 2 at T2, and 1 at T1. Most (n = 4) had primary lesions in the pancreatic head. Mean pretrial tumor diameter was 33.3 ± 13.4 mm. On day 2 CT, 5 lesions demonstrated a zone of necrosis measuring a mean diameter of 15.7 ± 5.5 mm; 3 cases did not develop necrosis. No adverse events were noted during the procedure or postprocedure observation period (days 1-3), and no changes in patient-reported outcomes were noted.
Conclusions: In this pilot study, EUS-guided verteporfin PDT is feasible and shows promise as a minimally invasive ablative therapy for LAPC in select patients. Tumor necrosis is visible within 48 hours after treatment. Patient enrollment and data collection are ongoing. (Clinical trial registration number: NCT03033225.).

Non-Photoinduced Biological Properties of Verteporfin

Curr Med Chem2016;23(11):1171-84.PMID: 26980565DOI: 10.2174/0929867323666160316125048

Background: Verteporfin is a porphyrinic photosensitizer clinically used for the photodynamic treatment of age-related macular degeneration. It has been identified almost simultaneously as a YAP/TEAD and an autophagosome inhibitor. Over the last few years, YAP (TAZ), the downstream effectors of the Hippo pathway, have emerged as promising anticancer targets, as shown by several experimental lines of evidence, showing the overproduction of YAP in several cancers. However, YAP was also found to be closely connected to autophagy, mitochondria and reactive oxygen/nitrogen species. We herein, review the recent studies where VP was used without photoactivation as a YAP/TEAD inhibitor or protein oligomerization promoter, focusing on its effects on the YAP/TEAD gene targets and other biomarkers related to autophagy.
Results: Since the identification of VP as YAP/TEAD inhibitor, several in vitro and in vivo studies have revealed the new potential of this molecule in different cancers, where YAP is overexpressed. However, detailed structural information about its interaction with YAP is still lacking. Concomitantly, VP was identified as autophagosome inhibitor by promoting oligomerization of p62. Moreover, VP proves to be tumor-selective proteotoxic (by oligomerization of p62, STAT3) in colorectal cancer. Knowledge on the biological properties of the only YAP inhibitor available to date is vital for its pharmacological use on cellular and animal models.
Conclusion: VP is a multi-target drug interacting with several proteins implicated in major cellular processes. Although this does not impact its clinical use, VP does not seem to be the ideal drug for pharmacological inhibitions of YAP/TEAD.

Verteporfin inhibits lipopolysaccharide-induced inflammation by multiple functions in RAW 264.7 cells

Toxicol Appl Pharmacol2020 Jan 15;387:114852.PMID: 31812773DOI: 10.1016/j.taap.2019.114852

Inflammation is a physiologic response to damage triggered by infection, injury or chemical irritation. Chronic inflammation produces repeated damage to cells and tissues, which can induce a variety of human diseases including cancer. Verteporfin, an FDA approved drug, is used for the treatment of age-related macular degeneration. The anti-tumor effects of verteporfin have been demonstrated by a number of studies. However, fewer studies focus on the anti-inflammatory functions of this drug. In this study, we investigated the anti-inflammatory effects and potential mechanisms of verteporfin. The classic lipopolysaccharide (LPS)-induced inflammation cell model was used. RAW 264.7 cells were pre-treated with verteporfin or vehicle control, followed by LPS stimulation. Verteporfin inhibited IL-6 and TNF-α at mRNA and protein expression levels. This effect was mediated through inhibition of the NF-κB and JAK/STAT pathways. Finally, verteporfin exhibited an anti-inflammation effect by crosslinking of protein such as NF-κB p65, JAK1, JAK2, STAT1, or STAT3 leading to inflammation. Taken together, these results indicate that verteporfin has the potential to be an effective therapeutic agent against inflammatory diseases.


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