Verteporfin liposome
Liposomal verteporfin is a liposome-encapsulated form of Verteporfin (HY-B0146). Verteporfin is a photosensitizer used in photodynamic therapy, which generates reactive oxygen species (ROS) upon irradiation at 690 nm to mediate photodynamic effects. Liposomal verteporfin can promote the release of Oxaliplatin (HY-17371) from endolysosomes via photochemical internalization (PCI), prolong the drug circulation time and enable sustained release, accumulate the drug in neovascular vessels, and enhance its cytotoxicity in tumor models. Liposomal verteporfin can be used in studies related to neovascular eye diseases and pancreatic cancer[1][2][3].
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Biological Activity
Verteporfin liposome (0.01-0.8 μM; 1 h) exhibits extremely low dark toxicity in MIA PaCa-2 and PANC-1 pancreatic cancer cells, and induces concentration-dependent cytotoxicity after irradiation with 0.5 J/cm2[1].
Verteporfin liposome (25-250 μM; 0.5-24 h) is taken up by MIA PaCa-2 and PANC-1 3D microtumors in a time-dependent manner[1].
Photodynamic therapy (PDT) with Verteporfin liposome (100 μM; 8 h) synergizes with Oxaliplatin (HY-17371) to reduce the viability of 3D pancreatic cancer microtumors of MIA PaCa-2 and PANC-1[1].
Verteporfin liposomes are taken up faster by LDL receptor-enriched human colon cancer cell lines than aqueous sodium hematoporphyrin[3].
Strong lysosomal colocalization is observed in MIA PaCa-2 and PANC-1 pancreatic cancer cells treated with Verteporfin liposome (200 μM; 2, 8, 24 h)[1].
The binding rate of Verteporfin liposome to plasma lipoproteins in vitro reaches up to 91%, with a balanced distribution among major lipoprotein fractions[3].
Verteporfin liposomes are selectively taken up by LDL receptor-positive cell lines in vitro via LDL receptor-mediated binding[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MIA PaCa-2, PANC-1
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Concentration:200 μM
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Incubation Time:2, 8, 24 h
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Result:Showed strong colocalization with lysosomes after 8 hours of incubation, with average Pearson’s correlation coefficients of 0.8 in both cell lines.
Maintained high colocalization coefficients across all time points for NLBPD and FLBPD, while CLBPD showed a decrease in colocalization at 24 hours in both cell lines.
Exhibited fluorescence across cellular membranes, indicating non-exclusive lysosomal localization.
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Cell Line:MIA PaCa-2, PANC-1 3D microtumor cultures
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Concentration:25, 50, 100, 200, 250 μM (dark toxicity); 100 μM (uptake kinetics)
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Incubation Time:24 h (dark toxicity); 30 minutes, 1, 2, 4, 8, 16, 24 h (uptake kinetics)
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Result:Increased in uptake over time, with maximal uptake observed at 24 hours.
Showed the highest uptake for CLBPD in PANC-1 microtumors.
Demonstrated non-toxicity at 100 μM to microtumors.
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Cell Line:MIA PaCa-2, PANC-1 3D microtumor cultures
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Concentration:100 μM
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Incubation Time:8 h
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Result:Reduced MIA PaCa-2 microtumor viability to 55%, 59%, and 50% respectively for NLBPD, FLBPD, or CLBPD monotherapy.
Reduced MIA PaCa-2 microtumor viability to 20% when combining FLBPD PDT with oxaliplatin, a significant decrease compared to monotherapies.
Achieved a global synergy score of 29.41 for MIA PaCa-2, with radiant exposures ≥2.5 J/cm2 synergistic with all oxaliplatin doses.
Maintained PANC-1 microtumor viability at 71%, 68%, and 74% respectively for NLBPD, FLBPD, or CLBPD monotherapy.
Reduced PANC-1 microtumor viability to 45%, 56%, and 56% respectively when combining NLBPD, FLBPD, or CLBPD PDT with oxaliplatin.
Achieved a global synergy score of 8.75 for PANC-1, with synergy observed at select dose combinations.
Diminished combination treatment efficacy in both cell lines when dynasore was added.
Verteporfin liposome (intravenous injection; single dose) achieves higher tumor tissue concentrations in tumor-bearing mice with abundant LDL receptors than water-soluble Verteporfin (HY-B0146)[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Rj: NMRI-Foxn1nu/nu nude mice (female, 6 weeks old, orthotopic implantation of luciferase-expressing PANC-1 cells)[1]
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Dosage:0.5 mg/kg (liposomal verteporfin); 5 mg/kg (oxaliplatin)
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Administration:i.p. (liposomal verteporfin, followed by 690 nm light irradiation at 150 mW/cm2 for 50 J/cm2); i.p. (oxaliplatin, immediate post-irradiation)
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Result:Achieved the lowest tumor volumes and heterogeneity compared to monotherapies or sham treatment.
Showed 58% of mice had tumor response, with mean bioluminescence signal reduction significantly greater than oxaliplatin monotherapy and near-significantly greater than PDT monotherapy.
Maintained stable body weight profiles confirming tolerability.
Chemical Information
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SMILES
[Verteporfin liposome]
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Synonyms
Liposomal verteporfin
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Verteporfin liposome Related Classifications
HY-185390 Related Classifications
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- Verteporfin liposome
- Liposomal verteporfin
- Liposome
- YAP
- Reactive Oxygen Species (ROS)
- age-related macular degeneration
- MIA PaCa-2
- PANC-1
- pancreatic ductal adenocarcinoma
- pancreatic cancer cells
- LDL receptor
- subfoveal choroidal neovascularisation
- pathological myopia
- orthotopic pancreatic tumors
- presumed ocular histoplasmosis syndrome
- Inhibitor
- inhibitor
- inhibit