TPP-Ce6
TPP-Ce6 is a mitochondria-targeted photosensitizer formed by the ester bond conjugation of chlorophyll e6 (Ce6) with triphenylphosphine (TPP). Under light irradiation or ultrasound exposure, TPP-Ce6 generates reactive oxygen species, induces cell apoptosis, and triggers immunogenic cell death. TPP-Ce6 can serve as a component of carrier-free co-delivery systems, undergo enzyme-induced self-assembly within tumors, and modulate tumor hypoxia. TPP-Ce6 is applicable to research on breast cancer and glioblastoma.
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- No. CAS: 3030629-73-0
- Fòrmula: C94H90N4O6P33+
- Peso molecular:1464.66
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Actividad biológica
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Chemical Information
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Actividad biológica
TPP-Ce6 (0.3 μg/mL (Ce6 equivalent); 2 h, 4 h, 6 h, 12 h) exhibits rapid, time-dependent cellular uptake by 4T1 mouse breast cancer cells, with greater uptake efficiency than free Ce6 but lower efficiency than TPP-Ce6@siPD-L1 NPs at all tested time points (2 h, 4 h, 6 h, 12 h) at a concentration of 0.3 μg/mL (Ce6 equivalent)[1].
TPP-Ce6 (0.3 μg/mL (Ce6 equivalent); 12 h treatment, 5 min 660 nm laser irradiation (15 mW/cm2), 2 h post-irradiation incubation) induces significant intracellular ROS generation in 4T1 mouse breast cancer cells when activated by 660 nm light (15 mW/cm2 for 5 min) following 12 h treatment at 0.3 μg/mL (Ce6 equivalent), with greater ROS generation than free Ce6 but lower generation than TPP-Ce6@siPD-L1 NPs[1].
TPP-Ce6 (0.3 μg/mL (Ce6 equivalent); 6 h treatment, 30 min Mito-Tracker Green incubation) effectively targets the mitochondria of 4T1 mouse breast cancer cells, with a higher colocalization Pearson correlation coefficient (0.645) than free Ce6 but a lower coefficient than TPP-Ce6@siPD-L1 NPs following 6 h treatment at 0.3 μg/mL (Ce6 equivalent)[1].
TPP-Ce6 (0.1-0.6 μg/mL (Ce6 equivalent); 6 h treatment, 10 min 660 nm laser irradiation (15 mW/cm2), 2 h post-irradiation incubation) exhibits low dark cytotoxicity (cell viability >95% at all concentrations) and concentration-dependent light-activated cytotoxicity in 4T1 mouse breast cancer cells, with greater cytotoxicity than free Ce6 but lower cytotoxicity than TPP-Ce6@siPD-L1 NPs under 660 nm light irradiation (15 mW/cm2 for 10 min) following 6 h treatment at 0.1, 0.2, 0.3, 0.4, 0.5, 0.6 μg/mL (Ce6 equivalent)[1].
TPP-Ce6 (0.3 μg/mL (Ce6 equivalent); 6 h treatment, 5 min 660 nm laser irradiation (15 mW/cm2), 30 min MPTP reagent incubation) activates mitochondrial permeability transition pores in 4T1 mouse breast cancer cells when activated by 660 nm light (15 mW/cm2 for 5 min) following 6 h treatment at 0.3 μg/mL (Ce6 equivalent), with a more pronounced effect than free Ce6 but a less pronounced effect than TPP-Ce6@siPD-L1 NPs[1].
TPP-Ce6 (TCe6) (4 h treatment; 30 min staining) effectively targets mitochondria in GL261 and U87 glioblastoma cells, as demonstrated by co-localization with MitoTracker Green FM[3].
TPP-Ce6 functions as a sonosensitizer in a cell-free system, with enhanced ROS generation when encapsulated in extracellular vesicles (EVs) upon US irradiation[4].
TPP-Ce6 (10 μM (Ce6 equivalent); 4 h) shows significantly lower cellular uptake than EV-encapsulated TPP-Ce6 in both MCF-7 human breast cancer cells and hDFB human dermal fibroblast cells[4].
TPP-Ce6 (10 μM (Ce6 equivalent); 4 h pretreatment) induces mitochondrial membrane depolarization in MCF-7 human breast cancer cells upon US irradiation, with enhanced mitochondrial damage when encapsulated in EVs, and maximal depolarization when co-encapsulated with PL in EVs[4].
TPP-Ce6 (10 μM (Ce6 equivalent); 4 h pretreatment, 8 h post-US incubation) induces apoptosis in MCF-7 human breast cancer cells upon US irradiation, with a higher total apoptotic rate observed when TPP-Ce6 is co-encapsulated with PL in EVs and combined with US[4].
TPP-Ce6 effectively targets MCF-7 breast cancer cell mitochondria, enhances ROS production under US irradiation, and when encapsulated in EVs with PL, achieves synergistic chemo-sonodynamic therapy efficacy via amplified ROS generation[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MCF-7 human breast cancer cells, human dermal fibroblast (hDFB) cells
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Concentration:5 μM T-Ce6
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Incubation Time:4 h; 2 min US exposure (1 MHz, 0.3 W/cm2)
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Result:Caused significant reduction in cell viability for both MCF-7 and hDFB cells when combined with US.
Exhibited the most substantial cytotoxicity in both cell lines with T80(T-Ce6/PL) plus US, with significantly greater viability reduction in MCF-7 cells compared to hDFB cells.
TPP-Ce6 (1.71 μmol/kg; i.v. via tail vein; single dose; followed by 660-nm laser irradiation 4 hours post-injection) inhibits orthotopic glioblastoma growth in athymic mice, with tumor growth suppression significantly less potent than bEV(TPP-Ce6)+L, and causes no systemic toxicity[2].
TPP-Ce6 (2 mg/kg; i.v.; single injection via tail vein) followed by NIR light irradiation suppresses orthotopic glioblastoma multiforme growth, induces cuproptosis, activates the cGAS-STING immune pathway, and enhances systemic anti-tumor immunity in male C57BL/6 mice with minimal systemic toxicity[3].
TPP-Ce6 (2 mg/kg; i.v.; single injection via tail vein) followed by NIR light irradiation induces glioblastoma multiforme regression, suppresses distant tumor growth, activates systemic anti-tumor immunity, and exhibits low systemic toxicity in male C57BL/6 mice[3].
Free TPP-Ce6 (0.8 mg/kg; i.v.; single dose) combined with ultrasound provides moderate tumor growth inhibition, reducing tumor volume to ~125% of baseline by day 20 without systemic toxicity[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:athymic mice (male, 5 weeks old, 20-30 g, orthotopic glioblastoma xenograft model via stereotactic injection of U87MG-luc cells)[2]
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Dosage:1.71 μmol/kg
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Administration:i.v. via tail vein; single dose; followed by 660-nm laser irradiation (150 mW, 5 min) at 4 hours post-injection
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Result:Suppressed tumor growth, with bioluminescence intensity reaching ~1500% of day 0 values by day 9.
Showed no significant body weight changes over the 9-day period.
Resulted in the smallest tumor size and largest area of necrotic change and nuclear shrinkage in tumor tissue compared to other treatment groups.
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Animal Model:C57BL/6 (male, 5-6 weeks old, 18-22 g, orthotopic brain tumor model induced by intracranial inoculation of 1×106 GL261-luc cells)[3]
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Dosage:2 mg/kg (based on TCe6 component of TCe6@Cu/TP5 NPs)
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Administration:i.v.; single injection via tail vein
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Result:Suppressed tumor progression with lower bioluminescence signals relative to control groups.
Caused notable orthotopic tumor tissue damage.
Reduced expression of proliferation marker Ki67 in tumor tissue.
Upregulated expression of cuproptosis-related proteins DLAT and FDX1 in tumor tissue.
Increased expression of cGAS-STING pathway-related proteins cGAS and STING in tumor tissue.
Increased CD4+ T cells, CD8+ T cells, and DC cells in spleen tissue.
Decreased Treg cells in spleen tissue.
Showed no significant morphologic alterations in major organs (heart, liver, spleen, lung, kidney).
Maintained stable body weight.
Chemical Information
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No. CAS 3030629-73-0
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Peso molecular 1464.66
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Fòrmula C94H90N4O6P33+
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SMILES
O=C(C1=C2/C(CC(OCC[P+](C3=CC=CC=C3)(C4=CC=CC=C4)C5=CC=CC=C5)=O)=C6[C@H]([C@@H](C(/C=C7N/C(C(C=C)=C\7C)=C\C8=N/C(C(CC)=C8C)=C\C(N2)=C1C)=N/6)C)CCC(OCC[P+](C9=CC=CC=C9)(C%10=CC=CC=C%10)C%11=CC=CC=C%11)=O)OCC[P+](C%12=CC=CC=C%12)(C%13=CC=CC=C%13)C%14=CC=CC=C%14
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
[1]. Luo Y, et al. Carrier-free Nanotherapeutics unleashed: Ce6/siPD-L1 co-delivery system synergizes photodynamic and RNAi therapies to combat breast cancer. Int J Biol Macromol. 2025;318(Pt 1):144962. [Content Brief]
[2]. Nguyen Cao TG, et al. Brain endothelial cell-derived extracellular vesicles with a mitochondria-targeting photosensitizer effectively treat glioblastoma by hijacking the blood‒brain barrier. Acta Pharm Sin B. 2023;13(9):3834-3848. [Content Brief]
[3]. Chen Y, et al. Copper-coordination driven brain-targeting nanoassembly for efficient glioblastoma multiforme immunotherapy by cuproptosis-mediated tumor immune microenvironment reprogramming. J Nanobiotechnology. 2024;22(1):801. Published 2024 Dec 28. [Content Brief]
[4]. Nguyen Cao TG, et al. Mitochondria-targeting sonosensitizer-loaded extracellular vesicles for chemo-sonodynamic therapy. J Control Release. 2023;354:651-663. [Content Brief]
[5]. Ali MS, et al. Triphenylphosphine-Based Mitochondrial Targeting Nanocarriers: Advancing Cancer Therapy. Clin Pharmacol. 2025;17:119-141. Published 2025 Jun 10. [Content Brief]
[6]. Quan Z, et al. ROS Regulation in CNS Disorder Therapy: Unveiling the Dual Roles of Nanomedicine. Small. 2025;21(5):e2410031. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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