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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- CAS 番号: 3030629-73-0
- 分子式: C94H90N4O6P33+
- 分子量:1464.66
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保管条件:
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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生物活性
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化学情報
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
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.
化学情報
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CAS 番号 3030629-73-0
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分子量 1464.66
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
[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
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TPP-Ce6 関連分類
HY-158189 関連分類
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