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^{[1][2][3][4][5][6]}.

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.

TPP-Ce6 (i.v.; on day 1 and day 4; 6 hours post-injection, 660 nm laser irradiation at 30 W/cm² for 10 minutes per dose) achieves 33% tumor growth inhibition in BALB/c mice with 4T1 breast cancer, induces tumor cell apoptosis to a moderate degree, enhances anti-tumor immune responses, and exhibits favorable in vivo safety^[1].
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.

1464.66

C₉₄H₉₀N₄O₆P₃³⁺

3030629-73-0

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

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.

  [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.

  [4]. Nguyen Cao TG, et al. Mitochondria-targeting sonosensitizer-loaded extracellular vesicles for chemo-sonodynamic therapy. J Control Release. 2023;354:651-663.

  [5]. Ali MS, et al. Triphenylphosphine-Based Mitochondrial Targeting Nanocarriers: Advancing Cancer Therapy. Clin Pharmacol. 2025;17:119-141. Published 2025 Jun 10.

  [6]. Quan Z, et al. ROS Regulation in CNS Disorder Therapy: Unveiling the Dual Roles of Nanomedicine. Small. 2025;21(5):e2410031.