Antitumor photosensitizer-10
Antitumor photosensitizer-10 is an antitumor photosensitizer. Upon near-infrared irradiation, Antitumor photosensitizer-10 generates superoxide anions, reduces the copper-binding capacity of glutathione, releases copper ions, and thereby induces cuproptosis in tumor cells (cuproptosis). Antitumor photosensitizer-10 can be used in breast cancer-related research.
For research use only. We do not sell to patients.
- Formula: C36H37Cl2CuN5O2S2+
- Molecular Weight:738.23
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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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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Upon irradiation with 660 nm light, Antitumor photosensitizer-10 (Compound NC) (10 μM; 1-7 min) generates abundant superoxide anion radicals in a cell-free PBS system[1].
Antitumor photosensitizer-10 (1 μM; 4-16 h) effectively delivers copper ions to 4T1 cells, and the intracellular copper level increases in a time-dependent manner after 4 h and 16 h of incubation[1].
Antitumor photosensitizer-10 (0.125-2 μM) exhibits enhanced phototoxicity against 4T1 cells under irradiation at 660 nm, with an IC50 of 216 nM under the condition of 6 J cm-2[1].
Treatment with Antitumor photosensitizer-10 (250 nM; 24 h) followed by 660 nm irradiation induces significant death of 4T1 cells; compared with the dark control group and NQ treatment group, this treatment leads to enhanced PI staining and reduced calcein-AM staining, which confirms this result[1].
Upon irradiation at 660 nm, Antitumor photosensitizer-10 (250 nM; 12 h) generates intracellular reactive oxygen species (ROS) in 4T1 cells[1].
Antitumor photosensitizer-10 (250 nM; 24 h) induces cuproptosis-related changes in HCT116 and 4T1 cells under irradiation at 660 nm, including decreased FDX1 expression and increased DLAT aggregation[1].
Antitumor photosensitizer-10 (250 nM; 24 h) induces DLAT aggregation (a hallmark event of cuproptosis) in 4T1 cells solely under 660 nm irradiation, and this result is confirmed by immunofluorescence imaging[1].
Pretreatment with BSO enhances the cuproptosis induced by Antitumor photosensitizer-10 (0.25-2 μM; 36 h) in 4T1 cells under high-concentration dark conditions; after 660 nm irradiation, its phototoxicity is synergistically enhanced, which confirms that glutathione (GSH) depletion mediates the synergistic effect between photodynamic therapy (PDT) and cuproptosis[1].
Antitumor photosensitizer-10 (250 nM; 12 h) generates reactive oxygen species (ROS) upon irradiation at 660 nm, which mediates glutathione (GSH) depletion and subsequent DLAT aggregation in 4T1 cells; in contrast, pretreatment with BSO combined with low-dose irradiation synergistically induces DLAT aggregation associated with cuproptosis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HCT116 human colon cancer cells, 4T1 mouse breast cancer cells
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Concentration:250 nM
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Incubation Time:12 h (treatment); 200 s (irradiation at 20 mW cm-2); 12 h (post-treatment incubation)
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Result:Reduced FDX1 expression markedly in HCT116 cells under light, similar to the positive control (elesclomol + CuCl2).
Induced DLAT aggregation (oligomer formation) in 4T1 cells under light, with more aggregation bands than the positive control (8-HQ-COOH + CuCl2).
Did not alter FDX1 or DLAT levels in the dark compared to controls.
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Cell Line:4T1 mouse breast cancer cells
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Concentration:250 nM
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Incubation Time:12 h (treatment); 200 s (irradiation at 20 mW cm-2); 12 h (post-treatment incubation)
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Result:Induced DLAT foci (indicative of aggregation) only in the NC + light group, similar to the positive control (elesclomol + CuCl2).
Showed DLAT fluorescence patterns identical to the control group (no visible aggregation foci) in NC dark, NQ dark, and NQ light conditions.
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Cell Line:4T1 mouse breast cancer cells
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Concentration:0.25-2 μM (NC); 20 μM (BSO)
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Incubation Time:12 h (BSO preincubation); 12 h (NC treatment); 200 s (irradiation at 20 mW cm-2); 12 h (post-treatment incubation)
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Result:Showed no effect on NC's dark cytotoxicity at low concentrations with BSO pre-treatment, but reduced cell survival at higher concentrations, indicating sensitization to cuproptosis.
Enhanced NC's phototoxicity beyond additive effects of BSO and PDT alone under light irradiation, with greater reduction in cell survival than BSO + NQ light groups at low concentrations.
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Cell Line:4T1 mouse breast cancer cells
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Concentration:250 nM (NC); 20 μM (BSO); 1 mM (Vc)
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Incubation Time:12 h (BSO preincubation); 5 min (Vc pre-irradiation treatment); 90-200 s (irradiation at 20 mW cm-2)
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Result:Induced marked DLAT foci in NC-treated cells when combined with BSO pre-treatment and low-dose light, while neither BSO alone nor low-dose light alone induced aggregation.
Induced DLAT foci in NC-treated cells with high-dose light alone, and addition of Vc markedly reduced these foci.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Balb/c mice (female, 5 weeks old, subcutaneously injected with 1 × 106 4T1 cells into the fourth mammary fat pad, tumors grown to ~100 mm3 before treatment)[1]
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Dosage:0.7 mg/kg (no light); 0.7 mg/kg (with light irradiation)
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Administration:intratumoral; single injection; 14 days observation period; 660 nm light irradiation at 100 mW cm-2 for 15 minutes (1 hour post-injection, light group only)
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Result:Showed no appreciable tumor growth inhibition in the absence of light.
Almost completely suppressed tumor growth over the 14-day observation period, with relative tumor volume remaining near baseline when combined with light irradiation.
Induced the most pronounced tumor destruction, TUNEL-positive cell death, and DLAT aggregation (a marker of cuproptosis) in the light-treated group.
Caused no abnormal changes in mouse body weight, and H&E staining of major organs showed no marked physiological damage.
Chemical Information
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Molecular Weight 738.23
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Formula C36H37Cl2CuN5O2S2+
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SMILES
CCN(CC)C1=CC(SC2=C/3)=C(C=C1)N=C2C4=CC=CC=C4C3=N\CCCCCCNC5=O[Cu+2]6(Cl)OC7=C8[N]6=C5C=CC8=CC=C7.Cl
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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)
Antitumor photosensitizer-10 Related Classifications
HY-182919 Related Classifications
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