1. Apoptosis NF-κB Metabolic Enzyme/Protease Immunology/Inflammation
  2. Photosensitizer Reactive Oxygen Species (ROS)
  3. Antitumor photosensitizer-11

Antitumor photosensitizer-11 is a type-I carbazole/benzindolium photosensitizer with antitumor activity. Antitumor photosensitizer-11 induces ROS generation via a type-I pathway, forming superoxide anions and hydroxyl radicals. Antitumor photosensitizer-11 triggers immunogenic cell death in cancer cells via enhanced oxidative stress. Antitumor photosensitizer-11 exhibits antiproliferative activity in normoxic and hypoxic environments, inhibits breast cancer tumor growth in vivo, and promotes dendritic cell maturation and T cell infiltration. Antitumor photosensitizer-11 can be used for the research of cancer, such as breast cancer.

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Antitumor photosensitizer-11

Antitumor photosensitizer-11 Chemical Structure

CAS No. : 2813319-14-9

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Description

Antitumor photosensitizer-11 is a type-I carbazole/benzindolium photosensitizer with antitumor activity. Antitumor photosensitizer-11 induces ROS generation via a type-I pathway, forming superoxide anions and hydroxyl radicals. Antitumor photosensitizer-11 triggers immunogenic cell death in cancer cells via enhanced oxidative stress. Antitumor photosensitizer-11 exhibits antiproliferative activity in normoxic and hypoxic environments, inhibits breast cancer tumor growth in vivo, and promotes dendritic cell maturation and T cell infiltration. Antitumor photosensitizer-11 can be used for the research of cancer, such as breast cancer[1].

In Vitro

Antitumor photosensitizer-11 (Compound 3a) acts as a photosensitizer, generating high levels of total ROS, superoxide anions, and hydroxyl radicals with minimal singlet oxygen production upon 520 nm light exposure[1].
Antitumor photosensitizer-11 (24 h) exhibits chemotherapeutic antiproliferative activity against normoxic 4T1 cells with an IC50 of 20.1 μM, and this activity is enhanced by 520 nm light exposure to an IC50 of 2.8 μM[1].
Antitumor photosensitizer-11 (24 h) exhibits chemotherapeutic antiproliferative activity against normoxic A549 cells with an IC50 of 9.4 μM, and this activity is enhanced by 520 nm light exposure to an IC50 of 3.1 μM[1].
Antitumor photosensitizer-11 (24 h) exhibits chemotherapeutic antiproliferative activity against normoxic HT29 cells with an IC50 of 15.1 μM, and this activity is enhanced by 520 nm light exposure to an IC50 of 2.8 μM[1].
Antitumor photosensitizer-11 (24 h) exhibits chemotherapeutic antiproliferative activity against hypoxic 4T1 cells with an IC50 of 15.4 μM, and this activity is enhanced by 520 nm light exposure to an IC50 of 2.4 μM[1].
Antitumor photosensitizer-11 (24 h) exhibits chemotherapeutic antiproliferative activity against hypoxic A549 cells with an IC50 of 18.5 μM, and this activity is enhanced by 520 nm light exposure to an IC50 of 5.5 μM[1].
Antitumor photosensitizer-11 (24 h) exhibits chemotherapeutic antiproliferative activity against hypoxic HT29 cells with an IC50 of 19.4 μM, and this activity is enhanced by 520 nm light exposure to an IC50 of 4.3 μM[1].
Antitumor photosensitizer-11 is stable in PBS, DMEM, and pH 5-7 solutions for up to 12 hours, and exhibits strong photostability after 10 min of 520 nm light exposure[1].
Antitumor photosensitizer-11 induces significant intracellular total ROS and superoxide anion generation in 4T1 cells only when combined with 520 nm light exposure, under both normoxic and hypoxic conditions[1].
Antitumor photosensitizer-11 (20 μM) combined with 520 nm light exposure induces immunogenic cell death in 4T1 cells, as evidenced by increased CRT exposure, decreased HMGB1 release, and ~15.86-fold higher ATP secretion[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay[1]

Cell Line: normoxic 4T1 murine breast cancer cells
Concentration: 20.1 μM (without light); 2.8 μM (with light)
Incubation Time: 24 h
Result: Inhibited 4T1 cell growth with an IC50 of 20.1 μM without light.
Enhanced antiproliferative activity with an IC50 of 2.8 μM with 520 nm light exposure.
In Vivo

Antitumor photosensitizer-11 (Compound 3a) (5 mg/kg; i.t.; on day 0, 3, 6, 9, 12 with 520 nm laser irradiation (60 J/cm2)) exhibits potent in vivo chemo/photodynamic/immune antitumor activity against 4T1 breast cancer, achieving a 93.1% tumor growth inhibition rate when combined with 520 nm laser irradiation, with low acute toxicity and favorable biocompatibility[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Breast cancer BALB/c mice(female, inoculated with 4T1 tumor cells)[1]
Dosage: 5 mg/kg
Administration: Intratumoral injection; on day 0, 3, 6, 9, 12 with 520 nm laser irradiation (60 J/cm2)
Result: Achieved a 75.8% tumor growth inhibition rate, reduced tumor weight by 71.8% versus the PBS group, and increased tumor apoptosis relative to PBS.
Achieved a 93.1% tumor growth inhibition rate when combined with 520 nm laser irradiation, reduced tumor weight by 89.4% versus the PBS group, increased tumor apoptosis to over 60%.
Reduced Ki67 proliferation marker expression to near baseline levels, increased CD80+CD86+ mature dendritic cells to 33.4% in tumor-associated lymph nodes and 38.2% in tumor sites, and raised CD3+CD8+ T cell proportion to 34.1% in tumor-associated lymph nodes when combined with 520 nm laser irradiation.
Showed liver (ALT, AST) and kidney (creatinine, BUN, uric acid) biomarker levels comparable to PBS controls, with no histopathological organ damage observed.
Reached a median lethal dose (LD50) of 82.2 mg/kg in mice.
Molecular Weight

559.40

Formula

C28H22IN3O2

CAS No.
SMILES

CCN1C2=CC=C([N+]([O-])=O)C=C2C3=C1C=CC(/C=C/C4=[N+](C)C5=CC=CC6=CC=CC4=C56)=C3.[I-]

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Antitumor photosensitizer-11
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