Antitumor photosensitizer-9
Antitumor photosensitizer-9 is a near-infrared Photosensitizer (PS) with a high singlet oxygen production rate (relative rate = 1.79). Antitumor photosensitizer-9 exhibits strong phototoxicity against various cancer cells and induces ROS generation under light irradiation. Antitumor photosensitizer-9 inhibits tumor growth in vivo and exhibits excellent anticancer photodynamic therapy (PDT) efficacy at low drug and light doses. Antitumor photosensitizer-9 can be used in photodynamic therapy research.
For research use only. We do not sell to patients.
- Formula: C44H41BIN5O2
- Molecular Weight:809.54
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Antitumor photosensitizer-9 (Compound A1) (2 h) shows Light dose-related photo-toxicity against HeLa cells, with IC50s < 5.0 nM[1].
Antitumor photosensitizer-9 (2 h) shows phototoxicity (IC50s = 3.7, 3.6, 4.5, 3.7 nM) and dark cytotoxicity (IC50s = 11.5, 13.5, 12.7, 10.7 μM) in HeLa, HepG 2, B16–F10, HUVEC cells[1].
Antitumor photosensitizer-9 (5 μM, 2 h) reaches peak intracellular accumulation and mainly accumulates in the ER in HeLa cells[1].
Antitumor photosensitizer-9 (0-500 nM,2 h) induces the production of ROS under light irradiation in HeLa cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Female BALB/c Nude mice (6-8 weeks old, 20-22 g) bearing HeLa cells (5 × 106 cells, 0.1 mL, s.c.) [1]
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Dosage:2 mg/kg
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Administration:i.v., once, 24 days of PDT treatment
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Result:Inhibited tumor growth, with tumor volume decreased by 78% and had no physiological toxicity, was more effective than photosensitizers Ce6 (HY-13594) and BDP4 (HY-D1452).
Chemical Information
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Molecular Weight 809.54
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Formula C44H41BIN5O2
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SMILES
IC(C(C1=CC=C(C=C1)OC)=[N]2C3=NC4=C(C=C(N4B2(C#CCN(C)C)C#CCN(C)C)C5=CC=C(C=C5)OC)C6=CC=CC=C6)=C3C7=CC=CC=C7
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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.
Protocols
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)