Anticancer agent 311
Anticancer agent 311 is an apoptosis inducer and p53 modulator. Anticancer agent 311 increases p53 levels, activates cleaved caspase-3, reduces p-Cdc25C levels, and disrupts p-p44/42 MAPK phosphorylation. Anticancer agent 311 induces G2/M phase arrest, inhibits cancer cell viability in a concentration- and time-dependent manner, and exhibits low toxicity to non-cancer cells. Anticancer agent 311 prevents tumor growth and angiogenesis in mouse xenograft models without detectable toxicity. Anticancer agent 311 can be used for the research of lung cancer.
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- CAS No.: 421579-95-5
- Formule: C23H18FNO5S
- Masse moléculaire:439.46
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Anticancer agent 311 (#2714) (48 h) potently inhibits the viability of murine Lewis lung carcinoma LL/2 cells with an IC50 of 5.43 μM and mouse mammary carcinoma 4T1 cells with an IC50 of 6.12 μM, while showing minimal toxicity to non-cancer NIH-3T3 and HK-2 cells (IC50 >40 μM)[1].
Anticancer agent 311 (4-20 μM; 24-72 h) inhibited LL/2 cell viability in a time- and concentration-dependent manner[1].
Anticancer agent 311 (5-20 μM; 48 h) induces G2/M phase arrest in murine Lewis lung carcinoma LL/2 cells, with 77.7% of cells accumulating in G2/M after treatment with 20 μM for 48 h[1].
Anticancer agent 311 (5-20 μM; 48 h) induces apoptosis in murine Lewis lung carcinoma LL/2 cells in a concentration-dependent manner, reaching 50.2% at 20 μM after 48 h, and disrupts mitochondrial membrane potential in these cells[1].
Anticancer agent 311 (2.5-10 μM; 24 h) downregulates p-Cdc25C, p-p44/42 MAPK, and p-Akt while upregulating p53 and cleaved caspase-3 in murine Lewis lung carcinoma LL/2 cells after 24 h of treatment, supporting G2/M phase arrest and caspase-dependent apoptosis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Lewis lung carcinoma LL/2 cells
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Concentration:4 μM; 8 μM; 12 μM; 16 μM; 20 μM;
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Incubation Time:24 h; 48 h; 72 h
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Result:Inhibited LL/2 cell viability in a time- and concentration-dependent manner.
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Cell Line:Lewis lung carcinoma LL/2 cells
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Concentration:5 μM; 10 μM; 20 μM
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Incubation Time:48 h
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Result:Increased the percentage of LL/2 cells in the G2/M phase to 77.7% at 20 μM, accompanied by decreases in the G0/G1 and S phases.
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Cell Line:Lewis lung carcinoma LL/2 cells
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Concentration:5 μM, 10 μM, 20 μM
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Incubation Time:48 h
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Result:Increased the apoptosis rate of LL/2 cells to 22.9% with 5 μM, 45.1% with 10 μM, and 50.2% with 20 μM after 48 h.
Caused a concentration-dependent decrease in Rho 123 fluorescence, indicating collapse of mitochondrial membrane potential (ΔΨm).
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Cell Line:Lewis lung carcinoma LL/2 cells
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Concentration:2.5 μM, 5 μM, 10 μM
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Incubation Time:24 h
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Result:Downregulated the expression of phosphorylated Cdc25C (p-Cdc25C), phosphorylated p44/42 MAPK (p-p44/42 MAPK), and phosphorylated Akt (p-Akt) in a concentration-dependent manner.
Upregulated the expression of p53 and cleaved caspase-3 in a concentration-dependent manner.
Anticancer agent 311 (#2714) (25-100 mg/kg; i.p.; daily; 28 days) exhibits potent anti-lung cancer efficacy in C57BL/6 mice, achieving up to 58.1% tumor growth inhibition at 100 mg/kg, while also increasing survival, reducing angiogenesis, and inducing tumor cell apoptosis with no detectable toxicity[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male and female, 18-22 g)[1]
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Dosage:25 mg/kg; 50 mg/kg; 100 mg/kg
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Administration:i.p.; daily; 14 days
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Result:Caused no mortality, adverse clinical signs, or obvious pathological damage in any treated group.
Showed no significant differences in hematological parameters (WBC, RBC, HGB, HCT, PLT) between treated groups and vehicle control.
Showed no significant differences in serum biochemical parameters (HDL, TG, CHOL, CREA, BUN, GLU, ALP, ALB, TP, AST, ALT) between treated groups and vehicle control.
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Animal Model:C57BL/6 (female, 6-8 weeks old, 18-22 g, subcutaneous implantation of LL/2 murine Lewis lung carcinoma cells)[1]
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Dosage:25 mg/kg; 50 mg/kg; 100 mg/kg
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Administration:i.p.; daily; 28 days
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Result:Achieved 45.1% tumor growth inhibition at 50 mg/kg compared to vehicle control.
Achieved 58.1% tumor growth inhibition at 100 mg/kg compared to vehicle control.
Significantly increased mouse survival compared to vehicle control across all doses.
Reduced CD31 staining by 37.4% in tumor tissues compared to vehicle control.
Reduced CD105 staining by 15.2% in tumor tissues compared to vehicle control.
Increased apoptotic tumor cells 11-fold compared to vehicle control.
Caused no significant changes in body weight during treatment.
Chemical Information
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CAS No. 421579-95-5
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Masse moléculaire 439.46
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Formule C23H18FNO5S
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SMILES
O=C(C1=C(C2=CC=CC=C2)OC3=C1C=C(NS(=O)(C4=CC=C(C=C4)F)=O)C=C3)OCC
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Anticancer agent 311 Related Classifications
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