Caspase-3/7 activator 4
Caspase-3/7 activator 4 is a caspase-3 activator and caspase-7 activator. Caspase-3/7 activator 4 inhibits key enzymes in estrogen biosynthesis, including aromatase (IC50 = 38.3 nM) and steroid sulfatase (IC50 = 12.7 µM), and selectively suppresses COX-2 (IC50 = 5.38 µM). Caspase-3/7 activator 4 shows strong antioxidant activity (DPPH: IC50 = 16.26 µM). Caspase-3/7 activator 4 inhibits estrogen synthesis, suppresses estrogen availability, reduces prostaglandin production, increases caspase-3/7 expression, induces G0/G1 cell cycle arrest, induces apoptotic cell death, reduces circulating TNF-α and VEGFR-II levels, restores hepatorenal function markers and histoarchitecture, restores antioxidant defense enzyme activity, reduces lipid peroxidation, exerts antiproliferative activity against breast cancer cells, exerts antitumor activity in the Ehrlich ascites carcinoma models. Caspase-3/7 activator 4 can be used for the research of breast cancer, ehrlich ascites carcinoma.
For research use only. We do not sell to patients.
- Formula: C14H14ClN3O4S
- Molecular Weight:355.80
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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
All Caspase Isoforms
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Biological Activity
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COX-2 5.38 μM (IC50) |
Caspase 3 |
Caspase-7 |
Aromatase 38.3 μM (IC50) |
Steroid Sulfatase 12.7 μM (IC50) |
Caspase-3/7 activator 4 (compound 6) (0.5-80 μM; hibits the proliferation of MDA-MB-231 and MCF-7 breast cancer cells with IC50 values of 2.25 μM and 6.70 μM, respectively, and shows high selectivity for cancer cells over non-tumorigenic MCF-10A cells[1].
Caspase-3/7 activator 4 (2.25 μM; 24 h) induces G0/G1 cell cycle arrest in MDA-MB-231 cells[1].
Caspase-3/7 activator 4 (2.25 μM; 24 h) induces substantial apoptotic cell death in MDA-MB-231 cells, with early apoptosis as the predominant mode[1].
Caspase-3/7 activator 4 (2.25 μM; 24 h) activates caspase-3 and caspase-7 in MDA-MB-231 cells, indicating induction of apoptotic pathways[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MDA-MB-231, MCF-7, MCF-10A
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Concentration:0.5 μM, 1 μM, 2.5 μM, 5 μM, 10 μM, 20 μM, 40 μM, 80 μM
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Incubation Time:48 h
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Result:Exhibited potent antiproliferative activity with IC50 values of 2.25 μM against MDA-MB-231 cells, 6.70 μM against MCF-7 cells, and 36.57 μM against non-tumorigenic MCF-10A cells.
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Cell Line:MDA-MB-231
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Concentration:2.25 μM
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Incubation Time:24 h
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Result:Induced a substantial accumulation in the G0/G1 phase (84.62%) with a concomitant decrease in the S phase (12.83%) and G2/M phase (2.55%) compared to untreated control cells.
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Cell Line:MDA-MB-231
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Concentration:2.25 μM
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Incubation Time:24 h
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Result:Resulted in a markedly higher total apoptosis/necrosis rate (24.81%) compared to untreated control cells (2.46%), with 16.26% early apoptosis, 5.61% late apoptosis, and 2.94% necrosis.
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Cell Line:MDA-MB-231
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Concentration:2.25 μM
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Incubation Time:24 h
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Result:Significantly increased caspase-3 levels to 428.56 pg/mL (3.69-fold increase) and caspase-7 levels to 2.916 ng/mL (4.83-fold increase) compared to untreated controls.
Caspase-3/7 activator 4 (1-200 mg/kg; i.p.; once) is administered to mice and closely monitored for 48 hours for death, behavioral changes, and obvious toxic symptoms. At doses up to 120 mg/kg , no mortality or abnormal behavioral manifestations were observed, and the animals maintained normal grooming, feeding, and locomotor activity, indicating a good safety margin at these concentra-
tions. In contrast, administration of 200 mg/kg resulted in complete mortality, establishing this dose as the approximate lethal dose (LD100)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Swiss albino female (20-25 g, Ehrlich ascites carcinoma model)[1]
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Dosage:2.5, 5, 10, 15, and 20 mg/kg
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Administration:i.p.; every other day; 10 days
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Result:Reduced viable EAC cell count to 125.94 × 106 (39.7% decrease vs. control) at 2.5 mg/kg.
Reduced viable EAC cell count to 78.76 × 106 (62.3% decrease vs. control) at 5 mg/kg.
Reduced viable EAC cell count to 58.64 × 106 (71.9% decrease vs. control) at 10 mg/kg.
Reduced viable EAC cell count to 42.17 × 106 (79.8% decrease vs. control) and ascitic tumor volume to 1.45 mL (74.3% decrease vs. control) at 15 mg/kg; reduced viable EAC cell count to 37.67 × 10⁶ (81.9% decrease vs. control) at 20 mg/kg; reduced serum TNF-α levels to 82.27 pg/mL (vs. EAC control 162.63 pg/mL); reduced serum VEGFR-II levels to 46.59 ng/mL; restored liver antioxidant markers (GSH: 31.20 pg/g tissue, CAT: 35.90 U/g tissue, SOD: 31.86 U/g tissue) and reduced MDA to 27.65 nmol/g tissue; improved liver function (ALT: 67.50 U/L, AST: 84.5 U/L) and renal function (creatinine: 0.98 mg/dL, urea: 60.50 mg/dL) vs. EAC control.
Chemical Information
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Molecular Weight 355.80
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Formula C14H14ClN3O4S
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SMILES
O=C(OC)CCN1/C(SCC1=O)=N\N=C\C2=CC(Cl)=CC=C2O
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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
[1]. El-Zend MA, et al. Design, synthesis, and multi-target anticancer evaluation of 1,3-thiazolodin-4-one analogues against breast cancer: mechanistic insights into estrogen metabolism, inflammation, angiogenesis, and oxidative stress. RSC Adv. 2026;16(3):2528-2554. Published 2026 Jan 12. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Caspase-3/7 activator 4 Related Classifications
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