Dicatenarin
Dicatenarin is a caspase‑3 activator with growth‑inhibitory activity against human cancer cells. Dicatenarin increases caspase‑3 activity, induces intracellular ROS generation, and activates the mitochondrial‑mediated apoptotic pathway. Dicatenarin exerts growth‑inhibitory effects against a panel of human cancer cell lines. Dicatenarin can be used in research on pancreatic cancer, lung cancer, colon cancer, breast cancer, prostate cancer, and ovarian cancer.
For research use only. We do not sell to patients.
- CAS No.: 1065-08-3
- Formula: C30H18O12
- Molecular Weight:570.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Biological Activity
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Caspase-3 |
Dicatenarin (1-100 µg/mL; 48 h) potently inhibits growth of human lung (A549), pancreatic (MIA PaCa-2), colon (HCT-116), breast (T47D), prostate (PC-3), and ovarian (OVCAR-3) cancer cell lines in vitro, with the lowest IC50 of 12 µg/mL against MIA PaCa-2 cells[1][2].
induces both early and late-stage apoptosisDicatenarin (5-20 µg/mL; 48 h) induces concentration-dependent apoptotic nuclear morphological changes in human pancreatic cancer (MIA PaCa-2) cells[1].
Dicatenarin (20 µg/mL; 48 h) induces both early and late-stage apoptosis in human pancreatic cancer (MIA PaCa-2) cells[1].
Dicatenarin (5-20 µg/mL; 48 h) induces concentration-dependent intracellular ROS generation in human pancreatic cancer (MIA PaCa-2) cells[1].
Dicatenarin (5-20 µg/mL; 48 h) induces concentration-dependent loss of mitochondrial transmembrane potential in human pancreatic cancer (MIA PaCa-2) cells[1].
Dicatenarin (5-20 µg/mL; 48 h) induces concentration-dependent release of cytochrome c from mitochondria to the cytosol in human pancreatic cancer (MIA PaCa-2) cells[1].
Dicatenarin (5-20 µg/mL; 48 h) induces concentration-dependent activation of caspase-3 in human pancreatic cancer (MIA PaCa-2) cells[1].
Dicatenarin (5-20 µg/mL; 7 days) potently inhibits clonogenic survival of human pancreatic cancer (MIA PaCa-2) cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:A549, MIA PaCa-2, HCT-116, T47D, PC-3, OVCAR-3
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Concentration:1, 10, 30, 50, 100 µg/mL
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Incubation Time:48 h
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Result:Exhibited cytotoxicity against all tested cell lines, with IC50 values of 23 µg/mL (A549), 12 µg/mL (MIA PaCa-2), 17 µg/mL (HCT-116), 29 µg/mL (T47D), 35 µg/mL (PC-3), and 26 µg/mL (OVCAR-3).
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Cell Line:MIA PaCa-2
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Concentration:20 µg/mL
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Incubation Time:48 h
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Result:Resulted in significant phosphatidylserine externalization (early apoptosis) and late-stage apoptotic/necrotic PI-positive staining, with a higher proportion of annexin V-positive cells compared to skyrin treatment.
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Cell Line:MIA PaCa-2
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Concentration:5, 10, 20 µg/mL
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Incubation Time:48 h
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Result:Induced concentration-dependent release of cytochrome c from mitochondria into the cytosol.
Showed minimal release at 5 µg/mL, moderate release at 10 µg/mL, prominent, diffuse cytosolic cytochrome c staining at 20 µg/mL, indicating complete mitochondrial outer membrane permeabilization.
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Cell Line:MIA PaCa-2
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Concentration:5, 10, 20 µg/mL
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Incubation Time:7 days
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Result:Caused concentration-dependent inhibition of colony formation.
Reduced colony number to ~460 (from ~550 in controls) at 5 µg/mL, to ~210 at 10 µg/mL, to ~50 at 20 µg/mL, representing a 91% reduction in colony formation at the highest concentration.
Chemical Information
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CAS No. 1065-08-3
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Molecular Weight 570.46
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Formula C30H18O12
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SMILES
O=C1C2=C(C=C(C)C(O)=C2C(C3=C1C(O)=CC(O)=C3C(C(O)=CC(O)=C4C(C5=C(C=C(C)C(O)=C56)O)=O)=C4C6=O)=O)O
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Structure Classification
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Initial Source
Penicillium pinophilum
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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)
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