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.
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- CAS No.: 1065-08-3
- 화학식: C30H18O12
- 분자량:570.46
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보관:
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
- Protocol
- 순도&문서
- References
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Help & FAQs
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Biological Activity
제품 설명
IC50 & Target
[1]|
Caspase-3 |
In Vitro
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. Further protocols information, click here.
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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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분자량 570.46
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화학식 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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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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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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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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