Ephemeranthol A
Ephemeranthol A is a phenanthrene compound with anticancer and anti-inflammatory activities. Ephemeranthol A exerts significant anti-inflammatory effects in macrophages by inhibiting the NF-κB and MAPK signaling pathways. Ephemeranthol A induces apoptosis and inhibits metastasis of lung cancer cells by suppressing the FAK/Akt signaling and EMT processes. Ephemeranthol A can be used for the research of acute and chronic inflammatory diseases and non-small cell lung cancer.
For research use only. We do not sell to patients.
- CAS No.: 135545-86-7
- Formula: C16H16O4
- Molecular Weight:272.30
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
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NF-κB |
iNOS |
COX-2 |
IL-1β |
IL-6 |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | IC50 |
10 μM
Compound: 7
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Cytotoxicity against human A549 cells assessed as decrease in cell viability after 6 days by MTT assay
Cytotoxicity against human A549 cells assessed as decrease in cell viability after 6 days by MTT assay
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[PMID: 27310249] |
Ephemeranthol A (6.25-50 μg/mL; 25 h) shows no cytotoxicity against Raw 264.7 cells at concentrations ≤ 25 μg/mL, but reduces cell viability at 50 μg/mL[1].
Ephemeranthol A (6.25-50 μg/mL; 7-25 h) potently inhibits LPS-induced production of NO, iNOS, COX-2, TNF-α, IL-6 and IL-1β in Raw 264.7 cells[1].
Ephemeranthol A (25 μg/mL; 1.5-2 h) blocks LPS-induced IκB degradation and inhibits the nuclear translocation of NF-κB subunits p50 and p65 in Raw 264.7 cells [1].
Ephemeranthol A (6.25-25 μg/mL; 1 h) inhibits LPS-induced phosphorylation of p38 and JNK in Raw 264.7 cells[1].
Ephemeranthol A (5-200 μM; 24-48 h) reduces the viability of human non-small cell lung cancer H460 cells in a concentration- and time-dependent manner, with an IC50 > 200 μM at 24 h and an IC50 of 150.5 μM at 48 h[2].
Ephemeranthol A (10-100 μM; 24 h) induces apoptosis in human non-small cell lung cancer H460 cells in a concentration-dependent manner[2].
Ephemeranthol A (50-100 μM; 48 h) induces apoptosis in human non-small cell lung cancer H460 cells at 48 h by decreasing Bcl-2 levels and activating caspase-9, caspase-3 and PARP[2].
Ephemeranthol A (50-100 μM; 48 h) inhibits the activation of the FAK-Akt signaling pathway in human non-small cell lung cancer H460 cells at 48 h[2].
Ephemeranthol A (5-50 μM; 48 h) inhibits anchorage-independent growth of human non-small cell lung cancer H460 cells[2].
Ephemeranthol A (10-100 μM; 24-48 h) inhibits migration of human non-small cell lung cancer H460 cells[2].
Ephemeranthol A (5-100 μM; 24-48 h) inhibits epithelial-mesenchymal transition and induces epithelial morphological changes in human non-small cell lung cancer H460 cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Raw 264.7 murine macrophage cells
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Concentration:25 μg/mL
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Incubation Time:1 h pre-incubation; 6 h LPS stimulation
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Result:Reduced LPS-induced iNOS protein production in Raw 264.7 cells.\n
Reduced LPS-induced COX-2 protein production in Raw 264.7 cells.
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Cell Line:Raw 264.7 murine macrophage cells
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Concentration:25 μg/mL
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Incubation Time:1 h pre-incubation; 6 h LPS stimulation
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Result:Significantly decreased LPS-induced mRNA levels of TNF-α, IL-6, and IL-1β.
Reduced TNF-α and IL-6 mRNA levels to the level of the unstimulated control.
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Cell Line:Raw 264.7 murine macrophage cells
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Concentration:25 μg/mL
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Incubation Time:1 h pre-incubation; 24 h LPS stimulation
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Result:Significantly inhibited LPS-induced production of TNF-α, IL-6, and IL-1β protein in Raw 264.7 cells.
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Cell Line:Raw 264.7 murine macrophage cells
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Concentration:25 μg/mL
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Incubation Time:1 h pre-incubation; 30 min or 1 h LPS stimulation
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Result:Blocked LPS-induced IκB degradation at 30 min post-stimulation.
Sustained the inhibitory effect until 1 h post-stimulation.\n
Inhibited LPS-induced translocation of p50 and p65 into the nucleus at 30 min post-stimulation.
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Cell Line:Raw 264.7 murine macrophage cells
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Concentration:25 μg/mL (p38, JNK phosphorylation at 10/20 min); 6.25, 12.5 and 25 μg/mL (p38 phosphorylation at 10 min)
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Incubation Time:1 h pre-incubation; 10 min or 20 min LPS stimulation (p38, JNK phosphorylation); 1 h pre-incubation, 10 min LPS stimulation (p38 phosphorylation dose-response)
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Result:Reduced LPS-induced phosphorylation of p38 and JNK at 10 min and 20 min post-stimulation.
Sustained the inhibitory effect on JNK phosphorylation for 20 min.
Induced a dose-dependent reduction in LPS-induced p38 phosphorylation at 6.25, 12.5, and 25 μg/mL.
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Cell Line:human non-small cell lung cancer H460 cells
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Concentration:5, 10, 50, 100 and 200 μM
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Incubation Time:24 h; 48 h
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Result:Exhibited non-toxic to slightly toxic effects at concentrations ≤ 50 μM.
Caused significant cell viability reduction at 100 and 200 μM at both 24 and 48 h.
Reached an IC50 of > 200 μM at 24 h and 150.5 μM at 48 h.
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Cell Line:human non-small cell lung cancer H460 cells
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Concentration:10, 50 and 100 μM
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Incubation Time:24 h
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Result:Induced concentration-dependent increases in apoptotic cell number.
Resulted in a significant increase to ~17% apoptotic nuclei at 100 μM.
Kept necrotic cell numbers minimal across all concentrations.
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Cell Line:human non-small cell lung cancer H460 cells
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Concentration:50, 100 μM
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Incubation Time:48 h
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Result:Increased cleaved PARP levels 1.98-fold (50 μM) and 2.33-fold (100 μM).
Increased cleaved caspase-9 levels 1.52-fold (50 μM) and 1.73-fold (100 μM).
Increased cleaved caspase-3 levels 4.78-fold (100 μM).
Reduced Bcl-2 levels to 0.63-fold (100 μM).
Showed no significant effects on Mcl-1 or Bax levels.
Reduced the p-FAK/total FAK ratio to 0.82-fold (50 μM) and 0.59-fold (100 μM).
Reduced the p-Akt/total Akt ratio to 0.52-fold (100 μM).
Kept total FAK and total Akt levels largely unchanged.
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Cell Line:human non-small cell lung cancer H460 cells
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Concentration:10, 50 and 100 μM
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Incubation Time:24 h; 48 h
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Result:Showed no significant effect on wound closure at 24 h.
Reduced wound closure to 33.77% (50 μM) and 25.06% (100 μM) at 48 h, compared to untreated control wound closure of 38.40%.
Chemical Information
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CAS No. 135545-86-7
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Molecular Weight 272.30
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Formula C16H16O4
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SMILES
OC1=CC2=C(C3=C(C(OC)=C(C=C3CC2)OC)O)C=C1
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Structure Classification
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Initial Source
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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]. Kim JH, et al. Anti-inflammatory effects of Dendrobium nobile derived phenanthrenes in LPS-stimulated murine macrophages. Arch Pharm Res. 2015;38(6):1117-1126. [Content Brief]
[2]. Nonpanya N, et al. Ephemeranthol A Suppresses Epithelial to Mesenchymal Transition and FAK-Akt Signaling in Lung Cancer Cells. Anticancer Res. 2020;40(9):4989-4999. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)