1. NF-κB MAPK/ERK Pathway Protein Tyrosine Kinase/RTK PI3K/Akt/mTOR Apoptosis Immunology/Inflammation
  2. NF-κB p38 MAPK FAK Akt Apoptosis NO Synthase COX TNF Receptor Interleukin Related
  3. 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.

Ephemeranthol A

Ephemeranthol A Chemical Structure

CAS No. : 135545-86-7

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Description

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[2].

IC50 & Target[1]

NF-κB

 

iNOS

 

COX-2

 

IL-1β

 

IL-6

 

In Vitro

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.

Western Blot Analysis[1]

Cell Line: Raw 264.7 murine macrophage cells
Concentration: 25 μg/mL
Incubation Time: 1 h pre-incubation; 6 h LPS stimulation
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.

RT-PCR[1]

Cell Line: Raw 264.7 murine macrophage cells
Concentration: 25 μg/mL
Incubation Time: 1 h pre-incubation; 6 h LPS stimulation
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.

ELISA Assay[1]

Cell Line: Raw 264.7 murine macrophage cells
Concentration: 25 μg/mL
Incubation Time: 1 h pre-incubation; 24 h LPS stimulation
Result: Significantly inhibited LPS-induced production of TNF-α, IL-6, and IL-1β protein in Raw 264.7 cells.

Western Blot Analysis[1]

Cell Line: Raw 264.7 murine macrophage cells
Concentration: 25 μg/mL
Incubation Time: 1 h pre-incubation; 30 min or 1 h LPS stimulation
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.

Western Blot Analysis[1]

Cell Line: Raw 264.7 murine macrophage cells
Concentration: 25 μg/mL (p38, JNK phosphorylation at 10/20 min); 6.25, 12.5 and 25 μg/mL (p38 phosphorylation at 10 min)
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)
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.

Cell Cytotoxicity Assay[2]

Cell Line: human non-small cell lung cancer H460 cells
Concentration: 5, 10, 50, 100 and 200 μM
Incubation Time: 24 h; 48 h
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.

Apoptosis Analysis[2]

Cell Line: human non-small cell lung cancer H460 cells
Concentration: 10, 50 and 100 μM
Incubation Time: 24 h
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.

Western Blot Analysis[2]

Cell Line: human non-small cell lung cancer H460 cells
Concentration: 50, 100 μM
Incubation Time: 48 h
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.

Cell Migration Assay[2]

Cell Line: human non-small cell lung cancer H460 cells
Concentration: 10, 50 and 100 μM
Incubation Time: 24 h; 48 h
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%.
Molecular Weight

272.30

Formula

C16H16O4

CAS No.
SMILES

OC1=CC2=C(C3=C(C(OC)=C(C=C3CC2)OC)O)C=C1

Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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