Aurofusarin
Aurofusarin is a secondary metabolite. Aurofusarin catalytically inhibits topoisomerase II alpha, induces CYP1A1, p53, oxidative stress, DNA damage, and glutathione redox shift, intercalates into DNA, and causes S phase reduction accompanied by cytoskeletal/nuclear condensation. Aurofusarin disrupts intestinal epithelial barrier integrity, acts additively with deoxynivalenol, reduces mitochondrial activity, is cytotoxic to colon cells, and inhibits probiotic Gram-positive bacteria through outer membrane penetration without affecting Gram-negative bacteria. Aurofusarin can be used in research on colon cancer and bacterial infections.
For research use only. We do not sell to patients.
- CAS No.: 13191-64-5
- Formula: C30H18O12
- Molecular Weight:570.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Topoisomerase Isoforms
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Biological Activity
Description
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topoisomerase II alpha |
CYP1A1 |
p53 |
In Vitro
Aurofusarin shows relatively low toxicity against Spodoptera frugiperda Sf9 insect cells in the MTT assay[1].
Aurofusarin (5-10 µM; 24-72 h) decreases the TEER of differentiated IPEC-J2 at 10 µM, with a maximum reduction of 83% after 72 h, whereas 5 µM had no effect and viability was unaffected[2].
Aurofusarin (5 µM; 24-48 h) combined with DON (6-Diazo-5-oxo-L-nor-Leucine) (HY-108357) additively reduces the TEER of differentiated IPEC-J2 at 24 and 48 h without affecting viability[2].
Aurofusarin (1-10 μM; 1 h) inhibits human topoisomerase II α catalytic activity at concentrations ≥1 μM in a cell-free decatenation assay[3].
Aurofusarin (10 μM; 24 h) increases CYP1A1 activity in HT29 cells[3].
Aurofusarin (0.01-10 μM; 24 h) reduces mitochondrial activity in HT29 and HCEC-1CT cells[3].
Aurofusarin (0.01-10 μM; 24-72 h) inhibits the proliferation of HT29 and HCEC-1CT cells, with HCEC-1CT responding at 0.1 μM after 72 h, and both cell lines being strongly inhibited at 10 μM[3].
Aurofusarin (5-10 μM; 1-24 h) induces p53 but not γ-H2AX in HT29 and HCEC-1CT cells, and disrupts actin cytoskeleton morphology, especially in HCEC-1CT cells[3].
Aurofusarin (5-10 μM; 24 h) reduces S-phase cells in HT29 cells without altering the cell cycle distribution of HCEC-1CT cells[3].
Aurofusarin (0.01-10 μM; 1 h) induces DNA strand breaks in HT29 cells at 1 μM and induces fpg-sensitive oxidative DNA damage at concentrations ≥0.1 μM[3].
Aurofusarin (0.01-10 μM; 1-3 h) induces reactive oxygen species in HT29 cells[3].
Aurofusarin (0.01-10 μM; 1-24 h) alters the glutathione redox state in HT29 cells, decreasing tGSH and increasing the GSSG/GSH ratio[3].
Aurofusarin (0.01-10 μM; 3-24 h) induces CYP1A1 transcription in HT29 cells, reaching 8.1-fold after 3 h at 5 μM and 6.5-fold after 24 h at 10 μM, while decreasing γGCL after 3 h at 10 μM[3].
Aurofusarin (2-256 µM; 6 h) inhibits the growth of Lactobacillus acidophilus in vitro with an IC50 of 8 µM, and had no effect on Escherichia coli, Staphylococcus aureus, or Salmonella typhimurium[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HT29 and HCEC-1CT cells
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Concentration:0.01, 0.1, 1, 5, 10 μM
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Incubation Time:1 h; 24 h
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Result:After 24 h, 5 μM AURO reduced mitochondrial activity to 76% in HT29 and 77% in HCEC-1CT; 10 μM reduced activity to 70% in HT29 and 60% in HCEC-1CT.
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Cell Line:HT29 and HCEC-1CT cells
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Concentration:0.01, 0.1, 1, 5, 10 μM
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Incubation Time:24, 48, 72 h
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Result:In HCEC-1CT, 0.1 μM AURO for 72 h reduced proliferation to 74% of solvent control; in HT29, 1 μ
M for 72 h reduced proliferation to 77%.
In both cell lines, 5 and 10 μM AURO decreased proliferation after all three incubation times; after 72 h, 10 μM AURO left 12% proliferating HT29 cells and 7% HCEC-1CT cells.
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Cell Line:HT29 and HCEC-1CT cells
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Concentration:5, 10 μM
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Incubation Time:24 h
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Result:In HT29 cells, 10 μM AURO decreased the proportion of cells in S-phase and slightly increased cells in G2/M-phase.
In HCEC-1CT cells, no changes in cell cycle distribution were observed.
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Cell Line:HT29 and HCEC-1CT cells
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Concentration:5, 10 μM
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Incubation Time:1, 3, 24 h
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Result:In HT29 cells, both 5 and 10 μM AURO increased p53 fluorescence after 3 h; HCEC-1CT cells showed no specific p53 differences after 3 h.
After 24 h, 10 μM AURO induced p53 in both cell lines.
Incubation with 5 and 10 μM AURO for 1 h did not increase γ-H2AX signal in HT29 or HCEC-1CT.
Morphologically, HT29 showed only a slight effect on filamentous actin after 3 h with 10 μM; HCEC-1CT showed loss of filamentous fine structure of the actin cytoskeleton, nuclear condensation, and kidney-shaped nuclei after 3 h, more pronounced after 24 h.
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Cell Line:HT29 cells
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Concentration:0.01, 0.1, 1, 5, 10 μM
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Incubation Time:3 h and 24 h
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Result:After 3 h, 10 μM AURO decreased γGCL transcription to 0.48-fold of solvent control.
CYP1A1 transcription after 3 h was 1.9-fold at 1 μM, 8.1-fold at 5 μM, and 2.5-fold at 10 μM.
After 24 h, CYP1A1 transcription was 4.1-fold at 5 μM and 6.5-fold at 10 μM; Nrf2 transcription was 1.1-fold at 10 μM.
- EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
- Flow cytometric DNA-content cell-cycle staining
- ROS/oxidative-stress fluorescent staining
- BrdU Incorporation Assay
- Transepithelial/transendothelial electrical resistance assay
- Protocol for Cell Cycle
- Gram Staining of Tissue Sections
- Genotoxicity/Mutagenicity Study
- Phalloidin F-actin cytoskeleton staining
- Cell Viability Determination by MTT Colorimetric Assay
Chemical Information
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CAS No. 13191-64-5
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Molecular Weight 570.46
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Formula C30H18O12
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SMILES
O=C(C=C(C)O1)C(C1=C2)=C(O)C(C(C(C(C(C3=C4C=C5C(C(C=C(C)O5)=O)=C3O)=O)=C(OC)C4=O)=C6OC)=O)=C2C6=O
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)