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. Further protocols information, click here.
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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.
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.
Protocols
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EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
The EdU incorporation assay measures DNA synthesis by adding the thymidine analog 5-ethynyl-2′-deoxyuridine to cells or tissues, where it is incorporated into newly synthesized DNA during S phase. Incorporated EdU is detected by copper-catalyzed azide-alkyne cycloaddition, in which a fluorescent azide covalently reacts with the ethynyl group on EdU, allowing S-phase cells to be detected by fluorescence microscopy, flow cytometry, or high-content imaging. EdU detection does not require DNA denaturation or anti-BrdU antibody access, which preserves sample structure and improves compatibility with immunostaining and multiparameter cytometry compared with BrdU-based detection. EdU can be cytotoxic in a cell-type- and exposure-dependent manner, so pulse duration, concentration, and continuous-labeling designs should be validated for each cell type.
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Flow cytometric DNA-content cell-cycle staining
Flow cytometric DNA-content cell-cycle staining measures the fluorescence intensity of DNA-bound fluorochromes in single cells or nuclei to estimate DNA content distributions, allowing assignment of populations to G0/G1, S, and G2/M phases by DNA histogram deconvolution. Propidium iodide (PI) intercalates into DNA, and PI fluorescence is proportional to cellular DNA content when staining is performed under conditions that make DNA accessible and minimize non-DNA signal. Cells with G2/M DNA content are expected to show approximately twice the fluorescence intensity of G0/G1 cells, while S-phase cells occupy intermediate fluorescence values. PI-based DNA-content analysis can also detect cells with fractional DNA content, often reported as sub-G1, when DNA fragmentation and extraction during staining reduce retained DNA signal in apoptotic cells. DAPI is an alternative DNA fluorochrome for univariate DNA-content analysis, while bivariate approaches combining DNA content with proliferation
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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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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Transepithelial/transendothelial electrical resistance assay
TEER measures electrical resistance across epithelial or endothelial monolayers cultured on permeable supports, and the readout reflects ionic conductance through the cell barrier, especially the paracellular pathway regulated by junctional integrity. TEER can be measured without destroying the monolayer and is commonly used before or during transport, permeability, barrier-disruption, and barrier-maturation experiments. TEER values are influenced by biological maturation and technical conditions; reported factors include temperature, medium formulation, passage number, electrode geometry, membrane properties, and junctional length during early monolayer maturation. Therefore, TEER should be interpreted with blank-insert subtraction, area normalization, repeated readings, and, when possible, orthogonal barrier readouts such as FITC-dextran flux or tight-junction staining.
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Gram Staining of Tissue Sections
Gram staining of tissue sections is a histochemical technique used to differentiate Gram-positive and Gram-negative bacteria within histological specimens based on differences in bacterial cell wall structure and dye retention, adapted from classical bacteriological Gram staining into tissue-compatible “histological Gram stain” variants. In tissue applications, modifications of the Brown-Hopps and Brown-Brenn methods are commonly used to improve differentiation of microorganisms embedded within host connective tissue and to reduce overstaining or loss of Gram-negative signal, which are known limitations of earlier approaches. The principle relies on crystal violet-iodine complex retention in Gram-positive organisms and subsequent decolorization and counterstaining steps that allow contrast visualization of Gram-negative organisms against tissue background.
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
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Phalloidin F-actin cytoskeleton staining
Phalloidin F-actin staining detects polymerized filamentous actin in fixed and permeabilized specimens by using fluorescent phalloidin or phalloidin-derived phallotoxins that bind actin filaments and generate a fluorescence microscopy readout corresponding to F-actin organization, including stress fibers, cortical actin, filament bundles, and tissue-specific actin networks. Phalloidin stabilizes F-actin by reducing actin subunit dissociation from filament ends, and fluorescent phallotoxins were established as tools for visualizing actin-containing structures in eukaryotic cells.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)