Altertoxin I
Based on 1 Customer Validation
Altertoxin I (Dihydroalterperylenol; ATX-I) is a quinone mycotoxin with immunosuppressive, mutagenic and anticancer activities. Altertoxin I inhibits LPS (HY-D1056)-mediated NF-κB activation and estrogen-dependent alkaline phosphatase activity. Altertoxin I activates the AhR signaling pathway, induces the expression of CYP 1A1/1A2/1B1 and the enzymatic activity of EROD. Altertoxin I can be used in breast cancer research.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 99.16%
- CAS. Nr.: 56258-32-3
- Formel: C20H16O6
- Molecular Weight:352.34
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Speicherung:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
In Vitro
Altertoxin I (0.001-20 μM; 20 h) suppresses LPS-induced NF-κB pathway activation in THP1-Lucia™ monocytes with significant effects starting at 1 μM, and does not induce cytotoxicity at concentrations up to 20 μM[1].
Altertoxin I (0.0002-10 μM; 48 h) exerts antiestrogenic effects in Ishikawa cells by suppressing E2-induced alkaline phosphatase activity with significant effects starting at 2 μM, and does not induce cytotoxicity at concentrations up to 10 μM[1].
Altertoxin I (0.01-5 µM; 24 h) dose-dependently induces EROD enzyme activity in MCF-7 human mammary breast cancer cells, with significant activation starting at 2.5 µM[2].
Altertoxin I (0.01-5 µM; 24 h) enhances metabolic activity in MCF-7 human mammary breast cancer cells at 5 µM without reducing cell metabolic activity at lower tested concentrations[2].
Altertoxin I (20 μM; 24 h) exhibits minimal cytotoxicity in A549, HeLa, U2OS, and HepG2 cancer cell lines[3].
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:human mammary breast cancer MCF-7 cells
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Concentration:0.01 µM, 0.1 µM, 1 µM, 2.5 µM, 5 µM
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Incubation Time:24 h
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Result:Did not compromise cell metabolic activity at any tested concentration.
Induced a significant enhancement of metabolic activity at 5 µM, reaching approximately 130% of solvent control.
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Cell Line:A549, HeLa, U2OS, HepG2
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Concentration:20 μM
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Incubation Time:24 h
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Result:Maintained cell viability near control levels across all four tested cancer cell lines.
Showed no significant growth inhibition.
Chemical Information
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CAS. Nr. 56258-32-3
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Appearance Solid
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Molecular Weight 352.34
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Formel C20H16O6
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Color Light yellow to yellow
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SMILES
O=C(C1=C2C3=CC=C1O)CC[C@]2([C@@]([H])(C4=C3C=CC(O)=C45)[C@H](CC5=O)O)O
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Synonyms
Dihydroalterperylenol; ATX-I
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Structure Classification
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Initial Source
Alternaria alternata
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protokoll
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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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.
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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.
Reinheit & Dokumentation
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Data Sheet (278 KB)
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SDS (480 KB)
- English - EN (480 KB)
- Français - FR (480 KB)
- Deutsch - DE (480 KB)
- Norwegian - NO (480 KB)
- Español - ES (480 KB)
- Swedish - SV (480 KB)
- Italian - IT (480 KB)
- Korean - KR (480 KB)
- Portuguese - PT (480 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Crudo F, et al. Discovery of the Alternaria mycotoxins alterperylenol and altertoxin I as novel immunosuppressive and antiestrogenic compounds in vitro. Archives of toxicology. 2025 Jan;99(1):407-421. [Content Brief]
[2].
Hohenbichler J, et al Alternaria alternata Toxins Synergistically Activate the Aryl Hydrocarbon Receptor Pathway In Vitro. Biomolecules. 2020 Jul 9;10(7):1018.
[Content Brief]
[3]. Xi J, et al. Alterperylenol as a Novel Thioredoxin Reductase Inhibitor Induces Liver Cancer Cell Apoptosis and Ferroptosis. Journal of agricultural and food chemistry. 2022 Dec 21;70(50):15763-15775. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Altertoxin I Related Classifications
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