Bischloroanthrabenzoxocinone
Bischloroanthrabenzoxocinone is a potent Type II fatty acid synthesis (FASII) inhibitor. Bischloroanthrabenzoxocinone inhibits fatty acid synthesis. Bischloroanthrabenzoxocinone shows antibacterial activities and inhibits phospholipid, DNA, RNA, protein, and cell wall synthesis.
For research use only. We do not sell to patients.
- CAS No.: 866022-28-8
- Formula: C28H24Cl2O7
- Molecular Weight:543.39
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Bischloroanthrabenzoxocinone (0.01-333 µg/mL) inhibits fatty acid synthesis with the IC50 values of 11.4, 35.3 µg/mL for Staphylococcus aureus and Escherichia coli, respectively[1].
Bischloroanthrabenzoxocinone (0-250 µg/mL) shows antibacterial activities with MIC values of 0.2, >250 µg/mL for Staphylococcus aureus and wild type Escherichia coli, respectively[1].
Ischloroanthrabenzoxocinone inhibits phospholipid synthesis with an IC50 value of 0.21 μg/ml, and it also inhibits DNA, RNA, protein, and cell wall syntheses in Staphylococcus aureus and Escherichia coli[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 866022-28-8
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Molecular Weight 543.39
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Formula C28H24Cl2O7
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SMILES
OC1=C(C(C2)=CC(C(C)(C3=C4Cl)C)=C1C(C3=C(C(Cl)=C4O)O)=O)[C@](O[C@@]25C)([H])C(C(O5)=CC(OC)=C6)=C6C
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Synonyms
(-)-BABX
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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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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)