2-Deethoxy-2-hydroxyphantomolin
2-Deethoxy-2-hydroxyphantomolin, Germacranolide, is an Antifungal and Antibacterial agent. 2-Deethoxy-2-hydroxyphantomolin can be isolated from Elephantopus tomentosus Linn and E. mollis. 2-Deethoxy-2-hydroxyphantomolin is moderately active against Candida albicans (14 mm clearing zone) and slightly active against Escherichia coli (12 mm), Pseudomonas aeruginosa (12 mm), Bacillus subtilis (14 mm), and Trichophyton mentagrophytes (13 mm).
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- CAS No.: 821799-76-2
- Formule: C19H22O6
- Masse moléculaire:346.37
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
In Vitro
2-Deethoxy-2-hydroxyphantomolin (20.0 mg/mL; 24 h) inhibits Staphylococcus aureus with an inhibition zone diameter of 31.0 mm in an in vitro disk diffusion assay[1].
2-Deethoxy-2-hydroxyphantomolin is moderately active against Candida albicans (14 mm clearing zone, AI = 0.4) and slightly active against Escherichia coli (12 mm, AI = 0.2), Pseudomonas aeruginosa (12 mm, AI = 0.2), Bacillus subtilis (14 mm, AI = 0.4), and Trichophyton mentagrophytes (13 mm, AI = 0.3), with no activity against Staphylococcus aureus and Aspergillus niger[2].
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. 821799-76-2
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Masse moléculaire 346.37
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Formule C19H22O6
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SMILES
CC(C(O[C@@H]1[C@]2([H])[C@@](OC(C2=C)=O)([H])[C@@]3([H])O[C@](C=C3C)(/C=C(C1)/C)O)=O)=C
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)