Antifungal agent 182
Antifungal agent 182 is a mitochondrial complex III (Qo site) inhibitor with an IC50 of 7.05 mg/L. Antifungal agent 182 binds to the Qo pocket, blocking electron transfer and impairing ATP synthesis. Antifungal agent 182 exhibits inhibitory activity against R. solani and P. capsici. Antifungal agent 182 can be used for research on rice sheath blight and Phytophthora capsici infection in pepper.
For research use only. We do not sell to patients.
- CAS No.: 3134776-29-4
- Formula: C17H12O3S
- Molecular Weight:296.34
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Antifungal agent 182 (A21) exhibits potent broad-spectrum antifungal activity, especially against P. capsici (EC50 = 0.59 mg/L) and R. solani (EC50 = 0.69 mg/L)[1].
Antifungal agent 182 causes visible morphological disruption to R. solani and P. capsici mycelia at their respective EC50 concentrations[1].
Antifungal agent 182 causes severe toxicological damage to the cellular structures of R. solani and P. capsici, including mitochondrial degradation and vacuolar enlargement[1].
Antifungal agent 182 disrupts membrane integrity in P. capsici, leading to increased permeability and leakage of charged substances[1].
Antifungal agent 182 acts as an inhibitor of mitochondrial complex III (IC50 = 7.05 mg/L) in P. capsici[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. 3134776-29-4
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Molecular Weight 296.34
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Formula C17H12O3S
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SMILES
O=C1OC(C2=CC=CS2)C(C3=CC4=CC=CC=C4O3)C1=C
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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.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Antifungal agent 182
- 3134776-29-4
- Antifungal agent182
- Antifungal agent-182
- Mitochondrial Metabolism
- Fungal
- rice sheath blight
- R. solani
- mitochondrial complex III
- membrane permeability
- ATP synthesis
- Qo site
- P. capsici
- cell membrane integrity
- electron transport
- Phytophthora capsici infection
- Inhibitor
- inhibitor
- inhibit