SDH-IN-28
SDH-IN-28 is a succinate dehydrogenase inhibitor with an IC50 value of 2.65 mg/L. SDH-IN-28 demonstrates broad-spectrum fungicidal efficacy, with EC50 values of 0.21 (Valsa mali), 0.95 (Botrytis cinerea), 0.64 (Rhizoctonia solani), 1.33 (Fusarium graminearum), and 0.66 mg/L (Gaeumannomyces graminis). SDH-IN-28 effectively prevents V. mali infection in apples.
For research use only. We do not sell to patients.
- Formula: C20H15Cl2F4N5O2S
- Molecular Weight:536.33
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
SDH-IN-28 (Compound 4d) (20 mg/L) shows good fungicidal activities with inhibition rate of V. mali (100%), S. sclerotiorum (94.3%), B. cinerea (86.1%), R. solani (100%), F. graminearum (88.0%), G. graminis (100%), and P. capsici (66.1%) at 20 mg/L[1].
SDH-IN-28 (50 mg/L, 1-10 days) shows superior curative and protective efficiency in apples inoculated with V. mali for 24 h[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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Molecular Weight 536.33
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Formula C20H15Cl2F4N5O2S
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SMILES
O=C(NC1=C(SCC(NNC2=CC=C(F)C=C2)=O)C(C(F)(F)F)=NN1C)C3=CC(Cl)=CC(Cl)=C3
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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)