LEX-K02
LEX-K02 is a broad-spectrum and potent thiazole amide antifungal agent with an EC50 of 0.140 μM. LEX-K02 inhibits fungal growth by disrupting the fungal cell membrane to cause leakage of intracellular substances and targeting the map00510 pathway to interfere with N-glycan biosynthesis. LEX-K02 can be used in studies related to Gaeumannomyces graminis infection.
For research use only. We do not sell to patients.
- CAS No.: 3106140-37-5
- Formula: C28H22F4N2O3S
- Molecular Weight:542.54
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
LEX-K02 (0.05-100 μM; 24 h-7 days) potently inhibits mycelial growth of Gaeumannomyces graminis with an EC50 of 0.140 μM. It disrupts cell membrane integrity, increases cell membrane permeability, causes leakage of cytoplasmic contents, alters gene expression and metabolite levels in Gaeumannomyces graminis, and significantly impairs the N-glycan biosynthesis pathway[1].
LEX-K02 (6.25-100 μM) is safe for wheat; it exerts no adverse effects on seed germination or seedling growth at concentrations up to 100 μM, and exhibits a weak growth-promoting effect on roots and shoots[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. 3106140-37-5
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Molecular Weight 542.54
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Formula C28H22F4N2O3S
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SMILES
O=C(C1=CSC(C2=CC(F)=C(C=C2)F)=N1)N[C@@H](C)C(O[C@@H](C)C(C3=CC=C(C=C3)F)C4=CC=C(C=C4)F)=O
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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)
LEX-K02 Related Classifications
HY-189090 Related Classifications
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