Jietacin A
Jietacin A is a nematicide. Jietacin A exhibits nematicidal activity against pine wood nematodes. Jietacin A can be used in studies related to pine wood nematode infection and pine wilt disease.
For research use only. We do not sell to patients.
- CAS No.: 109766-61-2
- Formula: C18H34N2O2
- Molecular Weight:310.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Parasite Isoforms
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| ATN-1 | ED50 |
1.82 μg/mL
Compound: Jietacin A
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Antiproliferative activity against human ATN1 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay
Antiproliferative activity against human ATN1 cells assessed as reduction in cell viability measured after 24 hrs by MTT assay
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[PMID: 31226655] |
In Vitro
Jietacin A (Compound 1) potently inhibits the pine wood nematode (Bursaphelenchus lignicolus) with an IC50 of 0.038 μg/mL[1].
Jietacin A (0.250 μμg/mL) potently inhibits Bursaphelenchus xylophilus (pine wood nematode) in vitro, and induces 100% mortality[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. 109766-61-2
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Molecular Weight 310.47
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Formula C18H34N2O2
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SMILES
O=C(CCCCCC(C)C)CCCCCCCN=N(C=C)=O
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Structure Classification
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Initial Source
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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)