Evoxine
Evoxine (Haplophytin B) is a compound that selectively inhibits CO2-induced immunosuppression and has activity in inhibiting the expression of interleukin-6 and chemokine CCL2 in human THP-1 macrophages. Evoxine shows antimicrobial activity against a wide range of bacteria, especially performing well in minimum inhibitory concentration (MIC) tests against Escherichia coli, Bacillus subtilis, and Staphylococcus aureus. Evoxine extracts may find application in crude drug preparations in West Africa, provided that their in vivo toxicity results are negative.
For research use only. We do not sell to patients.
- CAS No.: 522-11-2
- Formula: C18H21NO6
- Molecular Weight:347.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 522-11-2
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Molecular Weight 347.36
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Formula C18H21NO6
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SMILES
COC1=C2C(C(OC)=C3C(OC=C3)=N2)=CC=C1OC[C@@H](O)C(C)(O)C
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Synonyms
Haplophytin B; Haplophytine B
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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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THP-1 macrophage-like differentiation
THP-1 monocytes are differentiated into macrophage-like adherent cells by exposure to phorbol 12-myristate 13-acetate (PMA), a phorbol ester used across published THP-1 macrophage differentiation studies; differentiation is assessed by adherence, macrophage-like morphology, altered macrophage-associated surface markers such as CD11b, CD14, CD36, and CD204, phagocytic capacity, lysosomal/mitochondrial enrichment, cytokine responsiveness, and transcriptomic or proteomic remodeling. Because PMA concentration, exposure duration, and post-PMA resting time change downstream phenotype and immune responses, this protocol treats PMA differentiation as a model-generation step rather than a universal macrophage replacement method; low-dose PMA with a rest period is preferred when subsequent inflammatory or infection assays are planned.
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THP-1 Cell Differentation
Macrophages are important immune effector cells and play an important role in innate and adaptive immune responses. THP-1 cells are usually induced to differentiate into macrophages with PMA.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)