Coriolus Versicolor Extract
Coriolus Versicolor Extract is a biological response modifier (BRM) with anti-cancer and anti-migratory properties. Coriolus Versicolor Extract can also inhibit the expression of tumorigenic factors associated with inflammation and can be used in cancer research.
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Coriolus Versicolor Extract (50-300μg/mL; 24-48 h) has cytotoxic effects on HUVEC (24 h) endothelial cells and MCF-7 (48 h) breast cancer cells stimulated by LPS (100 ng/mL-1 μg/mL; 24-48 h) (HY-D1056)[1].
Coriolus Versicolor Extract (100 μg/mL; 24-48 h) inhibits the production of IL-6, IL-8, and MMP-9 stimulated by LPS (20-100 ng/mL; 24-48 h) in HUVEC and MCF-7 cells. This effect was accompanied by a decrease in the expression of TLR4 and p-IκB[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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SMILES
[Coriolus Versicolor Extract]
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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 Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)