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.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
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
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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SMILES
[Coriolus Versicolor Extract]
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)