Isogosferol
Based on 1 publication(s) in Google Scholar
Isogosferol ((+)-Isogospherol; Isogospherol) is a potent anti-inflammatory agent. Isogosferol decreases LPS (HY-D1056)-stimulated NO and IL-1β expression. Isogosferol decreases the LPS (HY-D1056)-stimulated expression of iNOS, COX-2, NF-κB, and pERK1/2.
For research use only. We do not sell to patients.
- CAS No.: 53319-52-1
- Formula: C16H14O5
- Molecular Weight:286.28
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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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Publications Citing Use of MedChemExpress (MCE) Isogosferol
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Biological Activity
Description
In Vitro
Isogosferol (100, 200 µM; 1+16 h) decreases LPS (HY-D1056)-stimulated NO expression in RAW 264.7 cells[1].
Isogosferol (0, 25, 50, 100, 200 µM; 1+16 h) decreases LPS-stimulated expression of iNOS, COX-2 protein in a dose-dependent manner[1].
Isogosferol (0, 25, 50, 100, 200 µM; 1+1 h) decreases the LPS-stimulated expression of NF-κB and pERK1/2 in a dose-dependentmanner[1].
Isogosferol (50, 100, 200 µM µM; 1+16 h) decreases LPS-stimulated release of the pro-inflammatory cytokine, IL-1β[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:RAW 264.7 cells
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Concentration:100, 200 µM (stimulated with LPS (1 µg/mL))
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Incubation Time:1+16
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Result:Remarkably down-regulated the LPS-stimulated NO expression with an IC50 of 148 μM and shows no effect on cell viability.
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Cell Line:0, 25, 50, 100, 200 µM
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Concentration:1+16
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Incubation Time:1+16
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Result:Decreased the expression of iNOS, COX-2 protein in a dose-dependent manner.
Chemical Information
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CAS No. 53319-52-1
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Molecular Weight 286.28
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Formula C16H14O5
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SMILES
CC([C@@H](O)COC1=C(OC=C2)C2=CC(C=C3)=C1OC3=O)=C
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Synonyms
(+)-Isogospherol; Isogospherol
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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.
Publications (1)
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Journal Impact Factor
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Most Recent
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
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Isogosferol Related Classifications
HY-N3480 Related Classifications
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