(-)-γ-Cuparenol
(-)-γ-Cuparenol is a sesquiterpene compound with an IC50 of 23.6 μg/mL against porcine Na+/K+-ATPase. (-)-γ-Cuparenol reduces phytohemagglutinin (PHA)-induced activation of NF-AT and NF-κB in Jurkat cells. (-)-γ-Cuparenol inhibits the growth of Gram-positive bacteria and some Gram-negative bacteria. (-)-γ-Cuparenol exhibits weak inhibitory activity against Candida albicans. (-)-γ-Cuparenol is applicable for research related to immunoregulation, cardiovascular diseases and bacterial infections.
For research use only. We do not sell to patients.
- CAS No.: 1357469-94-3
- Formula: C15H22O
- Molecular Weight:218.33
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
(-)-γ-Cuparenol (10 μg/mL; 4 h) significantly reduces PHA-induced NF-AT and NF-κB activation in Jurkat T lymphocytes[1].
(-)-γ-Cuparenol (0.05-100 μg/mL; 24 h ) inhibits the growth of Staphylococcus aureus, Bacillus subtilis, Micrococcus luteus, Proteus vulgaris, and Salmonella typhimurium with an MIC of 50 μg/mL, but does not inhibit Escherichia coli growth at concentrations up to 100 μg/mL[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. 1357469-94-3
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Molecular Weight 218.33
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Formula C15H22O
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SMILES
C[C@@]1(C2=CC=C(C=C2)CO)C(C)(CCC1)C
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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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Gram Staining of Tissue Sections
Gram staining of tissue sections is a histochemical technique used to differentiate Gram-positive and Gram-negative bacteria within histological specimens based on differences in bacterial cell wall structure and dye retention, adapted from classical bacteriological Gram staining into tissue-compatible “histological Gram stain” variants. In tissue applications, modifications of the Brown-Hopps and Brown-Brenn methods are commonly used to improve differentiation of microorganisms embedded within host connective tissue and to reduce overstaining or loss of Gram-negative signal, which are known limitations of earlier approaches. The principle relies on crystal violet-iodine complex retention in Gram-positive organisms and subsequent decolorization and counterstaining steps that allow contrast visualization of Gram-negative organisms against tissue background.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)