Murrayanol
Murrayanol is a natural carbazole alkaloid with a variety of biological activities. Murrayanol shows anti-inflammatory, topoisomerase I and topoisomerase II (Topoisomerase) inhibition activities. Murrayanol also as a mosquitocidal and antimicrobial.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 144525-81-5
- 分子式: C24H29NO2
- 分子量:363.49
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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生物活性
製品説明
体外実験
Murrayanol (Compound 2) shows an IC50 of 109 μg/mL against human prostaglandin H synthase isozyme 1 (hPGHS-1) and an IC50 of 218 μg/mL against hPGHS-2 in anti-inflammatory assays[1].
Murrayanol (Compound 2) shows 100% mortality at 12.5 µg/mL concentrations for Aedes aegyptii[1].
Murrayanol (Compound 2) completely inhibits topoisomerase I and II activity at 50 µg/mL concentrations when tested on S. cerevisiae mutant strains[1].
Murrayanol (Compound 2) shows an MIC100 of 100 µg/mL against C. kruseii and E. coli but give an MIC100 against S. aureus and S. pyogenes at 25 µg/mL[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
化学情報
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CAS 番号 144525-81-5
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分子量 363.49
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分子式 C24H29NO2
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SMILES
OC1=C(C/C=C(C)/CC/C=C(C)\C)C(NC2=C3C=C(C)C(OC)=C2)=C3C=C1
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Structure Classification
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Initial Source
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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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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
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)