23-Hydroxyohchininolide
23-Hydroxyohchininolide is a limonoid found in the leaves of Melia azedarach L.. 23-Hydroxyohchininolide inhibits LPS (HY-D1056)-induced NO production and exerts cytotoxic activity against human leukemia and stomach cancer cells. 23-Hydroxyohchininolide inhibits TPA (HY-18739)-induced Epstein-Barr virus early antigen activation. 23-Hydroxyohchininolide can be used for the research of cancer, infection and inflammatory disease.
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- CAS No.: 1429747-10-3
- Formule: C36H42O10
- Masse moléculaire:634.71
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
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Activité biologique
Description
In Vitro
23-Hydroxyohchininolide (Compound 8) (48 h) exhibits cytotoxic activity against HL60 leukemia cells (IC50 = 25.1 ± 3.2 μM) and AZ521 stomach cancer cells (IC50 = 78.5 ± 2.9 μM), but not against A549 lung or SK-BR-3 breast cancer cells (IC50 >100μM)[1].
23-Hydroxyohchininolide (2 h pre-incubation, then 16 h with LPS) inhibits LPS (HY-D1056)-induced NO production in RAW 264.7 macrophages with an IC50 of 58.6 ± 1.9 μM, and does not exhibit cytotoxicity against these cells at concentrations up to 100 μM[1].
23-Hydroxyohchininolide inhibits TPA (HY-18739)-induced EBV-EA activation in Raji cells with an IC50 of 497 molar ratio relative to 32 pmol TPA[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:HL60 (leukemia), AZ521 (stomach), A549 (lung), SK-BR-3 (breast) human cancer cell lines
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Concentration:1×10-6 to 1×10-4 g/mL
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Incubation Time:48 h
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Result:Exhibited cytotoxicity against HL60 cells with an IC50 of 25.1 ± 3.2 μM.
Exhibited cytotoxicity against AZ521 cells with an IC50 of 78.5 ± 2.9 μM.
Showed no cytotoxicity (IC50 > 100 μM) against A549 and SK-BR-3 cells.
Chemical Information
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CAS No. 1429747-10-3
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Masse moléculaire 634.71
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Formule C36H42O10
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SMILES
C[C@]12[C@@]3([H])[C@](OC[C@@]3([C@@H](C[C@@H]2OC(/C=C/C4=CC=CC=C4)=O)O)C)([H])[C@]5([H])[C@]([C@@H]1CC(OC)=O)(C6=C(C)[C@H](C7=CC(OC7=O)O)C[C@@]6([H])O5)C
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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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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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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
23-Hydroxyohchininolide Related Classifications
HY-N18117A Related Classifications
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