Eudebeiolide B
Eudebeiolide B is a compound that can be isolated from Salvia plebeia R. Br. Eudebeiolide B inhibits osteoclastogenesis by regulating RANKL-induced NF-κB, c-Fos and calcium signaling. Eudebeiolide B can be used for osteoclast-related diseases research.
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- CAS. Nr.: 1934299-51-0
- Formel: C15H18O4
- Molecular Weight:262.30
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
Akt |
NF-κB |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HepG2 | IC50 |
27.8 μM
Compound: 10
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Down regulation of PCSK9 mRNA expression in human HepG2 cells incubated for 24 hrs by SYBR green dye-based qRT-PCR analysis
Down regulation of PCSK9 mRNA expression in human HepG2 cells incubated for 24 hrs by SYBR green dye-based qRT-PCR analysis
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[PMID: 33567826] |
| RAW264.7 | IC50 |
68.9 μM
Compound: 18
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Anti-inflammatory activity in mouse RAW264.7 cells assessed as reduction in LPS-induced NO production preincubated for 30 mins followed by LPS stimulation measured after 24 hrs by Griess assay
Anti-inflammatory activity in mouse RAW264.7 cells assessed as reduction in LPS-induced NO production preincubated for 30 mins followed by LPS stimulation measured after 24 hrs by Griess assay
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[PMID: 28960981] |
In Vitro
Eudebeiolide B (1-30 μΜ, 1 hour) suppresses RANKL-induced osteoclast differentiation and function in mouse bone marrow macrophages (BMMs)[1].
Eudebeiolide B (1-30 μΜ, 1 hour) inhibits the expression of osteoclastogenesis-related marker genes and RANKL-mediated cellular signaling [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:Bone marrow macrophages (BMMs)
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Concentration:1-30 μΜ
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Incubation Time:1 hours
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Result:Inhibited RANKL-induced osteoclast differentiation of BMMs, bone resorption, and promotes osteoblast differentiation.
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Cell Line:Bone marrow macrophages (BMMs), MC3T3-E1 cells
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Concentration:10 μΜ
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Incubation Time:1 hours
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Result:Downregulated the expression of NFATc1 and c-fos, transcription factors induced by RANKL.
Attenuated the RANKL-induced expression of osteoclastogenesis-related genes, including Ctsk, MMP9 and DC-STAMP.
Induced the expression of alkaline phosphatase (ALP) and calcium accumulation during MC3T3-E1 osteoblast differentiation.
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Cell Line:Bone marrow macrophages (BMMs)
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Concentration:10 μΜ
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Incubation Time:1 hours
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Result:Inhibited the phosphorylation of Akt and NF-κB p65.
Downregulated the expression of CREB, Btk and phospholipase PLCγ2 in RANKL-induced calcium signaling.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Ovariectomized (OVX) mouse model[1]
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Dosage:5 or 10 mg/kg
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Administration:After 6 weeks of ovarian resection, intragastric injection (i.g.) once daily for 6 weeks.
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Result:Prevented bone mineral density (BMD) loss and bone mineral content (BMC) loss compared to the OVX mice.
Chemical Information
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CAS. Nr. 1934299-51-0
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Molecular Weight 262.30
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Formel C15H18O4
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SMILES
O[C@]12C(C[C@@]3([H])[C@](C1)(C=CC([C@@H]3C)=O)C)=C(C(O2)=O)C
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Synonyms
Plebeiolide D
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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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Osteoclast differentiation from monocyte/macrophage precursors
Osteoclast differentiation is an in vitro induction assay in which monocyte/macrophage-lineage precursors are exposed to macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL), generating multinucleated osteoclasts that are commonly identified by tartrate-resistant acid phosphatase (TRAP) staining and functionally confirmed by resorption pits on dentin, bone, or mineralized substrates. M-CSF supports survival and expansion of osteoclast precursors, while RANKL binding to RANK drives osteoclast commitment, fusion, maturation, and resorptive function; osteoprotegerin inhibits this pathway by binding RANKL and preventing RANK activation. The main readouts are the number of TRAP-positive multinucleated cells, formation of F-actin rings, and resorbed surface area; TRAP-positive multinucleated cells indicate osteoclast differentiation, whereas pit formation on dentin, bone, or mineralized coating indicates functional bone-resorbing activity.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Eudebeiolide B Related Classifications
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