3β,15α-Dihydroxy-7,11,23-trioxo-lanost-8-dien-26-oic acid
3β,15α-Dihydroxy-7,11,23-trioxo-lanost-8-dien-26-oic acid is a triterpene compound that can be found in Ganoderma lucidum, and it inhibits nitric oxide (NO) production in BV-2 microglial cells induced by lipopolysaccharide (LPS, HY-D1056), with an IC50 of 6.50 μM, making it a potential candidate for anti-inflammatory research.
For research use only. We do not sell to patients.
- CAS No.: 117354-72-0
- Formula: C30H44O7
- Molecular Weight:516.67
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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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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| BV-2 | IC50 |
6.5 μM
Compound: 24
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Antiinflammatory activity in mouse BV2 cells assessed as inhibition of LPS-induced NO production incubated for 24 hrs measured after 15 mins by Griess assay
Antiinflammatory activity in mouse BV2 cells assessed as inhibition of LPS-induced NO production incubated for 24 hrs measured after 15 mins by Griess assay
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[PMID: 27335254] |
Chemical Information
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CAS No. 117354-72-0
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Molecular Weight 516.67
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Formula C30H44O7
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SMILES
C[C@]12C3=C(C(C[C@@]1([C@@](C[C@@H]2O)([H])[C@H](C)CC(CC(C)C(O)=O)=O)C)=O)[C@@]4([C@@](C(C)([C@H](CC4)O)C)([H])CC3=O)C
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Structure Classification
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Initial Source
Ganoderma lucidum
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
3β,15α-Dihydroxy-7,11,23-trioxo-lanost-8-dien-26-oic acid Related Classifications
HY-N13706 Related Classifications
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