Berkeleyacetal C
keleyacetal C, a meroterpenoid compound with anti-inflammatory effects via inhibiting NF-κB, ERK1/2 and IRF3 signaling pathways. Berkeleyacetal C significantly inhibits the expression of iNOS and the following NO production by macrophages. Berkeleyacetal C inhibits expression and secretion of key pro-inflammatory factors and chemokines (TNF-α, IL-6, IL-1β, MIP-1α, and MCP-1). Berkeleyacetal C also inhibits activation of neutrophils and reactive oxygen species (ROS) production. Berkeleyacetal C can be used for the study of inflammatory disorders.
For research use only. We do not sell to patients.
- CAS No.: 959772-67-9
- Formula: C24H26O8
- Molecular Weight:442.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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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
IC50 & Target
[1]|
iNOS |
ERK1 |
ERK2 |
NF-κB |
IL-6 |
IL-1β |
TNF-α |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| BV-2 | IC50 |
0.8 μM
Compound: 6
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Antineuroinflammatory activity in human BV2 cells assessed as inhibition of LPS-induced nitric oxide production preincubated for 10 mins followed by LPS stimulation for 24 hrs by Griess assay
Antineuroinflammatory activity in human BV2 cells assessed as inhibition of LPS-induced nitric oxide production preincubated for 10 mins followed by LPS stimulation for 24 hrs by Griess assay
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[PMID: 27120704] |
| RAW264.7 | IC50 |
4.3 μM
Compound: 11
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Inhibition of LPS-induced nitric oxide production in mouse RAW264.7 cells after 24 hrs by Griess assay
Inhibition of LPS-induced nitric oxide production in mouse RAW264.7 cells after 24 hrs by Griess assay
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[PMID: 28960979] |
Chemical Information
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CAS No. 959772-67-9
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Molecular Weight 442.46
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Formula C24H26O8
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SMILES
C[C@@]12[C@](C[C@@]3([C@]4([H])[C@@]2([H])C([C@@H](O[C@]4([H])OC3=O)C)=O)C)([H])[C@]5(CO5)C(C(C(C)(O6)C)=CC1=O)=CC6=O
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Structure Classification
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Initial Source
fungus Penicillium purpurogenum MHZ 111
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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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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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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