SRI-22818
SRI-22818 is a NF-κB activator with an EC50 of 0.5 μM. SRI-22818 upregulates the expression of NF-κB and promotes its activation. SRI-22818 increases the level of SOD2. SRI-22818 exhibits activity in the SOD1G93A model of amyotrophic lateral sclerosis (ALS). SRI-22818 can be used for research related to amyotrophic lateral sclerosis.
For research use only. We do not sell to patients.
- CAS No.: 1429221-68-0
- Formula: C16H12BrNO3
- Molecular Weight:346.18
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| SH-SY5Y | EC50 |
0.5 μM
Compound: Example 1
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Activation of NF-KappaB (unknown origin) expressed in SH-SY5Y cells co-transfected with pNFkappaB-Luc plasmid measured after 24 hrs by Bright-Glo luciferase assay
Activation of NF-KappaB (unknown origin) expressed in SH-SY5Y cells co-transfected with pNFkappaB-Luc plasmid measured after 24 hrs by Bright-Glo luciferase assay
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[PMID: 31857831] |
In Vitro
Chemical Information
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CAS No. 1429221-68-0
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Molecular Weight 346.18
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Formula C16H12BrNO3
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SMILES
BrC(C=CC=C1)=C1N/C=C\C(C2=CC=C(OCO3)C3=C2)=O
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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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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)