ADHPE
ADHPE is a stabilizer of 14-3-3σ and p65 protein complex. ADHPE inhibits NF-κB (p65) signaling pathway and reduces the inflammatory response. ADHPE can be used for pediatric pneumonia-related acute lung injury and acute respiratory distress syndrome study.
For research use only. We do not sell to patients.
- CAS No.: 138870-97-0
- Formula: C23H28O8
- Molecular Weight:432.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
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14-3-3α |
Chemical Information
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CAS No. 138870-97-0
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Molecular Weight 432.46
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Formula C23H28O8
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SMILES
OC(C=C1CC[C@H](OC(C)=O)C[C@@H](OC(C)=O)CCC2=CC(O)=C(C=C2)O)=C(C=C1)O
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Structure Classification
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Initial Source
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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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Immunoprecipitation
Immunoprecipitation (IP) is an experimental method that uses the principle of antibody specific binding to purify and enrich target proteins.
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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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Inhalation Toxicity Study
Inhalation toxicity studies expose rodents to a controlled aerosol, vapor, gas, or smoke atmosphere and assess respiratory and systemic toxicity using exposure-atmosphere characterization, clinical observations, body and organ weights, bronchoalveolar lavage fluid, histopathology, blood chemistry, hematology, and, when included, molecular endpoints such as transcriptomics, proteomics, lipidomics, or tissue burden analysis. The primary biological readouts are airway irritation, pulmonary inflammation, cytotoxicity, altered surfactant or lipid homeostasis, impaired particle clearance, and tissue remodeling, reflected by BALF cell differentials, BALF protein, LDH, phosphatase activities, cytokines, lung weight, microscopic respiratory-tract lesions, and retained lung burden.
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Co-Immunoprecipitation
Co-immunoprecipitation technology can verify protein interaction based on the specific immune reaction between antibodies and antigens.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)