CAY10397
CAY10397 is a selective and orally active 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitor. CAY10397 can inhibit 15-PGDH-dependent endogenous metabolite production. CAY10397 blocks the selenium-dependent protective in inflammation. CAY10397 can be used for the research of colitis.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 78028-01-0
- Formel: C17H16N2O5
- Molecular Weight:328.32
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Speicherung:
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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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Biologische Aktivität
Beschreibung
In Vitro
CAY10397 (50 μM; 10 min) potently inhibits 15-PGDH activity in LoVo cell lysates, reducing formation of 15-PGDH-dependent metabolites including 11-oxo-ETE by 92%[1].
CAY10397 (50 μM; 10 min) does not alter levels of 15-PGDH precursor metabolites in HCA-7 cell lysates, which express negligible 15-PGDH[1].
CAY10397 inhibits the activity of purified human recombinant 15-PGDH[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:DSS-induced acute colitis mice model
C57BL/6 (male, 3 weeks old, maintained on 0.4 ppm selenium diet for 10-12 weeks)[2] -
Dosage:100 mg/kg
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Administration:oral gavage; every alternate day; starting at day -1 relative to DSS treatment
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Result:Blocked the Se-mediated inhibition of colonic expression of TNF-α, IL-1β, IFN-
γ and COX-2.
Significantly reduced colonic expression of the anti-inflammatory/barrier-protective gene Muc-2 relative to vehicle controls.
Significantly increased colonic histopathological scores relative to vehicle controls.
Significantly reduced colonic 15-PGDH specific activity relative to vehicle controls.
Chemical Information
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CAS. Nr. 78028-01-0
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Molecular Weight 328.32
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Formel C17H16N2O5
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SMILES
OC1=C(C=C(C=C1)/N=N/C2=CC=C(C=C2)C(OCC)=O)CC(O)=O
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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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DSS-Induced Colitis
Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.
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TNBS-Induced Colitis
TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.
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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
Reinheit & Dokumentation
Verweise
[1]. Liu X, et al. 11-Oxoeicosatetraenoic acid is a cyclooxygenase-2/15-hydroxyprostaglandin dehydrogenase-derived antiproliferative eicosanoid. Chem Res Toxicol. 2011;24(12):2227-2236. [Content Brief]
[2]. Kaushal N, et al. Crucial role of macrophage selenoproteins in experimental colitis. J Immunol. 2014;193(7):3683-3692. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
CAY10397 Related Classifications
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