Tegoprazan-d6
Tegoprazan (CJ-12420; RQ-00000004), a potassium-competitive acid blocker, is a reversible, oral active and highly selective inhibitor of gastric H+/K+-ATPase that could control gastric acid secretion and motility, with IC50 values ranging from 0.29-0.52 μM for porcine, canine, and human H+/K+-ATPases in vitro. Tegoprazan significantly improves colitis in mice and enhances the intestinal epithelial barrier function. Tegoprazan is promising for research of Inflammatory bowel, gastric acid-related, motilityimpaired diseases.
For research use only. We do not sell to patients.
- Formula: C20H13D6F2N3O3
- Molecular Weight:393.42
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Tegoprazan (1.0 mM and 3.0 mM, 4 h) reduces DSS-induced colitis by maintaining high junction integrity of the epithelial mucosa in Caco-2 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Caco-2 cells
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Concentration:1.0 mM and 3.0 mM
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Incubation Time:4 h
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Result:Protected the intestinal epithelial tight junction barrier and inhibits the increase in intestinal permeability.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Pylorus-Ligated Rats[2]
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Dosage:3 mg/kg and 10 mg/kg
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Administration:p.o., a single dose
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Result:Inhibited basal gastric acid secretion in a dose-dependent manner and was effective at a single dose in Pylorus-Ligated rats.
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Animal Model:Naproxen-induced acute gastric ulcer rat model[2]
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Dosage:0.1, 1 and 10 mg/kg
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Administration:p.o., a single day or daily for 5 days
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Result:Exerted an antiulcer effect in a dose-dependent manner and was effective at a single dose in naproxen-induced acute gastric ulcer rat model.
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Animal Model:DNBS and Tegoprazan-induced rats[2]
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Dosage:30 mg/kg
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Administration:p.o., twice daily for 5 days
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Result:Reduced mRNA expression levels of proinflammatory cytokines, especially interleukin-17 (IL17) in DNBS and Tegoprazan-induced rats.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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Unlabeled CAS 942195-55-3
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Molecular Weight 393.42
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Formula C20H13D6F2N3O3
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SMILES
CC1=NC2=C(C=C(C=C2N1)C(N(C([2H])([2H])[2H])C([2H])([2H])[2H])=O)O[C@H]3CCOC4=C3C(F)=CC(F)=C4
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Synonyms
CJ-12420-d6; RQ-00000004-d6
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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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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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Transepithelial/transendothelial electrical resistance assay
TEER measures electrical resistance across epithelial or endothelial monolayers cultured on permeable supports, and the readout reflects ionic conductance through the cell barrier, especially the paracellular pathway regulated by junctional integrity. TEER can be measured without destroying the monolayer and is commonly used before or during transport, permeability, barrier-disruption, and barrier-maturation experiments. TEER values are influenced by biological maturation and technical conditions; reported factors include temperature, medium formulation, passage number, electrode geometry, membrane properties, and junctional length during early monolayer maturation. Therefore, TEER should be interpreted with blank-insert subtraction, area normalization, repeated readings, and, when possible, orthogonal barrier readouts such as FITC-dextran flux or tight-junction staining.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)