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MedChemExpressModel Tegoprazan - 942195-55-3

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Tegoprazan (CJ-12420), a potassium-competitive acid blocker, is a reversible, orally active and highly selective inhibitor of gastric H+/K+-ATPase. Tegoprazan inhibits gastric acid secretion and motility against porcine, canine and human H+/K+-ATPase with IC50 values ranging from 0.29-0.52 μM in vitro. Tegoprazan significantly improves colitis and enhances the intestinal epithelial barrier function in mice. Tegoprazan is promising for research of Inflammatory bowel, gastric acid-related, motilityimpaired diseases[1][2][3].
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Tegoprazan

MCE China:Tegoprazan

Brand:MedChemExpress (MCE)

Cat. No.HY-17623

CAS:942195-55-3

Synonyms:CJ-12420; RQ-00000004

Purity:99.76%

Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping:Room temperature in continental US; may vary elsewhere.

Description:Tegoprazan (CJ-12420), a potassium-competitive acid blocker, is a reversible, orally active and highly selective inhibitor of gastric H+/K+-ATPase. Tegoprazan inhibits gastric acid secretion and motility against porcine, canine and human H+/K+-ATPase with IC50 values ranging from 0.29-0.52 μM in vitro. Tegoprazan significantly improves colitis and enhances the intestinal epithelial barrier function in mice. Tegoprazan is promising for research of Inflammatory bowel, gastric acid-related, motilityimpaired diseases.

In Vitro:Tegoprazan (1.0 mM and 3.0 mM, 4 h) reduces dextran sulphate sodium (DSS)-induced colitis by maintaining high junction integrity of the epithelial mucosa in Caco-2 cells. Additionally, Tegoprazan protects the intestinal epithelial tight junction barrier and inhibits the increase in intestinal permeability in Caco-2 cells[1].

In Vivo:Tegoprazan (30 mg / kg, p.o., twice daily for 5 days) alleviates the severity of dinitrobenzene sulfonic acid (DNBS)-induced reduced colon length and colonic damage, as well as protecting against DNBS-induced colon inflammation in mice colon[1]. Tegoprazan (0.1, 1 and 10 mg/kg, p.o., a single day or daily for 5 days) exerts an antiulcer effect in Naproxen (HY-15030)-induced acute gastric ulcer rat model[2].

IC50 & Target:IC50: 0.29-0.52 μM (H+/K+-ATPase)[1]. In Vitro Tegoprazan (1.0 mM and 3.0 mM, 4 h) reduces dextran sulphate sodium (DSS)-induced colitis by maintaining high junction integrity of the epithelial mucosa in Caco-2 cells. Additionally, Tegoprazan protects the intestinal epithelial tight junction barrier and inhibits the increase in intestinal permeability in Caco-2 cells[1]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Tegoprazan Related Antibodies RT-PCR[1] Cell Line: Caco-2 cells

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References:

[1]. Son M, et al. Novel Potassium-Competitive Acid Blocker, Tegoprazan, Protects Against Colitis by Improving Gut Barrier Function[J]. Front Immunol. 2022 May 25;13:870817.  [Content Brief]

[2]. Kim DK, et al. Effects of Tegoprazan, a Novel Potassium-Competitive Acid Blocker, on Rat Models of Gastric Acid-Related Disease[J]. J Pharmacol Exp Ther. 2019 Jun;369(3):318-327.  [Content Brief]

[3]. Takahashi N, et al. Tegoprazan, a Novel Potassium-Competitive Acid Blocker to Control Gastric Acid Secretion and Motility. J Pharmacol Exp Ther. 2018 Feb;364(2):275-286.  [Content Brief]

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