KFP-H008
KFP-H008 is an orally active potassium-competitive acid blocker. KFP-H008 inhibits gastric acid secretion through blocking H+-K+-ATPase. KFP-H008 reduces ethanol-induced gastric ulcer index and malonaldehyde as well as proinflammatory cytokine expression in vivo. KFP-H008 downregulates p-p38 MAPK and p65 NF-κB expression. KFP-H008 blocks histamine-stimulated acid secretion in rat and dog models. KFP-H008 can be studied in research on acid-related disease, such as ethanol-induced gastric ulcer and gastric epithelial cell damage.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 1876453-55-2
- 分子式: C19H18N4O2S
- 分子量:366.44
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
化学情報
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CAS 番号 1876453-55-2
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分子量 366.44
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分子式 C19H18N4O2S
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SMILES
O=S(=O)(C=1C=NC=CC1)N2C=C(C=C2C3=CC=C4NC=CC4=C3)CNC
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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
純度とドキュメンテーション
参考文献
[1]. Su M, et al., Anti-ulcerogenic effect of KFP-H008 against ethanol-induced gastric ulcer via p38 MAPK/NF-κB pathway. RSC Adv. 2019 Jun 4;9(31):17591. [Content Brief]
[2]. Lu B, et al., Fertility and early embryonic development toxicity and toxicokinetic study of KFP-H008 in Sprague-Dawley rats. Birth Defects Res. 2022 May;114(8):304-313. [Content Brief]
[3]. Li CY, et al., KFP-H008 blocks gastric acid secretion through inhibiting H+-K+-ATPase. Eur J Pharmacol. 2017 Sep 5;810:112-119. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)