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.
For research use only. We do not sell to patients.
- CAS No.: 1876453-55-2
- Formula: C19H18N4O2S
- Molecular Weight:366.44
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
-
CAS No. 1876453-55-2
-
Molecular Weight 366.44
-
Formula C19H18N4O2S
-
SMILES
O=S(=O)(C=1C=NC=CC1)N2C=C(C=C2C3=CC=C4NC=CC4=C3)CNC
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
-
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
Purity & Documentation
References
[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
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)