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product name Ranitidine


Description: Ranitidine HCl (also known as AH19065) is a histamine H2-receptor antagonist with IC50 of 3.3 ± 1.4 uM. It is used to treat stomach or intestinal ulcers by inhibiting stomach acid production. Ranitidine HCl sensitizes hepatocytes to killing by cytotoxic products from activated neutrophils, whereas Famotidine lacks this ability. Ranitidine inhibits the production of tumor necrosis factor-alpha (TNF-alpha) in monocytes stimulated with lipopolysaccharide in vitro.

References: J Pharmacol Exp Ther. 2003 Oct;307(1):9-16; J Pharmacol Exp Ther. 2002 Jun;301(3):1157-65.



Molecular Weight (MW)

350.86
Formula

C13H22N4O3S.HCl
CAS No.

66357-59-3
Storage

-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)

DMSO: 70 mg/mL (199.5 mM)
Water: 70 mg/mL (199.5 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)

 
Synonyms

AH19065

other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19426940

In Vitro

In vitro activity: Ranitidine sensitizes hepatocytes to killing by cytotoxic products from activated neutrophils, whereas Famotidine lacks this ability. Ranitidine inhibits the production of tumor necrosis factor-alpha (TNF-alpha) in monocytes stimulated with lipopolysaccharide in vitro. Ranitidine reduces the Kel of morphine dose-dependently with a maximum effect of 50%, and increases the relative concentration of morphine-6-glucuronide to morphine-3-glucuronide in isolated guinea pig hepatocytes. Ranitidine gradually decreases the morphine-3-glucuronide/morphine-6-glucuronide ratio by up to 21%.


Kinase Assay


Cell Assay

In Vivo Ranitidine results in liver injury as evidence by increased in serum alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase activities within 6 hours after Ranitidine administration in rats. Ranitidine inhibits hepatic ischemia/reperfusion-induced increase in hepatic tissue levels of TNF-alpha, cytokine-induced neutrophil chemoattractant, and hepatic accumulation of neutrophils in rats. Ranitidine cotreatment enhances LPS-induced coagulation prior to liver injury, and anticoagulants reduce liver damage in LPS/RAN-treated rats. Ranitidine /LPS-treated rats results in the formation of fibrin clots in liver sinusoids, and prevention of fibrin deposition associated with reduced hepatocellular injury. Ranitidine cotreatment enhances the LPS-induced TNF increase before the onset of hepatocellular injury in rats. Ranitidine displays anxiolytic effects in the elevated plus-maze as indicated by an increase in time spent in the open arms, more open-arm scanning and more end-excursions in rats.
Animal model  
Formulation & Dosage  
References J Pharmacol Exp Ther. 2003 Oct;307(1):9-16; J Pharmacol Exp Ther. 2002 Jun;301(3):1157-65.

PTC125

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Author: Sodium channel