≥98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

盐酸lei尼替丁

Off-white to yellow solid

DMSO ：70 mg/mL (199.51 mM)
Water ：70 mg/mL (199.51 mM）

Histamine H2 receptor

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%.

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.