Disease relevance of lafutidine

• Preoperative oral lafutidine may be an alternative to ranitidine as a prophylaxis against aspiration pneumonia [1].
• The mucosal regeneration index of the gastric ulcer after 10 days' administration of FRG-8813 was significantly higher than that obtained with famotidine [2].
• CONCLUSIONS: Lafutidine 10 mg produces a prompter rise in intragastric pH than rabeprazole 20 mg in fasting and postprandial Helicobacter pylori-negative male subjects [3].
• Daily administration of lafutidine dose-dependently reduced the severity of DSS-induced colitis and significantly mitigated changes in the colon length and MPO activity [4].
• Considering the low recurrence rate of ulcers after FRG-8813 treatment, we suggest that FRG-8813 treatment may provide additional benefits in peptic ulcer therapy [2].

High impact information on lafutidine

• Effect of omeprazole 10 mg on intragastric pH in three different CYP2C19 genotypes, compared with omeprazole 20 mg and lafutidine 20 mg, a new H2-receptor antagonist [5].
• After a 7-day regimen of omeprazole 10 mg, 20 mg, lafutidine 20 mg (a novel H2-receptor antagonist) or water only (baseline data), intragastric pH was measured for 24 h [5].
• With lafutidine 20 mg, these parameters were not influenced by the genotype [5].
• Sensitizing effects of lafutidine on CGRP-containing afferent nerves in the rat stomach [6].
• The validated LC/ESI-MS method has been successfully applied to the bioequivalence study of lafutidine in 24 healthy male Chinese volunteers [7].

Chemical compound and disease context of lafutidine

• In this study we examined the effect of lafutidine on dextran sulfate Na (DSS)-induced ulcerative colitis in rats, in relation to capsaicin-sensitive afferent neurons [4].
• Lafutidine synergistically increased CGRP release from isolated rat dorsal root ganglion neurons in the presence of anandamide, but famotidine did not [8].
• We examined the effect of lafutidine, a novel histamine H(2)-receptor antagonist, on acid reflux esophagitis in rats in relation to capsaicin-sensitive afferent neurons [9].

Biological context of lafutidine

• The amounts released correlated with the AUC of lafutidine in humans [10].
• The proposed method enables the unambiguous identification and quantification of lafutidine for pharmacokinetic, bioavailability or bioequivalence studies [11].

Anatomical context of lafutidine

• Stimulation of mucin biosynthesis in rat gastric mucosa by FRG-8813 and its structural analogs [12].
• This study was designed to examine whether lafutidine, which is an H(2)-receptor antagonist and activates sensory neurons, inhibits neutrophil activation, thereby reducing WIR-induced gastric mucosal injury [8].
• In many cases of rats healed by FRG-8813, the regenerated mucosa was normal in contrast with the control of famotidine-healed animals [2].
• Topical application of NH2Cl (10 mmol/L) reduced transmucosal PD in ex-vivo stomachs of anaesthetized rats, but this PD response was also prevented by pre-exposure to lafutidine, in a dose-dependent and sensory neuron-sensitive manner [13].
• Lafutidine inhibits Helicobacter pylori-induced interleukin-8 production in human gastric epithelial cells [14].

Associations of lafutidine with other chemical compounds

• The chronotropic response to histamine in the guinea pig right atria was suppressed by FRG-8813 in a concentration-dependent fashion [12].
• METHODS: 122 outpatients with positive cultures and subsequent successful cultivation of H. pylori for antimicrobial susceptibility tests were randomized to receive a 7-day course of either lafutidine (20 mg twice daily) or lansoprazole (30 mg twice daily), plus clarithromycin (200 mg twice daily) and amoxicillin (750 mg twice daily) [15].
• It was also found that both lafutidine and capsaicin increased the secretion of mucus in the colonic mucosa [4].
• Although the acid-induced GMBF and DAS responses were significantly mitigated by both indomethacin and sensory deafferentation but not by ruthenium red (RT), the vanilloid receptor (VR)-1 antagonist, the responses were preserved in lafutidine-treated animals, even in the presence of indomethacin [16].
• We studied the inhibition of gastric acid secretion by lafutidine and rabeprazole, given in single doses to fasting and postprandial subjects [3].

Gene context of lafutidine

• Lafutidine significantly increased plasma CGRP levels at 1, 1.5, 2.5 and 4 h and the total amount of CGRP release (192 +/- 14.0 pg.h/mL) compared with the control group (128 +/- 21.5 pg.h/mL) [10].
• In the present study, we examined the effects of lafutidine on H. pylori-induced IL-8 release and H. pylori adhesion to MKN45 cells [14].
• Lafutidine also significantly inhibited H. pylori-induced IL-6 release [14].
• Both TNF-alpha and IL-1beta-induced IL-8 releases, conversely, were little affected by lafutidine up to a concentration of 10(-5) M [14].
• We compared the effect between lafutidine and capsaicin, with respect to the interaction with endogenous prostaglandins (PG), nitric oxide (NO) and the afferent neurons, including transient receptor potential vanilloid subtype 1 (TRPV1) [17].

Analytical, diagnostic and therapeutic context of lafutidine

• Certain chemical properties, which may determine the stimulatory actions of the new histamine H2 receptor antagonist, FRG-8813 (2-(furfurylsulfinyl)-N-(4-[4-(piperidinomethyl)-2-pyridyl]o xy-(Z)- 2-butenyl)acetamide), on mucin biosynthesis, were identified by considering the derivation of this drug using an organ culture system of the rat stomach [12].
• We investigated the recurrence of ulcers in rats after treatment with FRG-8813, (+/-)-2-(furfurylsulfinyl)-N-[4- [4-(piperidinomethyl)-2-pyridyl] oxy-(Z)-2-butenyl] acetamide, a novel histamine H(2)-receptor antagonist [2].
• It is unlikely that FRG-8813 works as a mild irritant because it showed a gastroprotective effect after intraperitoneal injection, but oral administration itself did not influence the rat gastric mucosa [18].
• Plasma lafutidine concentrations were determined by high pressure liquid chromatography [10].
• After the induction of gastric ulcer, lafutidine given twice daily for 2.5 days reduced the area of ulcer in a dose-dependent manner with a significant effect at 10 mg/kg, p.o., as compared with that of the control group [19].

References