Disease relevance of ROXATIDINE

• The present data suggests that a single bedtime dose of roxatidine acetate 150 mg produces effective duodenal ulcer healing and pain relief equivalent to that produced by a twice daily dosage regimen [1].
• Roxatidine acetate in the long term maintenance of gastric ulcers [2].
• Clinical studies on the use of roxatidine acetate for the treatment of peptic ulcer in Japan [3].
• A pharmacokinetic study of roxatidine acetate in chronic renal failure [4].
• One patient on roxatidine acetate withdrew from treatment because of a mild skin rash [5].

High impact information on ROXATIDINE

• Roxatidine acetate is an H2-receptor antagonist which has been well tolerated in clinical trials [6].
• Roxatidine acetate. A review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic potential in peptic ulcer disease and related disorders [6].
• A comparison of roxatidine acetate and ranitidine in duodenal ulcer healing [5].
• A comparison of roxatidine acetate and ranitidine in gastric ulcer healing [7].
• Pharmacokinetics of roxatidine in healthy volunteers [8].

Chemical compound and disease context of ROXATIDINE

• Quality of peptic ulcer healing induced by lansoprazole and roxatidine [9].
• We conclude that Roxatidine acetate is comparable to cimetidine in relieving pain and endoscopic healing of duodenal ulcer and has an excellent safety profile [10].
• It is concluded that roxatidine was more effective than famotidine for gastric juice suppression in patients with peptic ulcer [11].
• Erythrodermic drug eruption due to roxatidine acetate hydrochloride [12].
• Healing-promoting actions of KU-1257 (N-ethyl-N'-[3-[3-(piperidinomethyl)phenoxy]propyl]urea, CAS 120958-90-9) were investigated in chronic gastric and duodenal ulcer models induced by acetic acid in rats and the effects were compared with those of famotidine and roxatidine acetate by gross or histological evaluation [13].

Biological context of ROXATIDINE

• Furthermore, there was no interference in the bioavailability of roxatidine acetate 150 mg daily when administered alone or in combination with a meal or antacids [14].
• Extensive general pharmacological studies with roxatidine acetate demonstrate the lack of effects on the central nervous system, on gastrointestinal motility, the autonomic nervous system and the cardiovascular and urogenital systems [15].
• On the other hand, cell proliferation was dose-dependently and significantly enhanced by incubation with roxatidine and ranitidine [16].
• The apparent volume of distribution at steady-state was 1.70 l/kg, and the plasma protein binding of TZU-0460 or its active metabolite, desacetyl TZU-0460 was less than 10% in normal subjects [17].
• Cell proliferation was assessed by means of [3H] thymidine uptake and cell counts after incubation with roxatidine or ranitidine [16].

Anatomical context of ROXATIDINE

• Effect of roxatidine acetate on daytime and night-time peptone-stimulated gastric acid secretion [18].
• Thus, in rats roxatidine acetate inhibits gastric acid secretion with similar values following intraduodenal or intraperitoneal injection, indicating excellent absorption of the drug from the gastrointestinal tract [15].
• Roxatidine acetate is a histamine H2-receptor antagonist which, after almost complete oral absorption (greater than 95%), is rapidly converted to its active metabolite, roxatidine, by esterases in the small intestine, plasma and liver [6].
• 4. Specific [125I]-APT binding to the histamine H2 receptor of guinea pig brain membranes was inhibited by roxatidine and all structural analogues used in this study, except F (N-(3-[m-(N, N-dimethyl-aminomethyl)phenoxy]-propyl)acetamide) [19].
• The treatment group received 75 mg of roxatidine acetate hydrochloride at 9 PM and 12 to 13 hours later gastric juice secretion was measured with gastric x-ray films in both groups [20].

Associations of ROXATIDINE with other chemical compounds

• In conclusion, roxatidine acetate and its major metabolite roxatidine behave like competitive antagonists with potencies similar to ranitidine on H2-receptors on the guinea-pig parietal cell [21].
• In addition, roxatidine acetate produced reductions in nocturnal hydrochloric acid output of 75 to 92% with an associated rise in intragastric pH of around 2 units compared to placebo [18].
• Sixteen female, inbred Sprague-Dawley rats acted as lymphocyte donors and were treated for 8 days with either a roxatidine-levamisole combination, or levamisole alone, or roxatidine alone or placebo [22].
• [3H]Glucosamine incorporation was stimulated in the corpus region by the histamine H2 receptor antagonists which have a six-membered aromatic ring, roxatidine and FRG-8813, and the new H+,K(+)-ATPase inhibitor, NC-1300-O-3 [23].
• To evaluate in vitro inhibitory effects of four types of histamine H2-receptor antagonist (H2-receptor antagonists), famotidine, roxatidine, cimetidine and ranitidine, on platelet function, we examined aggregating potency and P-selectin levels with agonist-induced aggregation [24].

Gene context of ROXATIDINE

• However, incubation with roxatidine or ranitidine did not increase the steady-state mRNA expression of TGF-alpha or EGFR as assessed by northern blot analysis [16].
• In conclusion, both roxatidine and cimetidine were found to exert suppressive effects on the growth of colon cancer implants in mice by inhibiting angiogenesis via reducing VEGF expression [25].
• The pharmacodynamics and pharmacokinetics of multiple doses of the new H2-receptor antagonist, roxatidine acetate, in healthy men [26].
• Roxatidine-induced activation of mucin biosynthesis in the corpus tissue is mediated by nitric oxide [19].
• 1. Roxatidine acetate, a new histamine H2-receptor antagonist, was administered in the evening (75 mg p.o.) to eight patients with renal insufficiency (CLCR 8-17 ml min-1) for 12 days and plasma drug concentrations were measured [27].

Analytical, diagnostic and therapeutic context of ROXATIDINE

• Roxatidine acetate is almost completely (greater than 95%) absorbed after oral administration and is rapidly converted to roxatidine, its major active plasma and urinary metabolite [8].
• A non-comparative multicentre study of 105 patients with healed duodenal ulcers was conducted to determine the effect on ulcer recurrence of 6 months' maintenance treatment with roxatidine acetate 75 mg daily [28].
• A single bedtime oral premedication with roxatidine acetate 150 mg ensures a gastric pH above 2.5 until 11 am the following day [29].
• Serum and urine samples were analysed with capillary gas chromatography to measure the salt of the desacetyl metabolite of roxatidine acetate (roxatidine) [4].
• A randomised multicentre, double-blind study of the efficacy and safety of roxatidine acetate 150 mg at bedtime or 75 mg twice a day was conducted in 300 outpatients with endoscopically confirmed duodenal ulcers [1].

References