Roxatidine
(Synonyms: 罗沙替丁) 目录号 : GC49565A histamine H2 receptor antagonist and major active metabolite of roxatidine acetate
Cas No.:78273-80-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Roxatidine is a histamine H2 receptor antagonist and major active metabolite of roxatidine acetate .1 Roxatidine reduces histamine-induced adenylate cyclase production in guinea pig parietal cells (IC50 = 0.8 µM). It inhibits histamine-induced hydrogen ion accumulation in the same cells (pA2 = 7.03). Roxatidine (200 mg/kg) reduces small intestinal lesion area in a rat model of gastric mucosal injury induced by indomethacin .2
1.Sewing, K.-F., Beil, W., and Hannemann, H.Comparative pharmacology of histamine H2-receptor antagonistsDrugs35(Suppl. 3)25-29(1988) 2.Umegaki, E., Yoda, Y., Tokioka, S., et al.Protective effect of roxatidine against indomethacin induced small intestinal mucosal injury in ratsJ. Gastroenterol. Hepatol.25(Suppl. 1)S35-S40(2010)
| Cas No. | 78273-80-0 | SDF | Download SDF |
| 别名 | 罗沙替丁 | ||
| Canonical SMILES | O=C(CO)NCCCOC1=CC=CC(CN2CCCCC2)=C1 | ||
| 分子式 | C17H26N2O3 | 分子量 | 306.4 |
| 溶解度 | DMSO: up to 25 mg/ml | 储存条件 | -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.2637 mL | 16.3185 mL | 32.6371 mL |
| 5 mM | 0.6527 mL | 3.2637 mL | 6.5274 mL |
| 10 mM | 0.3264 mL | 1.6319 mL | 3.2637 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Roxatidine acetate. A review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic potential in peptic ulcer disease and related disorders
Drugs 1991 Aug;42(2):240-60.PMID:1717223DOI:10.2165/00003495-199142020-00006.
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. Roxatidine is a potent inhibitor of basal and stimulated gastric acid secretion in animals and humans and, like most other H2-receptor antagonists, has no anti-androgenic effects and does not interfere with the hepatic metabolism of other drugs. Large-scale trials have shown that Roxatidine acetate 150mg per day is as effective as standard doses of cimetidine and ranitidine in the treatment of patients with duodenal or gastric ulcer, and that Roxatidine acetate 75mg in the evening is likely to become a 'standard' regimen for the prevention of peptic ulcer recurrence. Preliminary data also suggest that Roxatidine acetate may be useful in the treatment of reflux oesophagitis and stomal ulcer, and in the prevention of pulmonary acid aspiration. Roxatidine acetate is an H2-receptor antagonist which has been well tolerated in clinical trials. However, broader experience is required before definitive statements about tolerability relative to other H2-receptor antagonists can be made, and before the role of Roxatidine acetate in the treatment of reflux oesophagitis and stomal ulcer, and the prophylaxis of acid aspiration pneumonitis, can be clearly defined.
Clinical characteristics of Roxatidine acetate: a review
Scand J Gastroenterol Suppl 1988;146:121-34.PMID:2906456DOI:10.3109/00365528809099138.
Pharmacodynamic studies revealed that 150 mg of Roxatidine acetate were optimal in suppressing gastric acid secretion, and that a single bedtime dose of 150 mg was more effective than a dose of 75 mg twice daily in terms of inhibiting nocturnal acid secretion. When administered orally as a capsule containing a granule formulation, the drug displayed modified-release properties, which led to a sustained suppression of gastric acid secretion. Clinical trials revealed that Roxatidine acetate, 75 mg twice daily and 150 mg at night, was highly effective in healing duodenal and gastric ulcers and in reducing ulcer pain, over 4, 6, and 8 weeks of therapy. A steady reduction in diameter was observed in those ulcers not completely healed during therapy. The single bedtime dose regimen, while producing the same degree of healing as the divided daily dose during controlled clinical trials, may be of greater value in therapeutic use owing to improved patient compliance. In all efficacy criteria (cure, reduction in ulcer size, and pain relief) there was no significant difference between Roxatidine acetate in a total daily dose of 150 mg, ranitidine in a total daily dose of 300 mg, and cimetidine in a total daily dose of 800 mg. Prevention of gastric and duodenal ulcer relapse was achieved by Roxatidine acetate, 75 mg at night for 6 months, in about 70% of patients, as determined in open, pilot studies--a rate comparable to those reported for cimetidine and ranitidine. Roxatidine acetate shares with ranitidine an improved safety profile when compared with cimetidine. Human pharmacology studies and short-term and long-term clinical trials have all shown that Roxatidine acetate is an exceptionally well tolerated compound, without the antiandrogenic activity and interference with hepatic drug metabolism which have characterized cimetidine treatment. A reason for the improved safety profile of Roxatidine acetate may be its greater potency than cimetidine (six times less potent) and ranitidine (half as potent), so that lower doses of Roxatidine acetate, representing a lower chemical load, are therapeutically effective. The novel structure of Roxatidine acetate probably also underlies the improved safety of the compound.
A review of the animal pharmacology of Roxatidine acetate
Drugs 1988;35 Suppl 3:30-40.PMID:2905247DOI:10.2165/00003495-198800353-00008.
Roxatidine acetate (TZU 0460/HOE 760) [N-(3-[3-(1-piperidinylmethyl)-phenoxy]-propyl)acetoxyacetamide hydrochloride] is a specific and competitive H2-receptor antagonist with a chemical structure different from those of cimetidine, ranitidine and famotidine. Roxatidine acetate and its main metabolite Roxatidine inhibit histamine-induced gastric acid secretion in vitro with a potency greater than that of cimetidine, and in the range of that produced by ranitidine. Gastric acid secretion following stimulation with dibutyryl cyclic adenosine monophosphate remains unaffected by Roxatidine acetate. In vivo experiments in rats and dogs confirm these in vitro findings. 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. In all studies it was shown that Roxatidine acetate was more potent than cimetidine. In rats single or repeated dosing with Roxatidine acetate did not influence drug metabolising enzymes in the liver nor did the drug show antiandrogenic activity in long term animal studies. 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. Studies on the pharmacokinetics and metabolism of Roxatidine acetate demonstrate that there is a presystemic deacetylation producing the main metabolite Roxatidine, which is responsible for the in vivo effects of the drug.
Roxatidine Attenuates Degradation of Extracellular Matrix
Biomed Pharmacother 2017 Nov;95:1156-1160.PMID:28926925DOI:10.1016/j.biopha.2017.08.130.
Degradation of extracellular matrix such as type II collagen and aggrecan induced by proinflammatory cytokines has been considered as an important hallmark of Osteoarthritis (OA). Roxatidine is a licensed specific competitive H (2) -receptor antagonist used for the treatment of gastric and duodenal ulcers. The pharmacological function of Roxatidine on Osteoarthritis (OA) remains unknown. In the current study, we report that Roxatidine attenuated TNF-α- induced degradation of type II collagen by suppressing the expression of MMP-3 and MMP-13 in human chondrosarcoma cell line SW1353 cells. In addition, Roxatidine ameliorated TNF-α- induced reduction of aggrecan by inhibiting the expression of ADAMTS-4 and ADAMTS-5. Notably, results indicate that Roxatidine ameliorated TNF-α- induced the phosphorylations of IKK, IκBα, and NF-κB p65 as well as nuclear translocation of NF-κB p65 and the transcriptional activity of NF-κB, suggesting that Roxatidine abolished the activation of NF-κB signaling pathway. Our findings implicate that Roxatidine might be considered as an anti-osteoarthritic agent.
Pharmacokinetic characteristics of Roxatidine
J Clin Gastroenterol 1989;11 Suppl 1:S6-19.PMID:2572622doi
This article reviews the published and unpublished results of pharmacokinetic studies with Roxatidine acetate in healthy volunteers of different ethnic origins, patients with various degrees of renal impairment, patients on maintenance hemodialysis, lactating women, and elderly patients. In addition, it reports on the findings of interaction studies with food and other drugs. The pharmacokinetic characteristics of Roxatidine were found to be nearly identical for different doses, formulations, and ethnic groups. The decrease in relative total clearance (oral clearance) in patients with renal impairment and in the elderly can be explained almost completely by their level of renal function. As expected from the pharmacokinetic characteristics in healthy volunteers, only a small amount of Roxatidine is removed by hemodialysis. Dose reduction is recommended in patients with renal impairment, but dose supplementation after hemodialysis is not necessary. Only a negligible fraction of the dose administered is excreted with breast milk. No pharmacokinetic interactions were found with theophylline, warfarin, propranolol, diazepam, and desmethyldiazepam, antipyrine or antacids. Food did not interfere with the absorption or disposition of Roxatidine.