Esomeprazole
(Synonyms: 埃索美拉唑镁,(S)-Omeprazole; (-)-Omeprazole) 目录号 : GC48984
An H+/K+-ATPase inhibitor
Cas No.:119141-88-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Esomeprazole is an inhibitor of the gastric H+/K+-ATPase and the (S) enantiomer of omeprazole .1 It reversibly inhibits the activity of the H+/K+-ATPase in an enzyme assay. Esomeprazole (30 mg/kg, s.c.) inhibits histamine-induced gastric acid secretion in rats. Formulations containing esomeprazole in complex with magnesium have been used as proton pump inhibitors (PPIs) in the treatment of gastroesophageal reflux disease (GERD), H. pylori eradication, and hypersecretory conditions, as well as in the prevention of non-steroidal anti-inflammatory drug-related gastric ulcer.
1.Shin, J.M., and Sachs, G.Restoration of acid secretion following treatment with proton pump inhibitorsGastroenterology123(5)1588-1597(2002)
| Cas No. | 119141-88-7 | SDF | |
| 别名 | 埃索美拉唑镁,(S)-Omeprazole; (-)-Omeprazole | ||
| Canonical SMILES | COC1=CC=C2C(N=C([S@](CC3=C(C)C(OC)=C(C)C=N3)=O)N2)=C1 | ||
| 分子式 | C17H19N3O3S | 分子量 | 345.4 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 20 mg/ml,Ethanol: 10 mg/ml,PBS (pH 7.2): 10 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 | 2.8952 mL | 14.476 mL | 28.9519 mL |
| 5 mM | 0.579 mL | 2.8952 mL | 5.7904 mL |
| 10 mM | 0.2895 mL | 1.4476 mL | 2.8952 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
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。
Comparative effectiveness and tolerability of Esomeprazole and omeprazole in gastro-esophageal reflux disease: A systematic review and meta-analysis
Int J Clin Pharmacol Ther 2015 Oct;53(10):803-10.PMID:26329348DOI:10.5414/CP202396.
This study aims to evaluate the effectiveness and tolerability of Esomeprazole and omeprazole in patients with gastroesophageal reflux disease (GERD). Electronic searches on PubMed, EMBASE, the Cochrane Library, and ClinicalTrials.gov databases were carried out for reports up to February 28, 2015. Ten eligible studies from 8 articles were found that enrolled a total of 10,286 patients for meta-analysis. These results revealed a significant difference between Esomeprazole vs. omeprazole (RR=1.06, 95% CI [1.01, 1.10], I2=72%, p=0.01) by subgroup according to dosage by random effects model, and a significant difference between Esomeprazole 40 mg vs. omeprazole 20 mg (RR=1.07, 95% CI [1.004, 1.14], I2=78%, p=0.04) based on healing rate as determined by endoscopy, using a random effects model. A significant difference between Esomeprazole 20 mg and omeprazole 40 mg (RR=0.68, 95% CI [0.47, 0.97], I2=not applicable, p=0.03) was also found in comparing relief of symptoms by random effects model. There were no significant differences in outcomes between other subgroups, including tolerability. Based on these results, a high dose of Esomeprazole is recommended for GERD treatment and control in adults.
Esomeprazole inhibits hypoxia/endothelial dysfunction-induced autophagy in preeclampsia
Cell Tissue Res 2022 Apr;388(1):181-194.PMID:35091806DOI:10.1007/s00441-022-03587-z.
Preeclampsia (PE) affects 3 to 5% of pregnant women worldwide and is associated with fetal and maternal morbidity and mortality. Although a complete understanding of PE remains elusive, it has been widely accepted that a dysfunction of the placenta plays a key role in the pathogenesis of PE. In this study, we investigated the role of excessive placental autophagy during PE pathogenesis and explored whether Esomeprazole ameliorates PE by inhibiting the autophagy in the placenta. The PE cellular model was established by treating the cells' L-NAME and hypoxia. The PE mice model was established by L-NAME administration and was confirmed by the increased systolic blood pressure (SBP) and urinary protein detected. The autophagy and key proteins were detected in human placental tissue, in cells, and in the mice model by Western blot and immunofluorescence staining. Results showed that excessive autophagy could be detected in human PE placental tissue, in the PE cellular model, and in the PE mice model. Hypoxia induces autophagy by activating AMPKα and inhibiting mTOR in vivo and in vitro. Esomeprazole inhibits L-NAME-induced autophagy in mice by inhibiting AMPKα and activating mTOR. In conclusion, this study demonstrates that the excessive autophagy induced by the SIRT1/AMPKα-mTOR pathway plays a significant role in the pathogenesis of PE. However, Esomeprazole treatment inhibits AMPKα but activates mTOR, resulting in the inhibition of autophagy in the placenta and, therefore, mitigates PE symptoms.
Night-time gastric acid suppression by tegoprazan compared to vonoprazan or Esomeprazole
Br J Clin Pharmacol 2022 Jul;88(7):3288-3296.PMID:35146797DOI:10.1111/bcp.15268.
Aims: Nocturnal acid breakthrough has been considered an unmet need of proton-pump inhibitors. Tegoprazan, a novel potassium-competitive acid blocker, is expected to show improved properties for this unmet need. This study was aimed to compare night-time acid suppression by tegoprazan with that by vonoprazan or Esomeprazole, and to explore the effect of CYP2C19 phenotypes on acid-suppressive effects. Methods: A randomized, open-label, 3-period, 6-sequence crossover study was conducted. A single oral dose of tegoprazan 50 mg, vonoprazan 20 mg or Esomeprazole 40 mg was administered at night in each period. Continuous intragastric pH was monitored at baseline and after each dosing. Results: Sixteen healthy subjects (6 CYP2C19 extensive metabolizers, 5 intermediate metabolizers, 5 poor metabolizers) completed the study. After a single dose of tegoprazan, intragastric pH increased more rapidly to over 4 at approximately 1 hour compared to the other treatments, and elevated intragastric pH was maintained stably at night. Tegoprazan exhibited night-time acid suppression for slightly but not significantly longer than vonoprazan, and greater than Esomeprazole; % time at pH ≥ 4 at night was 66.0%, 60.5% and 36.1% for tegoprazan, vonoprazan and Esomeprazole, respectively. Night-time acid suppression by tegoprazan and vonoprazan was not dependent on CYP2C19 phenotypes, while that by Esomeprazole tended to be influenced by CYP2C19 phenotypes. Conclusion: Tegoprazan produced more rapid, potent and well sustained night-time acid suppression vs. vonoprazan or Esomeprazole when administered at night. Furthermore, tegoprazan showed no CYP2C19 phenotype dependency in acid suppression. It suggests the potential of tegoprazan, especially in preventing nocturnal acid breakthrough.
Esomeprazole and aspirin in Barrett's oesophagus (AspECT): a randomised factorial trial
Lancet 2018 Aug 4;392(10145):400-408.PMID:30057104DOI:10.1016/S0140-6736(18)31388-6.
Background: Oesophageal adenocarcinoma is the sixth most common cause of cancer death worldwide and Barrett's oesophagus is the biggest risk factor. We aimed to evaluate the efficacy of high-dose Esomeprazole proton-pump inhibitor (PPI) and aspirin for improving outcomes in patients with Barrett's oesophagus. Methods: The Aspirin and Esomeprazole Chemoprevention in Barrett's metaplasia Trial had a 2 × 2 factorial design and was done at 84 centres in the UK and one in Canada. Patients with Barrett's oesophagus of 1 cm or more were randomised 1:1:1:1 using a computer-generated schedule held in a central trials unit to receive high-dose (40 mg twice-daily) or low-dose (20 mg once-daily) PPI, with or without aspirin (300 mg per day in the UK, 325 mg per day in Canada) for at least 8 years, in an unblinded manner. Reporting pathologists were masked to treatment allocation. The primary composite endpoint was time to all-cause mortality, oesophageal adenocarcinoma, or high-grade dysplasia, which was analysed with accelerated failure time modelling adjusted for minimisation factors (age, Barrett's oesophagus length, intestinal metaplasia) in all patients in the intention-to-treat population. This trial is registered with EudraCT, number 2004-003836-77. Findings: Between March 10, 2005, and March 1, 2009, 2557 patients were recruited. 705 patients were assigned to low-dose PPI and no aspirin, 704 to high-dose PPI and no aspirin, 571 to low-dose PPI and aspirin, and 577 to high-dose PPI and aspirin. Median follow-up and treatment duration was 8·9 years (IQR 8·2-9·8), and we collected 20 095 follow-up years and 99·9% of planned data. 313 primary events occurred. High-dose PPI (139 events in 1270 patients) was superior to low-dose PPI (174 events in 1265 patients; time ratio [TR] 1·27, 95% CI 1·01-1·58, p=0·038). Aspirin (127 events in 1138 patients) was not significantly better than no aspirin (154 events in 1142 patients; TR 1·24, 0·98-1·57, p=0·068). If patients using non-steroidal anti-inflammatory drugs were censored at the time of first use, aspirin was significantly better than no aspirin (TR 1·29, 1·01-1·66, p=0·043; n=2236). Combining high-dose PPI with aspirin had the strongest effect compared with low-dose PPI without aspirin (TR 1·59, 1·14-2·23, p=0·0068). The numbers needed to treat were 34 for PPI and 43 for aspirin. Only 28 (1%) participants reported study-treatment-related serious adverse events. Interpretation: High-dose PPI and aspirin chemoprevention therapy, especially in combination, significantly and safely improved outcomes in patients with Barrett's oesophagus. Funding: Cancer Research UK, AstraZeneca, Wellcome Trust, and Health Technology Assessment.
Acid-inhibitory effects of vonoprazan 20 mg compared with Esomeprazole 20 mg or rabeprazole 10 mg in healthy adult male subjects--a randomised open-label cross-over study
Aliment Pharmacol Ther 2015 Sep;42(6):719-30.PMID:26193978DOI:10.1111/apt.13325.
Background: Proton pump inhibitors (PPIs) are widely used for the treatment of acid-related diseases. Vonoprazan is a member of a new class of acid suppressants; potassium-competitive acid blockers. Vonoprazan may thus be an alternative to PPIs. Aim: To evaluate efficacy, rapidity and duration of acid-inhibitory effects of vonoprazan vs. two control PPIs, Esomeprazole and rabeprazole, in 20 healthy Japanese adult male volunteers with CYP2C19 extensive metaboliser genotype. Methods: In this randomised, open-label, two-period cross-over study, vonoprazan 20 mg and Esomeprazole 20 mg (Study V vs. E) or rabeprazole 10 mg (Study V vs. R) were orally administered daily for 7 days. Primary pharmacodynamic endpoint was gastric pH over 24 h measured as percentage of time pH ≥3, ≥4 and ≥5 (pH holding time ratios; HTRs) and mean gastric pH. Results: Acid-inhibitory effect (pH4 HTR) of vonoprazan was significantly greater than that of Esomeprazole or rabeprazole on both Days 1 and 7; Day 7 difference in pH4 HTR for vonoprazan vs. Esomeprazole was 24.6% [95% confidence interval (CI): 16.2-33.1] and for vonoprazan vs. rabeprazole 28.8% [95% CI: 17.2-40.4]. The Day 1 to Day 7 ratio of 24-h pH4 HTRs was >0.8 for vonoprazan, compared with 0.370 for Esomeprazole and 0.393 for rabeprazole. Vonoprazan was generally well tolerated. One vonoprazan subject withdrew due to a rash which resolved after discontinuation. Conclusions: This study demonstrated a more rapid and sustained acid-inhibitory effect of vonoprazan 20 mg vs. Esomeprazole 20 mg or rabeprazole 10 mg. Therefore, vonoprazan may be a potentially new treatment for acid-related diseases.