Rabeprazole 10mg gastro-resistant tablets
Requires a prescription from a doctor or prescriber
Rabeprazole is an antiulcer drug in the class of proton pump inhibitors.
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Drug safety updates
MHRA alerts for Rabeprazole
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Rabeprazole
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Rabeprazole
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
24 branded products available
MHRA licensed products
View all licensed products for Rabeprazole on the MHRA register
Pariet 10mg gastro-resistant tablets
Pariet 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
Rabeprazole 10mg gastro-resistant tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
20 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 5 · Randomised trials: 19 · 2004–2026
Showing the 50 most relevant studies, sorted by most relevant.
A. McNicholl, P. M. Linares, O. Nyssen, et al.
Alimentary Pharmacology & Therapeutics, 2012
Al Hayek M, Lucendo AJ, Barberio B, et al.
2026
BackgroundErosive esophagitis (EE) is commonly managed with proton pump inhibitors (PPIs), yet many patients experience incomplete healing or recurrence. Potassium-competitive acid blockers (P-CABs) have emerged as potential alternatives, but high-certainty comparative evidence across agents remains limited. We performed a network meta-analysis to evaluate the relative efficacy and safety of P-CABs versus PPIs and to assess the certainty of the evidence.MethodsWe systematically searched PubMed, the Cochrane Library, and Web of Science from inception through March 1, 2025, for randomized controlled trials (RCTs) comparing P-CAB, PPI, and/or placebo for the treatment of EE. Risk of bias was assessed using the Cochrane Risk of Bias 2.0 tool. Key outcomes were 8-week endoscopic healing and 24-week recurrence. Certainty of evidence was evaluated using GRADE. Risk difference (RD) estimates were calculated using random-effects models. The study protocol was registered with PROSPERO (CRD420251116179).FindingsThirty-nine RCTs were included; all evaluated once-daily dosing. At 8 weeks, zastaprazan 20 mg, vonoprazan 20 mg, and esomeprazole 40 mg demonstrated moderate-certainty superiority over rabeprazole 20 mg and omeprazole 20 mg with RDs ranging from 0.05 to 0.11, while only vonoprazan 20 mg demonstrated moderate-certainty benefit versus lansoprazole 30 mg (RD: 0.04). In Los Angeles (LA) grade C/D EE, vonoprazan 20 mg, esomeprazole 40 mg, and rabeprazole-ER 50 mg demonstrated moderate-to-high-certainty benefit over lansoprazole 30 mg and omeprazole 20 mg with RDs ranging from 0.05 to 0.15. Vonoprazan 20 mg and rabeprazole-ER 50 mg demonstrated moderate-certainty benefit compared with pantoprazole 40 mg (RDs: 0.12 and 0.09, respectively).At 24 weeks, vonoprazan 10 mg and 20 mg showed moderate-to-high-certainty benefit versus lansoprazole 15 mg (RDs: -0.11 and -0.13, respectively), while in direct comparisons, esomeprazole 20 mg outperformed lansoprazole 15 mg and pantoprazole 20 mg, with approximately 40-50% relative reductions in recurrence. In LA grade C/D EE, vonoprazan 10 mg and 20 mg demonstrated moderate-to-high-certainty superiority over lansoprazole 15 mg and pantoprazole 20 mg with RDs ranging from -0.12 to -0.20. Esomeprazole 20 mg showed a high-certainty benefit compared with pantoprazole 20 mg (RD: -0.16). At 8 and 24 weeks, safety profiles were generally comparable between P-CABs and PPIs.InterpretationAmong once-daily regimens, vonoprazan 20 mg, zastaprazan 20 mg, and esomeprazole 40 mg were most effective for healing EE, while vonoprazan 10 mg and 20 mg and esomeprazole 20 mg were most effective in preventing recurrence. Benefits were most pronounced in LA grade C/D EE and are supported by moderate to high-certainty evidence. Comparative trials evaluating newer P-CABs against optimized PPI strategies, including twice-daily dosing, are needed to evaluate efficacy and long-term safety, particularly with respect to hypergastrinemia and infection risk.FundingNone was received for the study.
Abstract licence: CC BY-NC-ND
Mei-si Lin, Siyuan Zhang, Minyue Zhang, et al.
Medicine, 2020
T. Takeuchi, T. Furuta, Y. Fujiwara, et al.
Alimentary Pharmacology & Therapeutics, 2020
Xiulian Zhang, Zhongfu Wang, Tingting Xu, et al.
European Journal of Medical Research, 2024
Hsu PI, Chen CL, Shih CA, et al.
2025
Li M, Wang X, Dong X, et al.
2025
BackgroundIncreasing antibiotic resistance compromises therapeutic options for Helicobacter pylori (H. pylori) infection, especially in penicillin-allergic individuals.ObjectivesThis trial aimed to assess the efficacy and safety of 14-day vonoprazan-minocycline (VM) dual therapy against bismuth-containing quadruple therapy (B-quadruple therapy), as initial treatment for H. pylori infection.DesignThis study was a single-center, open-label, and non-inferiority randomized controlled trial.MethodsIn this study, 240 individuals with H. pylori infection who have not received therapy were randomly assigned 1:1 to either the VM dual therapy group (vonoprazan 20 mg plus minocycline 100 mg, administered twice daily) or the B-quadruple therapy group (rabeprazole 10 mg, amoxicillin 1000 mg, clarithromycin 500 mg, and bismuth potassium citrate 220 mg, all administered twice daily). The primary outcome was to evaluate the non-inferiority of eradication rates between the two groups. Secondary outcomes included assessments of AEs and compliance.ResultsThe eradication rates of VM dual group and B-quadruple therapy group were 87.5% and 88.3%, respectively, by intention-to-treat (ITT) analysis; 92.1% and 94.6% by modified ITT (mITT) analysis; and 92.0% and 95.5% by per-protocol (PP) analysis. The eradication rates of the VM group were non-inferior to those of the B-quadruple therapy group in ITT, mITT, and PP analyses (one-sided p-values were 0.02, 0.01, and 0.02). The incidence of AEs was higher in the B-quadruple therapy group (28.3%) than in the VM group (16.7%, p = 0.03). Good compliance was achieved in both groups (p = 0.60).ConclusionThe VM dual therapy was not inferior to the B-quadruple therapy in the initial treatment of H. pylori infection, and the incidence of AEs was lower compared to B-quadruple therapy.Trial registrationThis trial was registered on the Chinese Clinical Trial Registry with the registration number ChiCTR2400081461.
Abstract licence: CC BY-NC
Wei-Chen Tai, Shih-Cheng Yang, Chih-Chien Yao, et al.
Infectious Diseases and Therapy, 2023
Wang H, Fei C, Cao Y, et al.
2026
- Helicobacter pylori
- Helicobacter Infections
- Amoxicillin
BACKGROUND: Both traditional proton pump inhibitors and the novel potassium-competitive acid blocker vonoprazan, when combined with high-dose amoxicillin in dual therapy, have shown promise for Helicobacter pylori (H. pylori) eradication. However, high-quality evidence directly comparing their efficacy and safety remains limited. This study aimed to compare the clinical efficacy and safety of rabeprazole-amoxicillin dual therapy versus vonoprazan-amoxicillin dual therapy for H. pylori eradication. METHODS: From April 1, 2024, to February 28, 2025, 318 H. pylori-positive patients were enrolled and randomly assigned in a 1:1 ratio to two treatment groups: the Rabeprazole Group (rabeprazole 20 mg twice daily; amoxicillin 1000 mg three times daily) and the Vonoprazan Group (vonoprazan 20 mg twice daily; amoxicillin 1000 mg three times daily). Both groups received a 14-day treatment course. A 13C-urea breath test was performed at least four weeks after treatment completion. H. pylori eradication rates, incidence of adverse events during treatment, and medication adherence were compared between the groups. RESULTS: In the intention-to-treat analysis, the eradication rates were 75.5% (95% CI: 68.8%-82.2%) in the Rabeprazole Group and 83.0% (95% CI: 77.2%-88.9%) in the Vonoprazan Group, with no statistically significant difference (P = 0.097). In the modified intention-to-treat analysis, the rates were 78.4% (95% CI: 71.9%-84.9%) and 88.6% (95% CI: 83.5%-93.7%), respectively, showing a significant difference (P = 0.018). In the per-protocol analysis, the rates were 79.7% (95% CI: 73.1%-86.3%) and 90.1% (95% CI: 85.1%-95.0%), respectively, also showing a significant difference (P = 0.015). The incidence of adverse events was low in both groups (10.5% vs. 12.8%, P = 0.533). Medication adherence did not differ significantly between the groups (P = 0.648). Manual labor occupation was identified as a risk factor for eradication failure (adjusted OR = 2.153, 95% CI: 1.067 to 4.346, P = 0.032). CONCLUSION: Vonoprazan-amoxicillin dual therapy achieves satisfactory outcomes for H. pylori eradication, with a significantly higher eradication rate than the traditional rabeprazole-amoxicillin dual regimen. As a novel acid suppressant, vonoprazan demonstrates significant clinical advantages and broad application potential in dual-therapy regimens for H. pylori eradication. CLINICAL TRIAL REGISTRATION: https://www.medicalresearch.org.cn/ , identifier ChiCTR2400082319. Registered on March 5, 2024.
Abstract licence: CC BY-NC-ND
Elias M, Yazbeck C, Zaarour A, et al.
2025
- Helicobacter pylori
- Helicobacter Infections
- Anti-Bacterial Agents
BackgroundThe aim of this study is to optimize Helicobacter pylori (H. pylori) eradication by increasing the proton pump inhibitor (PPI) dose and reducing the treatment duration of antibiotics without compromising the treatment's safety and efficacy.MethodsThis pilot randomized controlled trial included 120 patients from Notre Dame des Secours University Hospital in Byblos, Lebanon, between February 2023 and December 2023. Participants were Lebanese adults with H. pylori infection confirmed by upper gastrointestinal endoscopy. Exclusion criteria included pregnancy or nursing, malignancy or gastric mucosa-associated lymphoid tissue lymphoma, allergy or contraindications to study drugs, active upper gastrointestinal bleeding, prior gastric surgeries, recent use of PPIs or antibiotics, celiac disease, previous H. pylori treatment, or refusal to consent. Eligible patients (n = 113) were randomly assigned into three groups: Group A (n = 38) received a standard-dose of rabeprazole 20 mg twice daily for 14 days with concomitant therapy, Group B (n = 37) received a double-dose of rabeprazole (20 mg twice per day) for 10 days with concomitant therapy, and Group C (n = 38) received a high-dose of rabeprazole (20 mg three times per day) for 10 days with concomitant therapy. Eradication was assessed by urea breath test six weeks after treatment completion.ResultsOut of 120 participants, 101 patients were considered for analysis, while 19 patients were excluded (15.8%). Of these exclusions, 7 patients were excluded before randomization due to drug allergy and opted for alternative treatment (5.8%), while 12 were excluded after randomization due to loss to follow-up (12%). The results indicated that the high-dose PPI group C had the highest percentage of negative breath tests (100%), followed by the standard treatment group A with 94.7%, and then group B with 83.3%. However, given the pilot nature and sample size of this study, these results, particularly the 100% rate in Group C, should be interpreted as preliminary and require confirmation in a larger trial.ConclusionThe use of high-dose PPI with 10 days of concomitant therapy (Group C) demonstrated the highest eradication rate among the study groups. This promising finding suggests a potential benefit of the high-dose PPI regimen with 10-day concomitant therapy but must be interpreted with caution; it warrants further investigation in a larger and adequately powered randomized controlled trial to confirm its efficacy and generalizability, given the pilot nature of this study.Name of the registryLebanon clinical trial registry; TRAIL REGISTRATION NUMBER: LBCTR2025075755; DATE OF REGISTRATION IN PRIMARY REGISTRY: 14/08/2025.
Abstract licence: CC BY-NC-ND
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
1-2 hours
Mechanism
Rabeprazole belongs to a class of antisecretory compounds (substituted benzimida…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
52%
Half-life
1-2 hours
Protein binding
96.3%
Metabolism
Elimination
20 mg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1041 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). The release of the H(+) ion in the stomach lumen is followed by binding of K(+) ion converting the pump conformation back to the E1 state (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
ATC A02BD12
ATC A02BD13
ATC A02BC54
ATC A02BC04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Rabeprazole
Additional database identifiers
Drugs Product Database (DPD)
12149
ChemSpider
4853
BindingDB
50070209
HUGO Gene Nomenclature Committee (HGNC)
HGNC:819
GenAtlas
ATP4A
GeneCards
ATP4A
GenBank Gene Database
J05451
GenBank Protein Database
561634
Guide to Pharmacology
849
UniProt Accession
ATP4A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2595
GeneCards
CYP1A1
GenBank Gene Database
K03191
GenBank Protein Database
181276
Guide to Pharmacology
1318
UniProt Accession
CP1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72