Esomeprazole 10mg gastro-resistant granules sachets
Requires a prescription from a doctor or prescriber
Genetic variations that may affect drug response
2 known genetic variations may influence how your body responds to Esomeprazole 10mg gastro-resistant granules sachets.Gene involved: CYP2C19
These are known genetic variations. They don't mean the medicine won't work for you — speak to your doctor or a pharmacogenomics specialist for personalised advice. Source: DrugBank (CC BY-NC 4.0).
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Yellow Card reports
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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.
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Suspected adverse reactions reported for Esomeprazole
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7 branded products available
MHRA licensed products
View all licensed products for Esomeprazole on the MHRA register
Nexium 10mg gastro-resistant granules sachets
Nexium 10mg gastro-resistant granules sachets
Esomeprazole 10mg gastro-resistant granules sachets
Esomeprazole 10mg gastro-resistant granules sachets
Esomeprazole 10mg gastro-resistant granules sachets
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)
30 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.
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Codes for healthcare professionals and prescribing systems
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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: 9 · Randomised trials: 36 · 2010–2026
Showing the 50 most relevant studies, sorted by most relevant.
J. Jankowski, J. de Caestecker, S. Love, et al.
Lancet (London, England), 2018
Kwang-Jae Lee, B. Son, G. Kim, et al.
Alimentary Pharmacology & Therapeutics, 2019
Shibli F, Mari A, Fass R
2025
Background and objectiveErosive esophagitis (EE) is the second most common phenotype of gastroesophageal reflux disease (GERD). While proton pump inhibitors (PPIs) are considered the mainstay treatment for healing and maintaining remission of EE, a significant proportion of patients, particularly those with advanced grades, fail to respond adequately. This review provides an updated overview of the current pharmacological treatment options for EE.MethodsAn extensive electronic literature search was performed using PubMed database to identify relevant articles. The search included prospective clinical trials, observational trials, case-control studies, systematic reviews with or without meta-analysis, and narrative reviews describing pharmacological therapy for adult patients with EE. Articles were limited to English language publications. Search terms encompassed various treatment modalities including PPIs, potassium-competitive acid blockers (P-CABs), histamine 2 receptor antagonists (H2RAs), sucralfate, prokinetics, rebamipide and alginates.Key content and findingsResearch has shown varying effectiveness across different treatments for EE. While randomized controlled trials found alginates, sucralfate, and histamine-2 receptor antagonists to have limited healing efficacy, PPIs remain the most effective treatment, achieving healing rates of 75-95% after 8 weeks, though symptom resolution reaches about 60-85%. Among PPIs, esomeprazole shows slightly better healing outcomes compared to others. However, PPI effectiveness decreases in advanced EE cases [Los Angeles (LA) grades C/D], with healing rates dropping to 60-70%. More recently, P-CABs have demonstrated promising results, demonstrating healing rates non-inferior to PPIS but superior in patients with advanced EE or PPI-resistent EE. Given that most patients experience relapse upon discontinuation, maintaining PPI or PCAB therapy is crucial for preventing EE recurrence.ConclusionsThe future of EE management lies in a more personalized approach that takes into account disease severity, PPI response, and patient preferences. While PPIs remain the mainstay of treatment, P-CABs represent a promising new therapeutic option, particularly for severe and PPI-resistant cases. The addition of nighttime to bedtime H2RAs or use of double PPI dose may benefit refractory cases. Further studies are needed to directly compare PPIs and P-CABs in different EE grades and evaluate the value of adjunctive therapies.
Abstract licence: CC BY-NC-ND
Omar Abureesh, Ali Sohail, Yousef Yousef, et al.
Frontiers in Medicine, 2026
Simadibrata DM, Koo TH, Jiménez-Castillo RA, et al.
2026
Randomized controlled trials (RCTs) suggest that potassium-competitive acid blockers (PCABs) are non-inferior to standard-dose proton pump inhibitors (PPIs) for erosive esophagitis (EE). However, direct comparative data against double-dose or dual-delayed release PPIs remain limited. This network meta-analysis (NMA) ranks the efficacy of PCABs and PPIs (standard, double, and dual-delayed-release doses) for EE healing and maintenance. A systematic search of MEDLINE, EMBASE, and the Cochrane Library from inception through February 2, 2025 (updated on December 15, 2025) identified RCTs comparing PCABs or PPIs in adults with endoscopically confirmed EE or previously healed EE. Primary outcomes were EE healing at weeks 4 and 8, and maintenance at 6 months. A frequentist NMA estimated risk ratios (RRs) with 95% confidence intervals (95%CI), using vonoprazan 20 mg once daily (QD) and 10 mg QD as reference for healing and maintenance studies, respectively; ranking metrics (P-scores) were used descriptively. A total of 99 RCTs were included. At week 4, several regimens showed similar healing rate to vonoprazan 20 mg QD, including linaprazan 75 mg BID, linaprazan 50 mg BID, and zastaprazan 20 mg QD. At week 8, zastaprazan 20 mg QD was significantly better than vonoprazan 20 mg QD (RR 1.10; 95%CI 1.01-1.21; P-score = 0.92). For maintenance at 6 months, several standard-dose regimens (including esomeprazole 40 mg QD and vonoprazan 20 mg QD) showed similar efficacy, whereas lower-dose PPIs performed worse. Adverse events were comparable across therapies. Zastaprazan 20 mg QD and esomeprazole 40 mg QD demonstrated the highest efficacy for EE healing and maintenance, respectively. Overall, PCABs did not consistently outperform dual-delayed release or double-dose PPIs.
Abstract licence: CC BY
Bandyopadhyay S, Goenka M, Routh D, et al.
2026
Gastroesophageal reflux disease (GERD) is a chronic relapsing disorder often inadequately controlled with proton pump inhibitors (PPIs), particularly in patients with nocturnal acid breakthrough (NAB) or non-erosive reflux disease (NERD). Tegoprazan, a potassium-competitive acid blocker (PCAB), offers rapid, potent, and CYP2C19-independent acid suppression. This systematic review and meta-analysis evaluated randomized controlled trials comparing Tegoprazan with PPIs in adults with GERD and related disorders. Databases searched included PubMed, Cochrane, Wiley, and ClinicalTrials.gov (2015-2026). Eighteen studies met inclusion criteria. In erosive esophagitis, Tegoprazan 50 mg once daily achieved mucosal healing rates of 91.1%-99.1%, non-inferior to PPIs (93.5%-98.9%; pooled RR = 1.01, 95% CI 0.98-1.05). Pharmacodynamic and clinical studies demonstrated faster acid suppression and improved nocturnal pH control versus PPIs, achieving pH ≥ 4 within 30-60 min and maintaining levels throughout the 12-h period. In nocturnal symptom analyses, Tegoprazan achieved earlier relief (1.5 vs. 3 days to first heartburn-free night) and higher proportions of heartburn-free nights (57.8% vs. 43.1%), with significantly greater complete (p = 0.038) and partial (p = 0.034) nighttime symptom resolution than Esomeprazole. In NERD, symptom resolution ranged from 42.5% to 48.9% versus 24.2% with placebo. In open-label functional dyspepsia cohorts, improvements ranged from 74.6% to 86.7% in open-label cohorts. Seven trials (n = 2492) showed higher Helicobacter pylori eradication with Tegoprazan-based therapy (RR = 1.05, 95% CI 1.01-1.09; p = 0.006; I 2 = 0%). Adverse events were mild and comparable to PPIs. Tegoprazan provides rapid, sustained acid suppression, effective nocturnal symptom control, and a modest but statistically significant improvement in H. pylori eradication, representing a potential alternative to PPIs for patients with persistent or CYP2C19-related variable response.
Abstract licence: CC BY-NC-ND
Khan I, Ansab M, Nadeem A, et al.
2026
W. Tai, Chih‐Ming Liang, C. Kuo, et al.
The Journal of antimicrobial chemotherapy, 2019
Barzola-Farfán WA, Quispe-Vicuña C, Rivera-Lozada O, et al.
2026
Background: This investigation compared the efficacy and safety of fexuprazan 40 mg and esomeprazole 40 mg in patients with acid reflux-related disorders, including erosive esophagitis (EE) and laryngopharyngeal reflux disease (LPRD). Methods: A systematic search was conducted across five databases until January 2025. Primary outcomes included esophageal lesion healing, complete resolution of symptoms (CRS), and 24 h symptom-free days. Meta-analyses used random-effects models with the inverse variance method. The Risk of Bias 2.0 tool and the certainty of evidence (CoE) using GRADE methodology were assessed. Results: Three randomized controlled trials (n = 695) conducted in Asian countries were included. Fexuprazan may have little to no effect compared to esomeprazole on EE healing rate at 4 weeks (RR 1.02, 95% CI 0.93 to 1.12, I2 = 0%, n = 2 studies, CoE very low) and 8 weeks. No significant differences were found between treatments regarding CRS at 1 week (RR 1.29; 95% CI: 0.84 to 1.99; I2 = 0%; n = 2 studies; CoE very low) and 8 weeks, or in the 24 h symptom-free days at 1 week (MD 2.67 days, 95% CI -2.76 to 8.10, I2 = 41%, n = 2 studies, CoE very low) and 8 weeks. Fexuprazan also showed little to no effect on treatment-emergent adverse events (RR 1.00, 95% CI 0.83 to 1.20, I2 = 0%, n = 3 studies, CoE very low). Nonetheless, the evidence for all outcomes was rated as very uncertain. Conclusions: Fexuprazan 40 mg may provide similar efficacy compared to esomeprazole 40 mg in EE, with a comparable safety profile to esomeprazole in EE and LPRD patients. However, the evidence is highly uncertain, requiring further studies.
Abstract licence: CC BY
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
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
1-1.5 hours
Mechanism
Esomeprazole exerts its stomach acid-suppressing effects by preventing the final…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.5 hours
Half-life
1-1.5 hours
Protein binding
97%
Volume of distribution
16 L
Metabolism
3%
Elimination
1 to 1.5 hours
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Esomeprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole's duration of antisecretory effect persists longer than 24 hours.[FDA Label]
PPIs such as esomeprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes.[A177577][A177580]
Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as esomeprazole has been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal C. difficile), reduced absorption of micronutrients such as iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life.[A177571]
Rapid discontinuation of PPIs such as esomeprazole may cause a rebound effect and a short term increase in hypersecretion.[A177574] Esomeprazole doses should be slowly lowered, or tapered, before discontinuing to prevent this rebound effect.
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 407 interactions
Esomeprazole is the s-isomer of DB00338, which is a racemate of the S- and R-enantiomer. Esomeprazole has been shown to inhibit acid secretion to a similar extent as DB00338, without any significant differences between the two compounds in vitro.
PPIs such as esomeprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes.[A177577][A177580]
Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as esomeprazole has been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal C. difficile), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life.[A177571]
How the body processes this drug — absorption, distribution, metabolism, and elimination
The mean exposure (AUC) to esomeprazole increases from 4.32 μmol*hr/L on Day 1 to 11.2 μmol*hr/L on Day 5 after 40 mg once daily dosing. The AUC after administration of a single 40 mg dose of Esomeprazole is decreased by 43% to 53% after food intake compared to fasting conditions. Esomeprazole should be taken at least one hour before meals.[FDA Label]
Combination Therapy with Antimicrobials:
Esomeprazole magnesium 40 mg once daily was given in combination with DB01211 500 mg twice daily and DB01060 1000 mg twice daily for 7 days to 17 healthy male and female subjects.
The mean steady state AUC and Cmax of esomeprazole increased by 70% and 18%, respectively during triple combination therapy compared to treatment with esomeprazole alone. The observed increase in esomeprazole exposure during co-administration with clarithromycin and amoxicillin is not expected to produce significant safety concerns.
The remaining amount is dependent on CYP3A4 which forms the sulphone metabolite. CYP2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15 to 20% of Asians lack CYP2C19 and are termed Poor Metabolizers.[FDA Label] However, the influence of CYP 2C19 polymorphism is less pronounced for esomeprazole than for omeprazole.[F4495] At steady state, the ratio of AUC in Poor Metabolizers to AUC in the rest of the population (Extensive Metabolizers) is approximately 2.
Following administration of equimolar doses, the S- and R-isomers are metabolized differently by the liver, resulting in higher plasma levels of the S- than of the R-isomer.[FDA Label]
Nine major urinary metabolites have been detected. The two main metabolites have been identified as hydroxyesomeprazole and the corresponding carboxylic acid.
Three major metabolites have been identified in plasma: the 5-O-desmethyl- and sulphone derivatives and hydroxyesomeprazole. The major metabolites of esomeprazole have no effect on gastric acid secretion.[F4495]
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)
Interacts with the phosphorylation domain of the alpha subunit and functions as a ratchet, stabilizing the lumenal-open E2 conformation and preventing the reverse reaction of the transport cycle (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
ATC A02BD06
ATC A02BC05
ATC M01AE52
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)
Esomeprazole
Additional database identifiers
Drugs Product Database (DPD)
12371
ChemSpider
7843323
Guide to Pharmacology
4279
ZINC
ZINC000004693574
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:820
GenAtlas
ATP4B
GeneCards
ATP4B
GenBank Gene Database
M75110
GenBank Protein Database
184105
UniProt Accession
ATP4B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2715
GenAtlas
DDAH1
GeneCards
DDAH1
GenBank Gene Database
AB001915
GenBank Protein Database
4160666
Guide to Pharmacology
1247
UniProt Accession
DDAH1_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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_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