ESOMEPRAZOLE

Details

Stereochemistry	ABSOLUTE
Molecular Formula	C17H19N3O3S
Molecular Weight	345.416
Optical Activity	( - )
Defined Stereocenters	1 / 1
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

COC1=CC2=C(NC(=N2)[S@@+]([O-])CC3=NC=C(C)C(OC)=C3C)C=C1

InChI

InChIKey=SUBDBMMJDZJVOS-DEOSSOPVSA-N

InChI=1S/C17H19N3O3S/c1-10-8-18-15(11(2)16(10)23-4)9-24(21)17-19-13-6-5-12(22-3)7-14(13)20-17/h5-8H,9H2,1-4H3,(H,19,20)/t24-/m0/s1

HIDE SMILES / InChI

Molecular Formula	C17H19N3O3S
Molecular Weight	345.416
Charge	0
Count

Stereochemistry	ACHIRAL
Additional Stereochemistry	No
Defined Stereocenters	0 / 0
E/Z Centers	0
Optical Activity	NONE

Description
Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/022056lbl.pdfhttps://www.accessdata.fda.gov/drugsatfda_docs/label/2014/202342s002lbl.pdf

Esomeprazole strontium is a proton pump inhibitor. It suppresses gastric acid secretion by specific inhibition H+/K+ ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. The drug is indicated for the treatment of gastroesophageal reflux disease, reduction the risk of NSAID-associated gastric ulcer, eradication of H.pylori, and pathological hypersecretory conditions.

CNS Activity

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
Potassium-transporting ATPase 38 Target ID: CHEMBL2095173 Sources: https://www.ncbi.nlm.nih.gov/pubmed/10411559	Inhibitor 8504

Conditions

Condition	Modality	Highest Phase	Product
Heartburn 24 Sources: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=477cfda2-44cf-4d0e-bdc4-e30bf16bfea9	Primary	Approved 8583	NEXIUM 24HR Approved Use treats frequent heartburn (occurs 2 or more days a week) Launch Date 2014
Duodenal ulcer 49 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/022056lbl.pdf	Primary	Approved 8583	PRILOSEC Approved Use PRILOSEC is a proton pump inhibitor indicated for: treatment of duodenal ulcer in adults, treatment of gastric ulcer in adults. Treatment of Gastroesophageal Reflux Disease. Maintenance of healing of erosive esophagitis in pediatric patients and adults. Treatment of pathological hypersecretory conditions in adults. Launch Date 2008
Gastric ulcer 74 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/022056lbl.pdf	Primary	Approved 8583	PRILOSEC Approved Use PRILOSEC is a proton pump inhibitor indicated for: treatment of duodenal ulcer in adults, treatment of gastric ulcer in adults. Treatment of Gastroesophageal Reflux Disease. Maintenance of healing of erosive esophagitis in pediatric patients and adults. Treatment of pathological hypersecretory conditions in adults. Launch Date 2008
Gastroesophageal reflux disease 68 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/022056lbl.pdf	Primary	Approved 8583	PRILOSEC Approved Use PRILOSEC is a proton pump inhibitor indicated for: treatment of duodenal ulcer in adults, treatment of gastric ulcer in adults. Treatment of Gastroesophageal Reflux Disease. Maintenance of healing of erosive esophagitis in pediatric patients and adults. Treatment of pathological hypersecretory conditions in adults. Launch Date 1989
Pathological hypersecretory conditions 9 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/022056lbl.pdf	Primary	Approved 8583	PRILOSEC Approved Use PRILOSEC is a proton pump inhibitor indicated for: treatment of duodenal ulcer in adults, treatment of gastric ulcer in adults. Treatment of Gastroesophageal Reflux Disease. Maintenance of healing of erosive esophagitis in pediatric patients and adults. Treatment of pathological hypersecretory conditions in adults. Launch Date 2008

C_max

Value	Dose	Co-administered	Analyte	Population
668 ng/mL DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf	1 mg/kg single, oral dose: 1 mg/kg route of administration: Oral experiment type: SINGLE co-administered:		OMEPRAZOLE plasma	Homo sapiens population: UNKNOWN age: ADULT sex: UNKNOWN food status: UNKNOWN
7.5 μM EXPERIMENT https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/021689Orig1s034lbl.pdf	40 mg 1 times / day multiple, intravenous dose: 40 mg route of administration: Intravenous experiment type: MULTIPLE co-administered:		ESOMEPRAZOLE plasma	Homo sapiens population: HEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN

AUC

Value	Dose	Analyte	Population
1200 nM*h Clinical Trial https://clinicaltrials.gov/ct2/show/NCT01361217	20 mg single, oral dose: 20 mg route of administration: oral experiment type: single co-administered:	OMEPRAZOLE plasma	Homo sapiens population: healthy age: adults sex: food status:
1220 ng × h/mL DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf	1 mg/kg single, oral dose: 1 mg/kg route of administration: Oral experiment type: SINGLE co-administered:	OMEPRAZOLE plasma	Homo sapiens population: UNKNOWN age: ADULT sex: UNKNOWN food status: UNKNOWN
1179 nM × h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/2350532	20 mg 1 times / day multiple, oral dose: 20 mg route of administration: Oral experiment type: MULTIPLE co-administered:	OMEPRAZOLE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
16.2 μM × h EXPERIMENT https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/021689Orig1s034lbl.pdf	40 mg 1 times / day multiple, intravenous dose: 40 mg route of administration: Intravenous experiment type: MULTIPLE co-administered:	ESOMEPRAZOLE plasma	Homo sapiens population: HEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN

T_1/2

Value	Dose	Co-administered	Analyte	Population
0.58 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/2350532	20 mg 1 times / day multiple, oral dose: 20 mg route of administration: Oral experiment type: MULTIPLE co-administered:		OMEPRAZOLE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
1.4 h EXPERIMENT https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/021689Orig1s034lbl.pdf	40 mg 1 times / day multiple, intravenous dose: 40 mg route of administration: Intravenous experiment type: MULTIPLE co-administered:		ESOMEPRAZOLE plasma	Homo sapiens population: HEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN

Doses

Dose	Population	Adverse events
20 mg 1 times / day multiple, oral Recommended Dose: 20 mg, 1 times / day Route: oral Route: multiple Dose: 20 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/11563998/	unhealthy, 45.2 Health Status: unhealthy Age Group: 45.2 Sex: M+F Sources: https://pubmed.ncbi.nlm.nih.gov/11563998/	Other AEs: Nausea, Diarrhoea... Other AEs: Nausea (7%) Diarrhoea (6%) Headache (3%) Sources: https://pubmed.ncbi.nlm.nih.gov/11563998/
20 mg 1 times / day multiple, oral Recommended Dose: 20 mg, 1 times / day Route: oral Route: multiple Dose: 20 mg, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/019810s088,022056s003lbl.pdf	unhealthy Health Status: unhealthy Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/019810s088,022056s003lbl.pdf	Other AEs: Headache, Abdominal pain... Other AEs: Headache (6.9%) Abdominal pain (5.2%) Nausea (4%) Diarrhea (3.7%) Vomiting (3.2%) Flatulence (2.7%) Esophageal acid reflux (1.9%) Upper respiratory infection (1.9%) Constipation (1.5%) Dizziness (1.5%) Rash (1.5%) Asthenia (1.3%) Back pain (1.1%) Cough (1.1%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/019810s088,022056s003lbl.pdf

AEs

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
inhibitor 2252 substrate 1946	inhibitor 2438 substrate 1193	inhibitor 2507

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
P-gp 1741 CYP2C19 2057 CYP1A2 2153 BCRP 910 OATP1B1 1079 OAT3 747 OAT1 725 MATE1 415 MATE2 267 OCT2 779 OCT1 620 OCT3 159 CYP2B6 926 CYP2C8 1057	P-gp 2052 CYP2C19 1119 CYP2C8 810 CYP2C18 149	MRP3 83 CYP1A1 151 CYP1A2 832 CYP1B1 71

Drug as perpetrator

Target	Modality	Activity	Clinical evidence
CYP2C19 2141	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/ \| https://pubmed.ncbi.nlm.nih.gov/30845361/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022101s014021957s017021153s050lbl.pdf	strong [IC50 3.7 uM]	yes (co-administration study) Comment: Esomeprazole administration resulted in a significant increase (1.67‐fold) in the AUC0–∞ of proguanil and a significant decrease (0.522‐fold) in that of cycloguanil Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/ \| https://pubmed.ncbi.nlm.nih.gov/30845361/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022101s014021957s017021153s050lbl.pdf
CYP1A2 2333	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/	weak [IC50 >40 uM]
CYP2B6 1160	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/	weak [IC50 >40 uM]
CYP2C8 1117	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/	weak [IC50 >40 uM]
CYP2C9 2497	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/	weak [IC50 >40 uM]
CYP2D6 2546	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/	weak [IC50 >40 uM]
CYP3A4 2633	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/22648560/	weak [IC50 >40 uM]
CYP1A2 2333	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/16248835/ \| https://pubmed.ncbi.nlm.nih.gov/10584979/	weak [Ki 150 uM]	weak (co-administration study) Comment: Omeprazole exerts a concentration-dependent inhibition of CYP1A2 activity in man. However, even after single oral doses up to 80 mg, this effect is weak and without clinical relevance Sources: https://pubmed.ncbi.nlm.nih.gov/16248835/ \| https://pubmed.ncbi.nlm.nih.gov/10584979/
CYP3A4 2633	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/11334262/ \| https://pubmed.ncbi.nlm.nih.gov/16248835/	weak [Ki 367.5 uM]
CYP2D6 2546	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/11334262/	weak [Ki 745.1 uM]
OAT3 749	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/28801980/	yes [IC50 1.2 uM]	likely (co-administration study) Comment: The frequency of delayed MTX elimination in patients administered esomeprazole was 71.4% Sources: https://pubmed.ncbi.nlm.nih.gov/28801980/
OCT1 656	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/21779389/	yes [IC50 15.7 uM]
BCRP 985	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/19076159/	yes [IC50 17.6 uM]
P-gp 1932	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/11770010/	yes [IC50 17.7 uM]
OCT3 161	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/21779389/	yes [IC50 22 uM]
OAT1 730	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/25239859/	yes [IC50 4.32 uM]
OCT2 782	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/20053795/ \| https://pubmed.ncbi.nlm.nih.gov/21779389/	yes [IC50 6.7 uM]
OAT3 749	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/25239859/	yes [IC50 6.8 uM]
OATP1B1 1095	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/25975815/	yes [IC50 84.3 uM]	unlikely (co-administration study) Comment: Coaministration with simvastatin acid unlikely results in DDIs Sources: https://pubmed.ncbi.nlm.nih.gov/25975815/
CYP2C19 2141	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/16248835/ \| https://pubmed.ncbi.nlm.nih.gov/11334262/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf	yes [Ki 7.1 uM]	yes (co-administration study) Comment: Omeprazole increased Cmax and AUC of cilostazol by 18% and 26% respectively Sources: https://pubmed.ncbi.nlm.nih.gov/16248835/ \| https://pubmed.ncbi.nlm.nih.gov/11334262/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf
CYP1A1 272	inducer 1966 Sources: https://pubmed.ncbi.nlm.nih.gov/10445394/	yes
CYP1A2 2333	inducer 1966 Sources: https://pubmed.ncbi.nlm.nih.gov/12623754/	yes
CYP1B1 93	inducer 1966 Sources: https://pubmed.ncbi.nlm.nih.gov/12623754/	yes
CYP2C9 2497	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/11334262/ \| https://pubmed.ncbi.nlm.nih.gov/16248835/	yes
MATE1 416	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/20053795/ \| https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.2020.34.s1.09069	yes
MATE2 267	inhibitor 4027 Sources: https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.2020.34.s1.09069	yes
MRP1 232	supressor 160 Sources: https://pubmed.ncbi.nlm.nih.gov/30349304/	yes
P-gp 1932	supressor 160 Sources: https://pubmed.ncbi.nlm.nih.gov/33049093/ \| https://pubmed.ncbi.nlm.nih.gov/30349304/	yes
MRP3 326	inducer 1966 Sources: https://pubmed.ncbi.nlm.nih.gov/12538803/	yes	yes (expression study) Comment: livers of patients treated with omeprazole showed higher MRP3 protein expression Sources: https://pubmed.ncbi.nlm.nih.gov/12538803/

Drug as victim

Target	Modality	Activity	Clinical evidence
CYP2C19 1119	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/16093273/ \| https://pubmed.ncbi.nlm.nih.gov/9353355/ \| https://pubmed.ncbi.nlm.nih.gov/10901708/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf	major	yes (co-administration study) Comment: When voriconazole was given with omeprazole to healthy subjects, it significantly increased the steady-state Cmax and AUC0-24 of omeprazole, an average of 2 times and 4 times, respectively Sources: https://pubmed.ncbi.nlm.nih.gov/16093273/ \| https://pubmed.ncbi.nlm.nih.gov/9353355/ \| https://pubmed.ncbi.nlm.nih.gov/10901708/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf
CYP3A4 1946	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/16093273/ \| https://pubmed.ncbi.nlm.nih.gov/9353355/ \| https://pubmed.ncbi.nlm.nih.gov/10901708/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf	major	yes (co-administration study) Comment: Drugs known to induce CYP2C19 or CYP3A4 (such as rifampin) may lead to decreased omeprazole serum levels. In a cross-over study in 12 healthy male subjects, St John’s wort, an inducer of CYP3A4, decreased the systemic exposure of omeprazole in CYP2C19 poor metabolisers (Cmax and AUC decreased by 37.5% and 37.9%, respectively) and extensive metabolisers (Cmax and AUC decreased by 49.6% and 43.9%, respectively) Sources: https://pubmed.ncbi.nlm.nih.gov/16093273/ \| https://pubmed.ncbi.nlm.nih.gov/9353355/ \| https://pubmed.ncbi.nlm.nih.gov/10901708/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019810s096lbl.pdf
CYP2C18 149	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/8894508/	minor
CYP2C8 810	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/8894508/	minor
CYP2C9 1193	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/8894508/	minor
P-gp 2052	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/11770010/	no
CYP3A4 1946	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022101s014021957s017021153s050lbl.pdf	yes	yes (co-administration study) Comment: Drugs which induce CYP2C19 or CYP3A4 (such as St. John’s Wort or rifampin) can substantially decrease esomeprazole concentrations Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022101s014021957s017021153s050lbl.pdf
CYP2C19 1119	substrate 4014 Sources: https://www.ncbi.nlm.nih.gov/books/NBK100896/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022101s014021957s017021153s050lbl.pdf	yes	yes (pharmacogenomic study) Comment: Drugs which induce CYP2C19 or CYP3A4 (such as St. John’s Wort or rifampin) can substantially decrease esomeprazole concentrations; The CYP2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15–20% of Asians lack CYP2C19 and are termed poor metabolizers. At steady state, the ratio of AUC in poor metabolizers to AUC in the rest of the population (normal metabolizers) is approximately 2 Sources: https://www.ncbi.nlm.nih.gov/books/NBK100896/ \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/022101s014021957s017021153s050lbl.pdf

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:50275	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:50275
MolPort	MolPort-023-330-012	https://www.molport.com/shop/molecule-link/MolPort-023-330-012
ZINC	ZINC000004693574	http://zinc15.docking.org/substances/ZINC000004693574

PubMed

Title	Date	PubMed
New OTC drugs and devices 2000: a selective review.	2001-04-12	11297337
From the Food and Drug Administration.	2001-04-04	11277810
Complete remission of primary high-grade B-cell gastric lymphoma after cure of Helicobacter pylori infection.	2001-04-01	11283137
Which patients with ulcer- or reflux-like dyspepsia will respond favorably to omeprazole?	2001-04	11300989
Antireflux surgery in children suffering from reflux-associated respiratory disease?	2001-04	11288221
Pantoprazole and cyclosporine or tacrolimus.	2001-04	11284790
Maximal acid reflux control for Barrett's oesophagus: feasible and effective.	2001-04	11284781
Nitrofurantoin quadruple therapy for Helicobacter pylori infection: effect of metronidazole resistance.	2001-04	11284780
Effects of lansoprazole, clarithromycin and pH gradient on uptake of [14C]amoxycillin into rat gastric tissue.	2001-04	11266411
A new cause of Zollinger-Ellison syndrome: non-small cell lung cancer.	2001-04	11266390
Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen.	2001-03-29	11274623
Omeprazole therapy and salivary flow rate in duodenal ulcer patients.	2001-03-21	11257735
Haloperidol-stomach lesions attenuation by pentadecapeptide BPC 157, omeprazole, bromocriptine, but not atropine, lansoprazole, pantoprazole, ranitidine, cimetidine and misoprostol in mice.	2001-03-09	11292068
[Heartburn. Only a harmless symptom?].	2001-03-08	11277116
Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated.	2001-03-06	11242498
The effect of culture results for Helicobacter pylori on the choice of treatment following failure of initial eradication.	2001-03	11303370
Electrochemical studies and differential pulse polarographic analysis of lansoprazole in pharmaceuticals.	2001-03	11284340
Efficacy and safety of esomeprazole compared with omeprazole in GERD patients with erosive esophagitis: a randomized controlled trial.	2001-03	11280530
Pharmacodynamic modeling of lansoprazole using an indirect irreversible response model.	2001-03	11269565
Pharmacokinetic differences between lansoprazole enantiomers and contribution of cytochrome P450 isoforms to enantioselective metabolism of lansoprazole in dogs.	2001-03	11256484
Effect of genotypic differences in CYP2C19 on cure rates for Helicobacter pylori infection by triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin.	2001-03	11240980
Stereoselective pharmacokinetics of pantoprazole, a proton pump inhibitor, in extensive and poor metabolizers of S-mephenytoin.	2001-03	11240974
A case of gastric plasmacytoma associated with Helicobacter pylori infection: improvement of abnormal endoscopic and EUS findings after H. pylori eradication.	2001-03	11231401
Bioequivalence evaluation of lansoprazole 30-mg capsules (Lanfast and Lanzor) in healthy volunteers.	2001-03	11226823
Differentiation between reinfection and recrudescence of helicobacter pylori strains using PCR-based restriction fragment length polymorphism analysis.	2001-02	11293500
Protective effect of famotidine, omeprazole, and melatonin against acetylsalicylic acid-induced gastric damage in rats.	2001-02	11281181
Improved high performance liquid chromatographic analysis of omeprazole in human plasma.	2001-02	11272330
Gastroesophageal reflux disease and Barrett's esophagus.	2001-02	11272213
[Suppressive effect of lansoprazole on anti-Candida activity of murine macrophages].	2001-02	11260880
Re: Ammonia cannot explain the effect of H. pylori on omeprazole-induced acid suppression.	2001-02	11232721
Recurrent ulcer bleeding: is intravenous omeprazole the solution?	2001-02	11232716
A randomized, pharmacokinetic and pharmacodynamic, cross-over study of duodenal or jejunal administration compared to nasogastric administration of omeprazole suspension in patients at risk for stress ulcers.	2001-02	11232677
Do some patients with Helicobacter pylori infection benefit from an extension to 2 weeks of a proton pump inhibitor-based triple eradication therapy?	2001-02	11232676
Increased acid and bile reflux in Barrett's esophagus compared to reflux esophagitis, and effect of proton pump inhibitor therapy.	2001-02	11232672
Comparison of the efficacy and safety of different formulations of omeprazole-based triple therapies in the treatment of Helicobacter pylori-positive peptic ulcer.	2001-02	11227677
Early stage gastric MALT lymphoma with high-grade component cured by Helicobacter pylori eradication.	2001-02	11227668
Aggressive acid control: minimizing progression of Barrett's esophagus.	2001-02	11225348
Continued (5-year) followup of a randomized clinical study comparing antireflux surgery and omeprazole in gastroesophageal reflux disease.	2001-02	11220717
[A strategy for second-line anti-Helicobacter pylori therapy in patients with previously failed treatment].	2001-02	11218406
[Usefulness of new triple therapy containing PPI].	2001-02	11218404
[Selection of antibiotics and planning of eradication for H. pylori infection].	2001-02	11218403
[Recent guidelines for the management of Helicobacter pylori infection].	2001-02	11218393
[Ulcer therapy with a new proton pump inhibitor. One week of treatment is enough].	2001-01-11	11216011
[Prevalence and treatment of Helicobacter pylori in gastro-duodenal ulcers. An experience in Liege].	2001-01	11256133
Upper gastrointestinal bleeding as a metastatic manifestation of breast cancer: a case report and review of the literature.	2001-01	11248910
Approach to the patient with unexplained chest pain.	2001-01	11216468
Gastroesophageal reflux disease: extraesophageal manifestations and therapy.	2001-01	11215855
Management of GERD: medical versus surgical.	2001-01	11215853
Pharmacokinetic study of esomeprazole in the elderly.	2001	11286324
Study of the electrospray ionization mass spectrometry of the proton pump inhibiting drug Omeprazole.	2001	11223960

Patents

Sample Use Guides

In Vivo Use Guide

Active Duodenal Ulcer: 20 mg Once daily for 4 weeks. Some patients may require an addition 4 weeks. Gastric Ulcer: oral dose is 40 mg once daily for 4-8 weeks. Gastroesophageal Reflux Disease: The recommended adult oral dose for the treatment of patients with symptomatic GERD and no esophageal lesions is 20 mg daily for up to 4 weeks. The recommended adult oral dose for the treatment of patients with erosive esophagitis and accompanying symptoms due to GERD is 20 mg daily for 4 to 8 weeks.

Route of Administration: Oral

In Vitro Use Guide

Pretreatment of omeprazole (10-6 - 10-4M) dose-dependently inhibits neutrophil adherence and respiratory burst induced by H. pylori. These evidences imply that omeprazole may exhibit a beneficial effect on H. pylori-associated gastric mucosal damage caused by activated neutrophils.

Substance Class	Chemical Created by `admin` on `Wed Apr 02 09:33:02 GMT 2025` Edited by `admin` on `Wed Apr 02 09:33:02 GMT 2025`
Record UNII	N3PA6559FT
Record Status	`Validated (UNII)`
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Name

Type

Language

ESOMEPRAZOLE

Official Name

English

INEXIUM PARANOVA

Preferred Name

English

H199/18

Common Name

English

A02BC05

Code

English

OMEPRAZOLE S-FORM [MI]

Common Name

English

ESOMEPRAZOLE [VANDF]

Common Name

English

1H-BENZIMIDAZOLE, 5-METHOXY-2-((S)-((4-METHOXY-3,5-DIMETHYL-2-PYRIDINYL)METHYL)SULFINYL)-

Systematic Name

English

Esomeprazole [WHO-DD]

Common Name

English

esomeprazole [INN]

Common Name

English

5-METHOXY-2-((S)-((4-METHOXY-3,5-DIMETHYL-2-PYRIDYL)METHYL)SULFINYL)BENZIMIDAZOLE

Systematic Name

English

ESOMEPRAZOLE [MART.]

Common Name

English

OMEPRAZOLE S-FORM

Common Name

English

OMEPRAZOLE, (S)-

Common Name

English

Classification Tree Code System Code

WHO-VATC

QB01AC56