Esomeprazole (original) (raw)
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Summary
Esomeprazole is a proton pump inhibitor used to treat GERD, reduce the risk of NSAID associated gastric ulcers, eradicate H. pylori, and to treat conditions causing gastric acid hypersecretion.
Brand Names
Nexium, Vimovo
Generic Name
Esomeprazole
DrugBank Accession Number
DB00736
Background
Esomeprazole, sold under the brand name Nexium, is a proton pump inhibitor (PPI) medication used for the management of gastroesophageal reflux disease (GERD), for gastric protection to prevent recurrence of stomach ulcers or gastric damage from chronic use of NSAIDs, and for the treatment of pathological hypersecretory conditions including Zollinger-Ellison (ZE) Syndrome. It can also be found in quadruple regimens for the treatment of H. pylori infections along with other antibiotics including Amoxicillin, Clarithromycin, and Metronidazole, for example.7,10 Its efficacy is considered similar to other medications within the PPI class including Omeprazole, Pantoprazole, Lansoprazole, Dexlansoprazole, and Rabeprazole. Esomeprazole is the s-isomer of Omeprazole, which is a racemate of the S- and R-enantiomer. Esomeprazole has been shown to inhibit acid secretion to a similar extent as Omeprazole, without any significant differences between the two compounds in vitro.
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.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.3,4
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.5
Rapid discontinuation of PPIs such as esomeprazole may cause a rebound effect and a short term increase in hypersecretion.6 Esomeprazole doses should be slowly lowered, or tapered, before discontinuing to prevent this rebound effect.
Type
Small Molecule
Groups
Approved, Investigational
Structure
Weight
Average: 345.416
Monoisotopic: 345.114712179
Chemical Formula
C17H19N3O3S
Synonyms
- (−)-omeprazole
- (S)-(−)-omeprazole
- (S)-omeprazole
- Esomeprazol
- Ésoméprazole
- Esomeprazole
- Esomeprazolum
- Omeprazole S-form
- Perprazole
- A02BC05
- H 199/18
Indication
Esomeprazole is indicated for the treatment of acid-reflux disorders including healing and maintenance of erosive esophagitis, and symptomatic gastroesophageal reflux disease (GERD), peptic ulcer disease, H. pylori eradication, prevention of gastrointestinal bleeds with NSAID use, and for the long-term treatment of pathological hypersecretory conditions including Zollinger-Ellison Syndrome.
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Associated Conditions
Contraindications & Blackbox Warnings
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Pharmacodynamics
Esomeprazole is a compound that inhibits gastric acid secretion and is indicated in the treatment of gastroesophageal reflux disease (GERD), the healing of erosive esophagitis, and H. pylori eradication to reduce the risk of duodenal ulcer recurrence. Esomeprazole belongs to a new class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonistic properties, but that suppress gastric acid secretion by specific inhibition of the H+/K+ ATPase at the secretory surface of the gastric parietal cell. By doing so, it inhibits acid secretion into the gsatric lumen. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus.
Esomeprazole is the s-isomer of Omeprazole, which is a racemate of the S- and R-enantiomer. Esomeprazole has been shown to inhibit acid secretion to a similar extent as Omeprazole, 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.3,4
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.5
Mechanism of action
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 that persists longer than 24 hours.Label
| Target | Actions | Organism |
|---|---|---|
| APotassium-transporting ATPase alpha chain 1 | inhibitor | Humans |
| APotassium-transporting ATPase subunit beta | modulator | Humans |
| UN(G),N(G)-dimethylarginine dimethylaminohydrolase 1 | Not Available | Humans |
Absorption
After oral administration, peak plasma levels (Cmax) occur at approximately 1.5 hours (Tmax). The Cmax increases proportionally when the dose is increased, and there is a three-fold increase in the area under the plasma concentration-time curve (AUC) from 20 to 40 mg. At repeated once-daily dosing with 40 mg, the systemic bioavailability is approximately 90% compared to 64% after a single dose of 40 mg. 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.Label
Combination Therapy with Antimicrobials:
Esomeprazole magnesium 40 mg once daily was given in combination with Clarithromycin 500 mg twice daily and Amoxicillin 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.
Volume of distribution
The apparent volume of distribution at steady state in healthy volunteers is approximately 16 L.Label
Protein binding
Esomeprazole is 97% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 2 to 20 µmol/L.Label
Metabolism
Esomeprazole is extensively metabolized in the liver by the cytochrome P450 (CYP) enzyme system. The metabolites of esomeprazole lack antisecretory activity. The major part of esomeprazole’s metabolism is dependent upon the CYP2C19 isoenzyme, which forms the hydroxy and desmethyl metabolites. 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.Label However, the influence of CYP 2C19 polymorphism is less pronounced for esomeprazole than for omeprazole.9 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.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.9
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Route of elimination
The plasma elimination half-life of esomeprazole is approximately 1 to 1.5 hours. Less than 1% of parent drug is excreted in the urine. Approximately 80% of an oral dose of esomeprazole is excreted as inactive metabolites in the urine, and the remainder is found as inactive metabolites in the feces.
Half-life
1-1.5 hours
Clearance
Not Available
Adverse Effects
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Toxicity
Blurred vision, confusion, drowsiness, dry mouth, flushing headache, nausea, rapid heartbeat, sweating
Pathways
| Pathway | Category |
|---|---|
| Esomeprazole Metabolism Pathway | Drug metabolism |
| Esomeprazole Action Pathway | Drug action |
| Interacting Gene/Enzyme | Allele name | Genotype(s) | Defining Change(s) | Type(s) | Description | Details |
|---|---|---|---|---|---|---|
| Cytochrome P450 2C19 | CYP2C19*2 | (A;A) | A Allele, homozygote | Effect Directly Studied | Patients with this genotype have reduced metabolism of esomeprazole. | Details |
| Cytochrome P450 2C19 | CYP2C19*3 | (A;A) | A Allele, homozygote | Effect Directly Studied | Patients with this genotype have reduced metabolism of esomeprazole. | Details |
| Cytochrome P450 2C19 | CYP2C19*2A | Not Available | 681G>A | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*2B | Not Available | 681G>A | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*4 | Not Available | 1A>G | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*5 | Not Available | 1297C>T | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*6 | Not Available | 395G>A | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*7 | Not Available | 19294T>A | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*22 | Not Available | 557G>C / 991A>G | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*24 | Not Available | 99C>T / 991A>G … show all | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
| Cytochrome P450 2C19 | CYP2C19*35 | Not Available | 12662A>G | Effect Inferred | Poor metabolizer, lower dose requirement, improved drug efficacy | Details |
This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
| Drug | Interaction |
|---|---|
| Integrate drug-drug interactions in your software | |
| Abametapir | The serum concentration of Esomeprazole can be increased when it is combined with Abametapir. |
| Abatacept | The metabolism of Esomeprazole can be increased when combined with Abatacept. |
| Abrocitinib | The metabolism of Abrocitinib can be decreased when combined with Esomeprazole. |
| Acenocoumarol | The metabolism of Acenocoumarol can be decreased when combined with Esomeprazole. |
| Acyclovir | The excretion of Acyclovir can be decreased when combined with Esomeprazole. |
Food Interactions
- Take with or without food. Co-administration with food slightly alters pharmacokinetics, but not to a clinically significant extent.
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| Ingredient | UNII | CAS | InChI Key |
|---|---|---|---|
| Esomeprazole magnesium | 925R0D7W1O | 161973-10-0 | KWORUUGOSLYAGD-YPPDDXJESA-N |
| Esomeprazole magnesium dihydrate | 36H71644EQ | 217087-10-0 | DBOUSUONOXEWHU-VCKZSRROSA-N |
| Esomeprazole magnesium trihydrate | R6DXU4WAY9 | 217087-09-7 | VEVZQDGATGBLIC-UHFFFAOYSA-N |
| Esomeprazole sodium | L2C9GWQ43H | 161796-78-7 | RYXPMWYHEBGTRV-JIDHJSLPSA-N |
| Esomeprazole strontium | SCC2RK476A | 914613-86-8 | FEVPVZSYBDUVGY-YPPDDXJESA-N |
| Esomeprazole strontium hydrate | C5N25H3803 | 934714-36-0 | NCGHIAKEJNQSMS-QLGOZJDFSA-N |
Product Images
International/Other Brands
Alenia (Delta) / Awa-Block (Usawa) / Axagon (Simesa) / Cor (Prater) / Cronopep (Biotoscana) / Emanera (Krka) / Emep (Aristopharma) / Emozul (HYGIA) / ES-OD (Piramal Healthcare) / Esmep (HYGIA) / Eso (Asiatic Lab) / Esofag (Micro Labs) / Esolok (Ibn Sina) / Esomarfan (Marfan) / Esomenta (RAK) / Esomep (ACI) / Esomeprazol Genfar (Genfar S.A) / Esopral (Maquifarma) / Esorest (Centaur) / Inexium paranova / Lucen (Malesci) / Nexiam (AstraZeneca)
Brand Name Prescription Products
Generic Prescription Products
Over the Counter Products
Mixture Products
| Name | Ingredients | Dosage | Route | Labeller | Marketing Start | Marketing End | Region | Image |
|---|---|---|---|---|---|---|---|---|
| PharmapureRx ESOMEP-EZS | Esomeprazole magnesium dihydrate (20 mg/1) | Kit | Oral | PureTek Corporation | 2017-07-26 | 2021-05-31 |  |
ATC Codes
A02BD06 — Esomeprazole, amoxicillin and clarithromycin
- A02BD — Combinations for eradication of Helicobacter pylori
- A02B — DRUGS FOR PEPTIC ULCER AND GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)
- A02 — DRUGS FOR ACID RELATED DISORDERS
- A — ALIMENTARY TRACT AND METABOLISM A02BC05 — Esomeprazole
- A02BC — Proton pump inhibitors
- A02B — DRUGS FOR PEPTIC ULCER AND GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)
- A02 — DRUGS FOR ACID RELATED DISORDERS
- A — ALIMENTARY TRACT AND METABOLISM M01AE52 — Naproxen and esomeprazole
- M01AE — Propionic acid derivatives
- M01A — ANTIINFLAMMATORY AND ANTIRHEUMATIC PRODUCTS, NON-STEROIDS
- M01 — ANTIINFLAMMATORY AND ANTIRHEUMATIC PRODUCTS
- M — MUSCULO-SKELETAL SYSTEM
Drug Categories
- 2-Pyridinylmethylsulfinylbenzimidazoles
- Acid Reducers
- Alimentary Tract and Metabolism
- Anti-Ulcer Agents
- Antiinflammatory and Antirheumatic Products
- Antiinflammatory and Antirheumatic Products, Non-Steroids
- Benzimidazoles
- Cytochrome P-450 CYP2C19 Inhibitors
- Cytochrome P-450 CYP2C19 Inhibitors (weak)
- Cytochrome P-450 CYP2C19 Substrates
- Cytochrome P-450 CYP3A Substrates
- Cytochrome P-450 CYP3A4 Substrates
- Cytochrome P-450 Enzyme Inhibitors
- Cytochrome P-450 Substrates
- Drugs causing inadvertant photosensitivity
- Drugs for Acid Related Disorders
- Drugs for Peptic Ulcer and Gastro-Oesophageal Reflux Disease (Gord)
- Enzyme Inhibitors
- Gastric Acid Lowering Agents
- Gastrointestinal Agents
- Heterocyclic Compounds, Fused-Ring
- Musculo-Skeletal System
- OAT3/SLC22A8 Inhibitors
- P-glycoprotein inhibitors
- P-glycoprotein substrates
- Photosensitizing Agents
- Propionates
- Proton Pump Inhibitors
- Proton-pump Inhibitors
- Pyridines
- Sulfoxides
- Sulfur Compounds
Chemical TaxonomyProvided by Classyfire
Description
This compound belongs to the class of organic compounds known as sulfinylbenzimidazoles. These are polycyclic aromatic compounds containing a sulfinyl group attached at the position 2 of a benzimidazole moiety.
Kingdom
Super Class
Class
Sub Class
Direct Parent
Alternative Parents
Anisoles / Methylpyridines / Alkyl aryl ethers / Imidazoles / Heteroaromatic compounds / Sulfoxides / Sulfinyl compounds / Azacyclic compounds / Organopnictogen compounds / Organonitrogen compounds / Organic oxides / Hydrocarbon derivatives show 2 more
Substituents
Alkyl aryl ether / Anisole / Aromatic heteropolycyclic compound / Azacycle / Azole / Benzenoid / Ether / Heteroaromatic compound / Hydrocarbon derivative / Imidazole / Methylpyridine / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organonitrogen compound / Organooxygen compound / Organopnictogen compound / Organosulfur compound / Pyridine / Sulfinyl compound / Sulfinylbenzimidazole / Sulfoxide show 12 more
Molecular Framework
Aromatic heteropolycyclic compounds
External Descriptors
5-methoxy-2-\{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl\}-1H-benzimidazole (CHEBI:50275)
Affected organisms
- Humans and other mammals
UNII
CAS number
119141-88-7
InChI Key
SUBDBMMJDZJVOS-DEOSSOPVSA-N
InChI
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
IUPAC Name
5-methoxy-2-[(S)-(4-methoxy-3,5-dimethylpyridin-2-yl)methanesulfinyl]-1H-1,3-benzodiazole
SMILES
COC1=CC2=C(NC(=N2)[S@@](=O)CC2=NC=C(C)C(OC)=C2C)C=C1
Synthesis Reference
Manne Reddy, "Amorphous hydrates of esomeprazole magnesium and process for the preparation thereof." U.S. Patent US20040167173, issued August 26, 2004.
General References
- Lind T, Rydberg L, Kyleback A, Jonsson A, Andersson T, Hasselgren G, Holmberg J, Rohss K: Esomeprazole provides improved acid control vs. omeprazole In patients with symptoms of gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 2000 Jul;14(7):861-7. [Article]
- Klotz U: Clinical impact of CYP2C19 polymorphism on the action of proton pump inhibitors: a review of a special problem. Int J Clin Pharmacol Ther. 2006 Jul;44(7):297-302. [Article]
- Ghebremariam YT, LePendu P, Lee JC, Erlanson DA, Slaviero A, Shah NH, Leiper J, Cooke JP: Unexpected effect of proton pump inhibitors: elevation of the cardiovascular risk factor asymmetric dimethylarginine. Circulation. 2013 Aug 20;128(8):845-53. doi: 10.1161/CIRCULATIONAHA.113.003602. Epub 2013 Jul 3. [Article]
- Tommasi S, Elliot DJ, Hulin JA, Lewis BC, McEvoy M, Mangoni AA: Human dimethylarginine dimethylaminohydrolase 1 inhibition by proton pump inhibitors and the cardiovascular risk marker asymmetric dimethylarginine: in vitro and in vivo significance. Sci Rep. 2017 Jun 6;7(1):2871. doi: 10.1038/s41598-017-03069-1. [Article]
- Haastrup PF, Thompson W, Sondergaard J, Jarbol DE: Side Effects of Long-Term Proton Pump Inhibitor Use: A Review. Basic Clin Pharmacol Toxicol. 2018 Aug;123(2):114-121. doi: 10.1111/bcpt.13023. Epub 2018 May 24. [Article]
- Reimer C, Sondergaard B, Hilsted L, Bytzer P: Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology. 2009 Jul;137(1):80-7, 87.e1. doi: 10.1053/j.gastro.2009.03.058. Epub 2009 Apr 10. [Article]
- Fallone CA, Chiba N, van Zanten SV, Fischbach L, Gisbert JP, Hunt RH, Jones NL, Render C, Leontiadis GI, Moayyedi P, Marshall JK: The Toronto Consensus for the Treatment of Helicobacter pylori Infection in Adults. Gastroenterology. 2016 Jul;151(1):51-69.e14. doi: 10.1053/j.gastro.2016.04.006. Epub 2016 Apr 19. [Article]
- DailyMed Label: NEXIUM (esomeprazole magnesium) delayed-release capsules or granules, for oral use [Link]
- Health Canada Label - Esomeprazole [File]
- TOP Guidelines - H pylori [File]
External Links
Human Metabolome Database
KEGG Drug
PubChem Compound
PubChem Substance
ChemSpider
RxNav
ChEBI
ChEMBL
ZINC
Therapeutic Targets Database
PharmGKB
Guide to Pharmacology
RxList
Drugs.com
Wikipedia
FDA label
Clinical Trials
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Manufacturers
- Astrazeneca lp
Packagers
- AQ Pharmaceuticals Inc.
- A-S Medication Solutions LLC
- AstraZeneca Inc.
- Cardinal Health
- Direct Pharmaceuticals Inc.
- Diversified Healthcare Services Inc.
- Innoviant Pharmacy Inc.
- Lake Erie Medical and Surgical Supply
- Merck & Co.
- Nucare Pharmaceuticals Inc.
- Palmetto Pharmaceuticals Inc.
- Physicians Total Care Inc.
- Prepackage Specialists
- Rebel Distributors Corp.
- Southwood Pharmaceuticals
- Stat Rx Usa
Dosage Forms
| Form | Route | Strength |
|---|---|---|
| Capsule | Oral | 40.00 mg |
| Capsule | Oral | 22.250 mg |
| Kit | Oral; Topical | |
| Injection, powder, for solution | 40 MG | |
| Tablet, film coated | ||
| Tablet, coated | Oral | 20 mg |
| Capsule, delayed release pellets | Oral | 20 mg |
| Capsule, delayed release pellets | Oral | 40 mg |
| Capsule | Oral | 20 mg |
| Capsule | Oral | 40 mg |
| Powder | Intravenous | 40 mg/1vial |
| Powder | Intravenous | 40 mg |
| Powder, for solution | Intravenous | 40 mg |
| Tablet | Oral | |
| Capsule, delayed release | Oral | 22.25 MG |
| Capsule, delayed release | Oral | 44.5 MG |
| Tablet, delayed release | Oral | 22.545 MG |
| Tablet, delayed release | Oral | 45.09 MG |
| Capsule, coated pellets | Oral | 20 mg |
| Capsule, coated pellets | Oral | 40 mg |
| Injection | Intravenous | 40 mg |
| Capsule, coated | Oral | 4000000 mg |
| Capsule, coated | Oral | 2000000 mg |
| Granule | Oral | 5 mg |
| Injection | Intravenous | |
| Tablet, delayed release | Oral | 20 mg |
| Tablet, delayed release | Oral | 40 mg |
| Tablet, delayed release | Oral | 4000000 mg |
| Injection, powder, for solution | Parenteral | |
| Tablet, delayed release | Oral | |
| Tablet, coated | Oral | 2000000 mg |
| Capsule | Oral | 20 mg/1 |
| Tablet, delayed release | Oral | 20 mg/1 |
| Tablet, orally disintegrating, delayed release | Oral | 20 mg/1 |
| Capsule, coated pellets | Oral | 20 mg/1 |
| Capsule, coated pellets | Oral | 40 mg/1 |
| Capsule, delayed release | Oral | 40 1/1 |
| Capsule, delayed release pellets | Oral | 20 mg/1 |
| Capsule, delayed release pellets | Oral | 40 mg/1 |
| For suspension | Oral | 20 mg/1 |
| For suspension | Oral | 40 mg/1 |
| Granule, for suspension, extended release | Oral | 10 mg/1 |
| Injection, powder, for solution | Intravenous | 40 mg |
| Injection | Intravenous | 40 mg/5mL |
| Injection, powder, for solution | 40 MG/ML | |
| Injection, powder, for solution | Intravenous | 40 mg/5ml |
| Injection, powder, for solution; injection, powder, lyophilized, for solution | Intravenous | 40 mg |
| Injection, powder, lyophilized, for solution | Intravenous | 120 mg |
| Injection, powder, lyophilized, for solution | Intravenous | 20 mg/1 |
| Injection, powder, lyophilized, for solution | Intravenous | 20 mg/5mL |
| Injection, powder, lyophilized, for solution | Intravenous | 40 mg/5mL |
| Injection, powder, lyophilized, for solution | Intravenous | 40 mg/1 |
| Capsule, delayed release | Oral | 24.65 mg/1 |
| Capsule, delayed release | Oral | 49.3 mg/1 |
| Tablet | Oral | 40 MG |
| Capsule, delayed release | Oral | |
| Powder, for solution | Parenteral | 40 MG |
| Tablet, delayed release | Oral | 22.21 mg |
| Capsule, coated | Oral | 20 mg |
| Capsule | Oral | |
| Powder | Oral | |
| Injection, powder, lyophilized, for solution | Intravenous | 40 mg |
| Tablet, coated | Oral | 20.00 mg |
| Tablet, coated | Oral | 40.00 mg |
| Injection, powder, for solution | ||
| Tablet, film coated | Oral | 20 mg |
| Tablet, delayed release | Oral | 22.264 Mg |
| Tablet, delayed release | Oral | 44.528 Mg |
| Capsule, coated | Oral | 41.2 mg |
| Capsule, coated | Oral | 40 mg |
| Tablet, coated | Oral | 40 mg |
| Granule | Oral | 10 MG |
| Injection, powder, for solution | Parenteral | 40 MG |
| Solution | Intravenous | 42.533 mg |
| Tablet | Oral | 41.400 mg |
| Granule | Oral | 2.500 mg |
| Tablet | Oral | 20.000 mg |
| Tablet, film coated | Oral | |
| Granule | Oral | 2.5 mg |
| Granule | Oral | 0.167 g |
| Granule | Oral | 20 mg |
| Granule | Oral | 40 mg |
| Injection, powder, for solution; injection, powder, lyophilized, for solution | 40 mg | |
| Capsule, delayed release | Oral | 20 mg/1 |
| Capsule, delayed release | Oral | 40 mg/1 |
| Granule | Oral | 11.1 MG |
| Granule, delayed release | Oral | 10 mg / sachet |
| Granule, delayed release | Oral | 10 mg/1 |
| Granule, delayed release | Oral | 2.5 mg/1 |
| Granule, delayed release | Oral | 20 mg/1 |
| Granule, delayed release | Oral | 40 mg/1 |
| Granule, delayed release | Oral | 5 mg/1 |
| Tablet, film coated | Oral | 40 mg |
| Granule, delayed release | Oral | 10 MG |
| Tablet | Oral | 20 mg/1 |
| Tablet | Oral | 20 MG |
| Injection | Intravenous | 20 mg/5mL |
| Solution | Parenteral | 40.000 mg |
| Tablet, film coated | Oral | |
| Tablet, coated | Oral | |
| Capsule | Oral | 44.500 mg |
| Capsule, extended release | Oral | 40 mg |
| Kit | Oral | 20 mg/1 |
| Capsule, delayed release | Oral | 20 mg |
| Capsule, delayed release | Oral | 40 mg |
| Injection, powder, lyophilized, for solution | Intravenous | 42.5 mg |
| Tablet, coated | Oral | 44.55 mg |
| Capsule, coated | Oral | |
| Tablet | Oral | 44.569 mg |
| Tablet, delayed release | Oral | 22545 Mg |
| Solution | Intravenous | 42.60 mg |
| Injection, powder, for solution | Intravenous | 40.00 mg |
| Capsule | Oral | 20.0000 mg |
| Solution | Intravenous | 42.547 mg |
| Tablet | Oral | |
| Tablet, delayed release | Oral | |
| Tablet, extended release | Oral | |
| Solution | 40.000 mg | |
| Injection, powder, for solution | 40 mg/1vial |
Prices
| Unit description | Cost | Unit |
|---|---|---|
| Nexium i.v. 20 mg vial | 33.91USD | vial |
| Nexium i.v. 40 mg vial | 33.91USD | vial |
| NexIUM 20 mg Delayed Release Capsule | 6.76USD | capsule |
| NexIUM 40 mg Delayed Release Capsule | 6.76USD | capsule |
| Nexium 10 mg packet | 6.5USD | each |
| Nexium 20 mg capsule | 6.5USD | capsule |
| Nexium 20 mg packet | 6.5USD | each |
| Nexium 40 mg capsule | 6.5USD | capsule |
| Nexium 40 mg packet | 6.5USD | each |
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
| Patent Number | Pediatric Extension | Approved | Expires (estimated) | Region |
|---|---|---|---|---|
| US5877192 | No | 1999-03-02 | 2014-05-27 | |
| CA1338377 | No | 1996-06-11 | 2013-06-11 |  |
| CA2346988 | No | 2009-02-10 | 2019-11-03 | |
| US6191148 | Yes | 2001-02-20 | 2019-04-09 | |
| US6147103 | Yes | 2000-11-14 | 2019-04-09 | |
| US6166213 | Yes | 2000-12-26 | 2019-04-09 | |
| US5900424 | Yes | 1999-05-04 | 2016-11-04 | |
| US6369085 | Yes | 2002-04-09 | 2018-11-25 | |
| US6428810 | Yes | 2002-08-06 | 2020-05-03 | |
| US7411070 | Yes | 2008-08-12 | 2018-11-25 | |
| US8466175 | Yes | 2013-06-18 | 2018-11-25 | |
| US8852636 | No | 2014-10-07 | 2022-05-31 | |
| US8858996 | No | 2014-10-14 | 2022-05-31 | |
| US6926907 | No | 2005-08-09 | 2023-02-28 | |
| US7745466 | No | 2010-06-29 | 2018-10-13 | |
| US9161920 | No | 2015-10-20 | 2022-05-31 | |
| US9198888 | No | 2015-12-01 | 2022-05-31 | |
| US8945621 | No | 2015-02-03 | 2031-10-17 | |
| US8557285 | No | 2013-10-15 | 2022-05-31 | |
| US9220698 | No | 2015-12-29 | 2031-03-10 | |
| US5714504 | Yes | 1998-02-03 | 2015-08-03 | |
| US9345695 | No | 2016-05-24 | 2022-05-31 | |
| US9393208 | No | 2016-07-19 | 2029-09-03 | |
| US9707181 | No | 2017-07-18 | 2022-05-31 | |
| US10076494 | No | 2018-09-18 | 2036-12-08 | |
| US10835488 | No | 2020-11-17 | 2036-12-08 | |
State
Solid
Experimental Properties
| Property | Value | Source |
|---|---|---|
| melting point (°C) | 155 °C | Not Available |
| water solubility | Very slightly soluble in water | Not Available |
| logP | 0.6 | Not Available |
Predicted Properties
| Property | Value | Source |
|---|---|---|
| Water Solubility | 0.353 mg/mL | ALOGPS |
| logP | 1.66 | ALOGPS |
| logP | 2.43 | Chemaxon |
| logS | -3 | ALOGPS |
| pKa (Strongest Acidic) | 9.68 | Chemaxon |
| pKa (Strongest Basic) | 4.77 | Chemaxon |
| Physiological Charge | 0 | Chemaxon |
| Hydrogen Acceptor Count | 5 | Chemaxon |
| Hydrogen Donor Count | 1 | Chemaxon |
| Polar Surface Area | 77.1 Å2 | Chemaxon |
| Rotatable Bond Count | 5 | Chemaxon |
| Refractivity | 93.66 m3·mol-1 | Chemaxon |
| Polarizability | 35.81 Å3 | Chemaxon |
| Number of Rings | 3 | Chemaxon |
| Bioavailability | 1 | Chemaxon |
| Rule of Five | Yes | Chemaxon |
| Ghose Filter | Yes | Chemaxon |
| Veber's Rule | No | Chemaxon |
| MDDR-like Rule | No | Chemaxon |
Predicted ADMET Features
| Property | Value | Probability |
|---|---|---|
| Human Intestinal Absorption | + | 0.9968 |
| Blood Brain Barrier | - | 0.6326 |
| Caco-2 permeable | + | 0.8867 |
| P-glycoprotein substrate | Non-substrate | 0.5573 |
| P-glycoprotein inhibitor I | Inhibitor | 0.6622 |
| P-glycoprotein inhibitor II | Non-inhibitor | 0.968 |
| Renal organic cation transporter | Non-inhibitor | 0.542 |
| CYP450 2C9 substrate | Non-substrate | 0.7838 |
| CYP450 2D6 substrate | Substrate | 0.6175 |
| CYP450 3A4 substrate | Substrate | 0.6901 |
| CYP450 1A2 substrate | Inhibitor | 0.7505 |
| CYP450 2C9 inhibitor | Non-inhibitor | 0.907 |
| CYP450 2D6 inhibitor | Non-inhibitor | 0.9231 |
| CYP450 2C19 inhibitor | Inhibitor | 0.8994 |
| CYP450 3A4 inhibitor | Inhibitor | 0.796 |
| CYP450 inhibitory promiscuity | High CYP Inhibitory Promiscuity | 0.7895 |
| Ames test | Non AMES toxic | 0.5692 |
| Carcinogenicity | Non-carcinogens | 0.8318 |
| Biodegradation | Not ready biodegradable | 0.9778 |
| Rat acute toxicity | 2.2254 LD50, mol/kg | Not applicable |
| hERG inhibition (predictor I) | Weak inhibitor | 0.719 |
| hERG inhibition (predictor II) | Non-inhibitor | 0.8977 |
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)
Mass Spec (NIST)
Not Available
Spectra
| Spectrum | Spectrum Type | Splash Key |
|---|---|---|
| Predicted GC-MS Spectrum - GC-MS | Predicted GC-MS | splash10-0udj-0902000000-d7c360235f936b712320 |
| Predicted MS/MS Spectrum - 10V, Positive (Annotated) | Predicted LC-MS/MS | splash10-0f6t-0049000000-dd6465ff98d6ab7b732e |
| Predicted MS/MS Spectrum - 10V, Negative (Annotated) | Predicted LC-MS/MS | splash10-0005-1904000000-2c0b41fb687c7276742c |
| Predicted MS/MS Spectrum - 20V, Positive (Annotated) | Predicted LC-MS/MS | splash10-0f6t-0935000000-8e10633e2e9d56c4305a |
| Predicted MS/MS Spectrum - 20V, Negative (Annotated) | Predicted LC-MS/MS | splash10-004i-0900000000-9fd0b7267901f29c8a26 |
| Predicted MS/MS Spectrum - 40V, Negative (Annotated) | Predicted LC-MS/MS | splash10-004i-4900000000-c49d95c2f14e14dc5350 |
| Predicted MS/MS Spectrum - 40V, Positive (Annotated) | Predicted LC-MS/MS | splash10-001i-0910000000-3cb2734362e389c7f316 |
| Predicted 1H NMR Spectrum | 1D NMR | Not Applicable |
| Predicted 13C NMR Spectrum | 1D NMR | Not Applicable |
Chromatographic Properties
Collision Cross Sections (CCS)
| Adduct | CCS Value (Å2) | Source type | Source |
|---|---|---|---|
| [M-H]- | 204.5956042 | predicted | DarkChem Lite v0.1.0 |
| [M-H]- | 204.4013042 | predicted | DarkChem Lite v0.1.0 |
| [M-H]- | 203.6952042 | predicted | DarkChem Lite v0.1.0 |
| [M-H]- | 181.43503 | predicted | DeepCCS 1.0 (2019) |
| [M+H]+ | 206.3136042 | predicted | DarkChem Lite v0.1.0 |
| [M+H]+ | 205.6878042 | predicted | DarkChem Lite v0.1.0 |
| [M+H]+ | 205.1514042 | predicted | DarkChem Lite v0.1.0 |
| [M+H]+ | 183.79305 | predicted | DeepCCS 1.0 (2019) |
| [M+Na]+ | 205.3173042 | predicted | DarkChem Lite v0.1.0 |
| [M+Na]+ | 204.4892042 | predicted | DarkChem Lite v0.1.0 |
| [M+Na]+ | 205.0212042 | predicted | DarkChem Lite v0.1.0 |
| [M+Na]+ | 190.64558 | predicted | DeepCCS 1.0 (2019) |
Targets
Build, predict & validate machine-learning modelsUse our structured and evidence-based datasets to unlock new insights and accelerate drug research.Use our structured and evidence-based datasets to unlock new insights and accelerate drug research.
Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
The catalytic subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Uses ATP as an energy source to pump H(+) ions to the gastric lumen while transporting K(+) ion from the lumen into the cell (By similarity). Remarkably generates a million-fold proton gradient across the gastric parietal cell membrane, acidifying the gastric juice down to pH 1 (By similarity). 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).
Specific Function
ATP binding
Gene Name
ATP4A
Uniprot ID
Uniprot Name
Potassium-transporting ATPase alpha chain 1
Molecular Weight
114117.74 Da
References
- Saccar CL: The pharmacology of esomeprazole and its role in gastric acid related diseases. Expert Opin Drug Metab Toxicol. 2009 Sep;5(9):1113-24. doi: 10.1517/17425250903124363. [Article]
- McKeage K, Blick SK, Croxtall JD, Lyseng-Williamson KA, Keating GM: Esomeprazole: a review of its use in the management of gastric acid-related diseases in adults. Drugs. 2008;68(11):1571-607. [Article]
- Vachhani R, Olds G, Velanovich V: Esomeprazole: a proton pump inhibitor. Expert Rev Gastroenterol Hepatol. 2009 Feb;3(1):15-27. doi: 10.1586/17474124.3.1.15. [Article]
- Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Modulator
General Function
The beta subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Plays a structural and regulatory role in the assembly and membrane targeting of a functionally active pump (By similarity). 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 of the alpha subunit that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). 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).
Specific Function
ATPase activator activity
Gene Name
ATP4B
Uniprot ID
Uniprot Name
Potassium-transporting ATPase subunit beta
Molecular Weight
33366.95 Da
References
- Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
General Function
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation.
Specific Function
amino acid binding
Gene Name
DDAH1
Uniprot ID
Uniprot Name
N(G),N(G)-dimethylarginine dimethylaminohydrolase 1
Molecular Weight
31121.5 Da
References
- Ghebremariam YT, LePendu P, Lee JC, Erlanson DA, Slaviero A, Shah NH, Leiper J, Cooke JP: Unexpected effect of proton pump inhibitors: elevation of the cardiovascular risk factor asymmetric dimethylarginine. Circulation. 2013 Aug 20;128(8):845-53. doi: 10.1161/CIRCULATIONAHA.113.003602. Epub 2013 Jul 3. [Article]
- Tommasi S, Elliot DJ, Hulin JA, Lewis BC, McEvoy M, Mangoni AA: Human dimethylarginine dimethylaminohydrolase 1 inhibition by proton pump inhibitors and the cardiovascular risk marker asymmetric dimethylarginine: in vitro and in vivo significance. Sci Rep. 2017 Jun 6;7(1):2871. doi: 10.1038/s41598-017-03069-1. [Article]
Enzymes
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
Inhibitor
General Function
A cytochrome P450 monooxygenase involved in the metabolism of polyunsaturated fatty acids (PUFA) (PubMed:18577768, PubMed:19965576, PubMed:20972997). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase) (PubMed:18577768, PubMed:19965576, PubMed:20972997). Catalyzes the hydroxylation of carbon-hydrogen bonds. Hydroxylates PUFA specifically at the omega-1 position (PubMed:18577768). Catalyzes the epoxidation of double bonds of PUFA (PubMed:19965576, PubMed:20972997). Also metabolizes plant monoterpenes such as limonene. Oxygenates (R)- and (S)-limonene to produce carveol and perillyl alcohol (PubMed:11950794). Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine. Hydroxylates fenbendazole at the 4' position (PubMed:23959307).
Specific Function
(R)-limonene 6-monooxygenase activity
Gene Name
CYP2C19
Uniprot ID
Uniprot Name
Cytochrome P450 2C19
Molecular Weight
55944.565 Da
References
- Klotz U: Clinical impact of CYP2C19 polymorphism on the action of proton pump inhibitors: a review of a special problem. Int J Clin Pharmacol Ther. 2006 Jul;44(7):297-302. [Article]
- Modak AS, Klyarytska I, Kriviy V, Tsapyak T, Rabotyagova Y: The effect of proton pump inhibitors on the CYP2C19 enzyme activity evaluated by the pantoprazole-(13)C breath test in GERD patients: clinical relevance for personalized medicine. J Breath Res. 2016 Dec 17;10(4):046017. doi: 10.1088/1752-7163/10/4/046017. [Article]
- Esomeprazole Therapy and CYP2C19 Genotype [Link]
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
General Function
A cytochrome P450 monooxygenase involved in the metabolism of sterols, steroid hormones, retinoids and fatty acids (PubMed:10681376, PubMed:11093772, PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:19965576, PubMed:20702771, PubMed:21490593, PubMed:21576599). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase). Catalyzes the hydroxylation of carbon-hydrogen bonds (PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:21490593, PubMed:21576599, PubMed:2732228). Exhibits high catalytic activity for the formation of hydroxyestrogens from estrone (E1) and 17beta-estradiol (E2), namely 2-hydroxy E1 and E2, as well as D-ring hydroxylated E1 and E2 at the C-16 position (PubMed:11555828, PubMed:12865317, PubMed:14559847). Plays a role in the metabolism of androgens, particularly in oxidative deactivation of testosterone (PubMed:15373842, PubMed:15764715, PubMed:22773874, PubMed:2732228). Metabolizes testosterone to less biologically active 2beta- and 6beta-hydroxytestosterones (PubMed:15373842, PubMed:15764715, PubMed:2732228). Contributes to the formation of hydroxycholesterols (oxysterols), particularly A-ring hydroxylated cholesterol at the C-4beta position, and side chain hydroxylated cholesterol at the C-25 position, likely contributing to cholesterol degradation and bile acid biosynthesis (PubMed:21576599). Catalyzes bisallylic hydroxylation of polyunsaturated fatty acids (PUFA) (PubMed:9435160). Catalyzes the epoxidation of double bonds of PUFA with a preference for the last double bond (PubMed:19965576). Metabolizes endocannabinoid arachidonoylethanolamide (anandamide) to 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid ethanolamides (EpETrE-EAs), potentially modulating endocannabinoid system signaling (PubMed:20702771). Plays a role in the metabolism of retinoids. Displays high catalytic activity for oxidation of all-trans-retinol to all-trans-retinal, a rate-limiting step for the biosynthesis of all-trans-retinoic acid (atRA) (PubMed:10681376). Further metabolizes atRA toward 4-hydroxyretinoate and may play a role in hepatic atRA clearance (PubMed:11093772). Responsible for oxidative metabolism of xenobiotics. Acts as a 2-exo-monooxygenase for plant lipid 1,8-cineole (eucalyptol) (PubMed:11159812). Metabolizes the majority of the administered drugs. Catalyzes sulfoxidation of the anthelmintics albendazole and fenbendazole (PubMed:10759686). Hydroxylates antimalarial drug quinine (PubMed:8968357). Acts as a 1,4-cineole 2-exo-monooxygenase (PubMed:11695850). Also involved in vitamin D catabolism and calcium homeostasis. Catalyzes the inactivation of the active hormone calcitriol (1-alpha,25-dihydroxyvitamin D(3)) (PubMed:29461981).
Specific Function
1,8-cineole 2-exo-monooxygenase activity
Gene Name
CYP3A4
Uniprot ID
Uniprot Name
Cytochrome P450 3A4
Molecular Weight
57342.67 Da
Transporters
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
Inhibitor
General Function
Translocates drugs and phospholipids across the membrane (PubMed:2897240, PubMed:35970996, PubMed:8898203, PubMed:9038218). 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 (PubMed:8898203). Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells (PubMed:2897240, PubMed:35970996, PubMed:9038218).
Specific Function
ABC-type xenobiotic transporter activity
Gene Name
ABCB1
Uniprot ID
Uniprot Name
ATP-dependent translocase ABCB1
Molecular Weight
141477.255 Da
References
- Pauli-Magnus C, Rekersbrink S, Klotz U, Fromm MF: Interaction of omeprazole, lansoprazole and pantoprazole with P-glycoprotein. Naunyn Schmiedebergs Arch Pharmacol. 2001 Dec;364(6):551-7. [Article]
- Wedemeyer RS, Blume H: Pharmacokinetic drug interaction profiles of proton pump inhibitors: an update. Drug Saf. 2014 Apr;37(4):201-11. doi: 10.1007/s40264-014-0144-0. [Article]
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Inhibitor
General Function
Functions as an organic anion/dicarboxylate exchanger that couples organic anion uptake indirectly to the sodium gradient (PubMed:14586168, PubMed:15644426, PubMed:15846473, PubMed:16455804, PubMed:31553721). Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) (PubMed:14586168, PubMed:15846473, PubMed:15864504, PubMed:22108572, PubMed:23832370). Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain (PubMed:11306713, PubMed:14586168, PubMed:15846473). E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange (PubMed:26377792). Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule (PubMed:11907186). Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate (PubMed:22108572, PubMed: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 (PubMed:28534121). May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside (PubMed: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 (PubMed:11669456, PubMed:15846473, PubMed: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) (PubMed:14675047). May contribute to the release of cortisol in the adrenals (PubMed: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).
Specific Function
organic anion transmembrane transporter activity
Gene Name
SLC22A8
Uniprot ID
Uniprot Name
Organic anion transporter 3
Molecular Weight
59855.585 Da
References
- Chioukh R, Noel-Hudson MS, Ribes S, Fournier N, Becquemont L, Verstuyft C: Proton pump inhibitors inhibit methotrexate transport by renal basolateral organic anion transporter hOAT3. Drug Metab Dispos. 2014 Dec;42(12):2041-8. doi: 10.1124/dmd.114.058529. Epub 2014 Sep 19. [Article]
Drug created at June 13, 2005 13:24 / Updated at October 01, 2024 12:45