Identification
- Summary
Dexlansoprazole is a proton pump inhibitor used to help gastrointestinal ulcers heal, to treat symptoms of gastroesophageal reflux disease (GERD), to eradicate Helicobacter pylori, and to treat hypersecretory conditions such as Zollinger-Ellison Syndrome.
- Brand Names
- Dexilant
- Generic Name
- Dexlansoprazole
- DrugBank Accession Number
- DB05351
- Background
Dexlansoprazole is a new generation proton pump inhibitor (PPI) used for the management of symptoms associated with gastroesophageal reflux disease (GERD) and erosive esophagitis. Dexlansoprazole is the R-enantiomer of Lansoprazole, which is composed of a racemic mixture of the R- and S-enantiomers. Compared to the older generation of PPIs (which includes Pantoprazole, Omeprazole, and Lansoprazole) 9, dexlansoprazole MR has a unique pharmacokinetic profile due to its delayed-release and dual-delivery release system. The active ingredient is released in two phases at different pH values and at different time points, resulting in two peak concentrations in the blood; 25% of the dose is released at pH 5.5 in the proximal duodenum, while the remaining 75% is released at pH 6.75 in the distal small intestine 2. As a result, dexlansoprazole has a peak concentration within 1-2 hours after dosing and another within 4-5 hours Label. Dexlansoprazole's unique pharmacokinetics addresses limitations of the older generation PPIs including short plasma half-life, break-through symptoms, and need for meal-associated dosing 3. These characteristics make dexlansoprazole a good option for people who struggle with adherence and strict dosage timing before meals10,1.
Dexlansoprazole exerts its stomach acid-suppressing effects in the same way as other drugs in the PPI family by inhibiting the final step in gastric acid production. Dexlansoprazole targets the (H+, K+)-ATPase enzyme, which is involved in the secretion of hydrochloric acid through the exchange of H+ ions from the cytoplasm for K+ ions. Normally functioning (H+, K+)-ATPase stimulates hydrochloric acid secretion into the gastric lumen thereby increasing stomach acidity and lowering pH. Once absorbed into circulation, dexlansoprazole covalently binds to the sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells, which leads to inhibition of both basal and stimulated gastric acid secretion. Despite dexlansoprazole's unique pharmacokinetic profile, efficacy in management of GERD symptoms is considered similar to other medications within the PPI class including Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, and Rabeprazole.
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 dexlansoprazole have 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 13. PPIs such as dexlansoprazole 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 dimethylarginine (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes 11,12.
Dexlansoprazole doses should be slowly lowered, or tapered, before discontinuing as rapid discontinuation of PPIs such as dexlansoprazole may cause a rebound effect and a short term increase in hypersecretion 14.
- Type
- Small Molecule
- Groups
- Approved, Investigational
- Structure
Structure for Dexlansoprazole (DB05351)
- Weight
- Average: 369.36
Monoisotopic: 369.075882366 - Chemical Formula
- C16H14F3N3O2S
- Synonyms
- 2-((R)-((3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridinyl)methyl)sulfinyl)-1H-benzimidazole
- Dexlansoprazole
- External IDs
- T-168390
- TAK-390
- TAK-390MR
Pharmacology
- Indication
Dexlansoprazole is indicated for healing all grades of erosive esophagitis (EE), maintaining and healing of EE and relief of heartburn, and treating heartburn associated with symptomatic non-erosive gastroesophageal reflux disease (GERD).
Reduce drug development failure ratesBuild, train, & validate machine-learning modelswith evidence-based and structured datasets.Build, train, & validate predictive machine-learning models with structured datasets.- Associated Conditions
- Contraindications & Blackbox Warnings
Avoid life-threatening adverse drug eventsImprove clinical decision support with information on contraindications & blackbox warnings, population restrictions, harmful risks, & more.Avoid life-threatening adverse drug events & improve clinical decision support.- Pharmacodynamics
Dexlansoprazole is a proton pump inhibitor (PPI) and is included in the drug class of antisecretory compounds. It blocks the final step of gastric acid secretion by specific inhibition of the (H+, K+)-ATPase at the secretory surface of the parietal cells on gastric mucosa.
- Mechanism of action
Dexlansoprazole inhibits the H/K ATPase enzyme, which is involved in the secretion of hydrochloric acid, hydrolyzing ATP and exchanging H+ ions from the cytoplasm for K+ ions in the secretory canaliculus, which results in HCl secretion into the gastric lumen. Dexlansoprazole inhibits this effect of H/K ATPase by demonstrating a high degree of activation in the acidic environment. After passing through the liver and reaching the gastric parietal cells activated by a meal, PPIs undergo protonation in the acidic pH environment, followed by conversion to sulphenamide which represents the active form of the drug. Sulphenamide inhibits the activity of the proton pump and hence the transport of hydrogen ions into the gastric lumen via covalent binding to the SH groups of the cysteine residues of H/K ATPase 2. The delivery technology of dexlansoprazole MR is designed to release the drug in two separate pH-dependent phases, the first in the proximal duodenum (25% of total drug dose) and the second (75% of total drug dose) in the more distal small intestine. Dexlansoprazole reduces both basal and stimulated gastric acid secretion.
Target Actions Organism APotassium-transporting ATPase subunit beta inhibitorHumans APotassium-transporting ATPase alpha chain 1 inhibitorHumans UN(G),N(G)-dimethylarginine dimethylaminohydrolase 1 Not Available Humans - Absorption
After oral administration, the peak plasma concentration increases approximately dose proportionally. The dual delayed release formulation achieves two plasma concentration peaks, where the first peak occurs one to two hours after administration, followed by a second peak within four to five hours. The delivery technology of dexlansoprazole MR is designed to release the drug in two separate pH-dependent phases, the first in the proximal duodenum (25% of total drug dose) and the second (75% of total drug dose) in the more distal small intestine. The median time (Tmax) to peak plasma concentrations (Cmax) of 30 mg dexlansoprazole was 4 hours and ranged from 1 to 6 hours with the Cmax value of 688 ng/mL. AUC was found to be 3275 (ng∙h/mL)Label.
- Volume of distribution
The apparent volume of distribution after multiple doses in symptomatic GERD patients was 40.3 L Label.
- Protein binding
Plasma protein binding of dexlansoprazole ranged from 96% to 99% in healthy subjects and was independent of concentration from 0.01 to 20 mcg/mL Label.
- Metabolism
Dexlansoprazole is extensively metabolized in the liver by oxidation, reduction, and subsequent formation of sulfate, glucuronide and glutathione conjugates to inactive metabolites. Oxidative metabolites are formed by the cytochrome P450 (CYP) enzyme system including hydroxylation mainly by CYP2C19, and oxidation to the sulfone by CYP3A4. Dexlansoprazole is the major circulating component in plasma regardless of CYP2C19 metabolizer status. In CYP2C19 intermediate and extensive metabolizers, the major plasma metabolites are 5-hydroxy dexlansoprazole and its glucuronide conjugate, while in CYP2C19 poor metabolizers dexlansoprazole sulfone is the major plasma metabolite.
Hover over products below to view reaction partners
- Route of elimination
Dexlansoprazole is cleared from the body by either fecal excretion (50.7%) or renal excretion (47.6%) following oral ingestion, with no unchanged drug detected in the urine.
- Half-life
Dexlansoprazole is eliminated with a half-life of approximately one to two hours in healthy subjects and in patients with symptomatic GERD.
- Clearance
Apparent clearance (CL/F) in healthy subjects was 11.4 to 11.6 L/hour, respectively, after five days of 30 or 60 mg once daily administration.
- Adverse Effects
Improve decision support & research outcomesWith structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates.Improve decision support & research outcomes with our structured adverse effects data.- Toxicity
Oral LD50 value in mice, rats and dogs is > 5,000 mg/kg. Most commonly reported adverse reactions are diarrhea, abdominal pain, nausea, upper respiratory tract infection, vomiting, and flatulence. There are no reports of significant overdose but serious adverse events of hypertension have been reported in association with twice daily doses of DEXILANT 60 mg. Nonclicnial toxicology of dexlansopraole was assessed using lansoprazole studies. In two 24-month carcinogenicity studies involving rats, lansoprazole induced dose-related gastric ECL cell hyperplasia and ECL cell carcinoids and increased the incidence of intestinal metaplasia of the gastric epithelium in both sexes of rats. Dexlansoprazole is expected to have no effect on fertility and the reproductive system.
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
Interacting Gene/Enzyme Allele name Genotype(s) Defining Change(s) Type(s) Description Details Cytochrome P450 2C19 CYP2C19*2A Not Available 681G>A Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*2B Not Available 681G>A Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*3 Not Available 636G>A Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*4 Not Available 1A>G Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*5 Not Available 1297C>T Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*6 Not Available 395G>A Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*7 Not Available 19294T>A Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*22 Not Available 557G>C / 991A>G Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*24 Not Available 99C>T / 991A>G … show all Effect Inferred Poor drug metabolizer. Details Cytochrome P450 2C19 CYP2C19*35 Not Available 12662A>G Effect Inferred Poor drug metabolizer. Details
Interactions
- Drug Interactions
- 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 softwareAbametapir The serum concentration of Dexlansoprazole can be increased when it is combined with Abametapir. Abatacept The metabolism of Dexlansoprazole can be increased when combined with Abatacept. Abrocitinib The metabolism of Abrocitinib can be decreased when combined with Dexlansoprazole. Acenocoumarol The metabolism of Acenocoumarol can be decreased when combined with Dexlansoprazole. Adalimumab The metabolism of Dexlansoprazole can be increased when combined with Adalimumab. Albendazole The metabolism of Albendazole can be decreased when combined with Dexlansoprazole. Alendronic acid The therapeutic efficacy of Alendronic acid can be decreased when used in combination with Dexlansoprazole. Alpelisib The metabolism of Dexlansoprazole can be decreased when combined with Alpelisib. Amiodarone The metabolism of Dexlansoprazole can be decreased when combined with Amiodarone. Amitriptyline The metabolism of Amitriptyline can be decreased when combined with Dexlansoprazole. 
Identify potential medication risksEasily compare up to 40 drugs with our drug interaction checker.Get severity rating, description, and management advice.Learn more - Food Interactions
- Avoid St. John's Wort. This may induce the CYP3A4 metabolism of dexlansoprazole, which may cause reduced efficacy.
- Take with or without food. Dexlansoprazole's dual delayed release formulation allows it to be taken without regard to food in contrast to other PPIs.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Product Images
- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Dexilant Capsule, delayed release 30 mg/1 Oral Takeda Pharmaceuticals America, Inc. 2010-04-12 Not applicable US 
Dexilant Capsule, delayed release 60 mg/1 Oral Physicians Total Care, Inc. 2010-08-19 Not applicable US 
Dexilant Capsule, delayed release 60 mg Nasogastric; Oral Takeda 2010-08-05 Not applicable Canada 
Dexilant Capsule, delayed release 60 mg/1 Oral A-S Medication Solutions 2010-04-12 Not applicable US Dexilant Capsule, delayed release 30 mg Nasogastric; Oral Takeda 2010-08-05 Not applicable Canada Dexilant Capsule, delayed release 60 mg/1 Oral Takeda Pharmaceuticals America, Inc. 2010-04-12 Not applicable US 
Dexilant Capsule, delayed release 60 mg/1 Oral Cardinal Health 107, LLC 2010-04-12 Not applicable US 
Dexilant SoluTab Tablet, orally disintegrating, delayed release 30 mg/1 Oral Takeda Pharmaceuticals America, Inc. 2016-01-26 2016-08-03 US Dexlansoprazole Capsule, delayed release 60 mg Nasogastric; Oral Takeda Not applicable Not applicable Canada Dexlansoprazole Capsule, delayed release 30 mg Nasogastric; Oral Takeda Not applicable Not applicable Canada - Generic Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Dexlansoprazole Capsule, delayed release 60 mg/1 Oral Par Pharmaceutical, Inc. 2022-11-22 Not applicable US Dexlansoprazole delayed release Capsule, delayed release 60 mg/1 Oral TWi Pharmaceuticals, Inc. 2022-01-01 Not applicable US Dexlansoprazole delayed release Capsule, delayed release 60 mg/1 Oral TWi Pharmaceuticals, Inc. 2022-12-01 Not applicable US Dexlansoprazole delayed release Capsule, delayed release 30 mg/1 Oral A-S Medication Solutions 2022-01-01 Not applicable US Dexlansoprazole delayed release Capsule, delayed release 30 mg/1 Oral TWi Pharmaceuticals, Inc. 2022-01-01 Not applicable US Dexlansoprazole delayed release Capsule, delayed release 30 mg/1 Oral TWi Pharmaceuticals, Inc. 2022-12-01 Not applicable US Dexlansoprazole delayed release Capsule, delayed release 60 mg/1 Oral A-S Medication Solutions 2022-01-01 Not applicable US - Mixture Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image DEXGARD 30/30 MG MR KAPSUL, 30 ADET Dexlansoprazole (30 mg) + Domperidone (30 mg) Capsule Oral NUVOMED İLAÇ SAN.TİC. A.Ş. 2020-08-14 2021-11-12 Turkey 
DEXGARD 30/30 MG MR KAPSUL, 60 ADET Dexlansoprazole (30 mg) + Domperidone (30 mg) Capsule Oral NUVOMED İLAÇ SAN.TİC. A.Ş. 2020-08-14 2021-11-12 Turkey DUEDOM 30/10 MG KAPSÜL, 30 ADET Dexlansoprazole (30 mg) + Domperidone (10 mg) Capsule Oral CELTİS İLAÇ SAN. VE TİC. A.Ş. 2020-08-14 Not applicable Turkey DUEDOM 60/10 MG KAPSÜL, 30 ADET Dexlansoprazole (60 mg) + Domperidone (10 mg) Capsule Oral CELTİS İLAÇ SAN. VE TİC. A.Ş. 2020-08-14 Not applicable Turkey
Categories
- ATC Codes
- A02BC06 — Dexlansoprazole
- Drug Categories
- 2-Pyridinylmethylsulfinylbenzimidazoles
- Acid Reducers
- Alimentary Tract and Metabolism
- Anti-Ulcer Agents
- 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 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
- 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
- Organic compounds
- Super Class
- Organoheterocyclic compounds
- Class
- Benzimidazoles
- Sub Class
- Sulfinylbenzimidazoles
- Direct Parent
- Sulfinylbenzimidazoles
- Alternative Parents
- Methylpyridines / Alkyl aryl ethers / Benzenoids / Imidazoles / Heteroaromatic compounds / Sulfoxides / Sulfinyl compounds / Azacyclic compounds / Organopnictogen compounds / Organonitrogen compounds show 4 more
- Substituents
- Alkyl aryl ether / Alkyl fluoride / Alkyl halide / Aromatic heteropolycyclic compound / Azacycle / Azole / Benzenoid / Ether / Heteroaromatic compound / Hydrocarbon derivative show 15 more
- Molecular Framework
- Aromatic heteropolycyclic compounds
- External Descriptors
- Not Available
- Affected organisms
- Not Available
Chemical Identifiers
- UNII
- UYE4T5I70X
- CAS number
- 138530-94-6
- InChI Key
- MJIHNNLFOKEZEW-RUZDIDTESA-N
- InChI
- InChI=1S/C16H14F3N3O2S/c1-10-13(20-7-6-14(10)24-9-16(17,18)19)8-25(23)15-21-11-4-2-3-5-12(11)22-15/h2-7H,8-9H2,1H3,(H,21,22)/t25-/m1/s1
- IUPAC Name
- 2-[(R)-[3-methyl-4-(2,2,2-trifluoroethoxy)pyridin-2-yl]methanesulfinyl]-1H-1,3-benzodiazole
- SMILES
- CC1=C(OCC(F)(F)F)C=CN=C1C[S@@](=O)C1=NC2=CC=CC=C2N1
References
- General References
- Behm BW, Peura DA: Dexlansoprazole MR for the management of gastroesophageal reflux disease. Expert Rev Gastroenterol Hepatol. 2011 Aug;5(4):439-45. doi: 10.1586/egh.11.37. [Article]
- Skrzydlo-Radomanska B, Radwan P: Dexlansoprazole - a new-generation proton pump inhibitor. Prz Gastroenterol. 2015;10(4):191-6. doi: 10.5114/pg.2015.56109. Epub 2015 Dec 16. [Article]
- Frye JW, Peura DA: Managing gastroesophageal reflux disease - comparative efficacy and outcomes of dexlansoprazole MR. Ther Clin Risk Manag. 2015 Oct 30;11:1649-56. doi: 10.2147/TCRM.S66680. eCollection 2015. [Article]
- Peura DA, Metz DC, Dabholkar AH, Paris MM, Yu P, Atkinson SN: Safety profile of dexlansoprazole MR, a proton pump inhibitor with a novel dual delayed release formulation: global clinical trial experience. Aliment Pharmacol Ther. 2009 Nov 15;30(10):1010-21. doi: 10.1111/j.1365-2036.2009.04137.x. Epub 2009 Sep 4. [Article]
- Kukulka M, Wu J, Perez MC: Pharmacokinetics and safety of dexlansoprazole MR in adolescents with symptomatic GERD. J Pediatr Gastroenterol Nutr. 2012 Jan;54(1):41-7. doi: 10.1097/MPG.0b013e31822a323a. [Article]
- Fass R, Frazier R: The role of dexlansoprazole modified-release in the management of gastroesophageal reflux disease. Therap Adv Gastroenterol. 2017 Feb;10(2):243-251. doi: 10.1177/1756283X16681701. Epub 2017 Jan 5. [Article]
- Wittbrodt ET, Baum C, Peura DA: Delayed release dexlansoprazole in the treatment of GERD and erosive esophagitis. Clin Exp Gastroenterol. 2009;2:117-28. Epub 2009 Nov 17. [Article]
- Grabowski B, Lee RD: Absorption, distribution, metabolism and excretion of [14C]dexlansoprazole in healthy male subjects. Clin Drug Investig. 2012 May 1;32(5):319-32. doi: 10.2165/11630930-000000000-00000. [Article]
- Tytgat GN: Shortcomings of the first-generation proton pump inhibitors. Eur J Gastroenterol Hepatol. 2001 May;13 Suppl 1:S29-33. [Article]
- Lee RD, Vakily M, Mulford D, Wu J, Atkinson SN: Clinical trial: the effect and timing of food on the pharmacokinetics and pharmacodynamics of dexlansoprazole MR, a novel Dual Delayed Release formulation of a proton pump inhibitor--evidence for dosing flexibility. Aliment Pharmacol Ther. 2009 Apr 15;29(8):824-33. doi: 10.1111/j.1365-2036.2009.03979.x. Epub 2008 Jan 20. [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]
- FDA Approved Drug Products: Dexilant (dexlansoprazole) delayed-release oral capsules [Link]
- External Links
- PubChem Compound
- 9578005
- PubChem Substance
- 347827723
- ChemSpider
- 7852369
- 816346
- ChEBI
- 135931
- ChEMBL
- CHEMBL1201863
- ZINC
- ZINC000003830986
- PharmGKB
- PA166110257
- Wikipedia
- Dexlansoprazole
- FDA label
- Download (284 KB)
- MSDS
- Download (201 KB)
Clinical Trials
- Clinical Trials
Phase Status Purpose Conditions Count 4 Completed Treatment Barrett's Esophagus / Inflammation 1 4 Completed Treatment Gastro-esophageal Reflux Disease (GERD) 2 4 Completed Treatment Gastro-esophageal Reflux Disease (GERD) / Proton Pump Inhibitors 1 4 Completed Treatment H Pylori Infection Eradication 1 4 Completed Treatment Helicobacter Pylori Infection 1 4 Completed Treatment Hypothyroidism;Postablative 1 4 Unknown Status Treatment Gastro-esophageal Reflux Disease (GERD) 1 4 Unknown Status Treatment Hypertrophy of Lingual Tonsil / Laryngopharyngeal Reflux (LPR) 1 4 Withdrawn Treatment Chest Pain / Gastrointestinal Reflux Disease 1 3 Completed Treatment Gastro-esophageal Reflux Disease (GERD) 4
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
Form Route Strength Tablet 30 mg Tablet 60 mg Capsule Oral Capsule, delayed release Nasogastric; Oral 30 mg Capsule, delayed release Nasogastric; Oral 60 mg Capsule, delayed release Oral 60 mg/1 Capsule Oral 30 mg Capsule Oral 60 mg Capsule, delayed release 60 mg Capsule, extended release Oral 60 MG Capsule, delayed release Oral Tablet, orally disintegrating, delayed release Oral 30 mg/1 Capsule, delayed release 30 mg Capsule, coated Oral 30 mg Capsule, delayed release Oral 30 mg Capsule, delayed release Oral 60 mg Capsule, delayed release Oral 30 mg/1 Capsule, coated Oral 60 mg Capsule, extended release Oral 30 mg - Prices
- Not Available
- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region CA1327010 No 1994-02-15 2011-02-15 Canada CA2375201 No 2010-02-09 2020-06-15 Canada US7399485 Yes 2008-07-15 2018-11-26 US US6328994 Yes 2001-12-11 2019-11-17 US US7875292 Yes 2011-01-25 2019-11-17 US US7431942 Yes 2008-10-07 2019-11-17 US US6462058 Yes 2002-10-08 2020-12-15 US US6939971 Yes 2005-09-06 2020-12-15 US US8173158 Yes 2012-05-08 2030-09-17 US US6664276 Yes 2003-12-16 2023-07-30 US US8784885 Yes 2014-07-22 2024-04-15 US US9233103 No 2016-01-12 2032-03-05 US US9011926 No 2015-04-21 2026-02-24 US US9238029 No 2016-01-19 2026-01-17 US US8722084 Yes 2014-05-13 2024-04-15 US US9145389 No 2015-09-29 2020-06-15 US US8871273 Yes 2014-10-28 2028-07-11 US US8461187 Yes 2013-06-11 2026-07-17 US US8105626 Yes 2012-01-31 2027-03-27 US US7285668 Yes 2007-10-23 2020-12-15 US US7790755 Yes 2010-09-07 2027-02-02 US US9241910 No 2016-01-26 2029-03-10 US US6238994 Yes 2001-05-29 2019-11-17 US
Properties
- State
- Solid
- Experimental Properties
Property Value Source melting point (°C) Decomposes at 140ºC MSDS water solubility 0.21mg/mL at pH7.0 MSDS logP 2.38 MSDS pKa 8.87 MSDS - Predicted Properties
Property Value Source Water Solubility 0.25 mg/mL ALOGPS logP 2.84 ALOGPS logP 3.03 Chemaxon logS -3.2 ALOGPS pKa (Strongest Acidic) 9.35 Chemaxon pKa (Strongest Basic) 4.16 Chemaxon Physiological Charge 0 Chemaxon Hydrogen Acceptor Count 4 Chemaxon Hydrogen Donor Count 1 Chemaxon Polar Surface Area 67.87 Å2 Chemaxon Rotatable Bond Count 6 Chemaxon Refractivity 87.61 m3·mol-1 Chemaxon Polarizability 34.5 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 Yes Chemaxon - Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
Spectrum Spectrum Type Splash Key Predicted MS/MS Spectrum - 10V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 10V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Negative (Annotated) Predicted LC-MS/MS Not Available
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Hydrogen:potassium-exchanging atpase activity
- Specific Function
- Required for stabilization and maturation of the catalytic proton pump alpha subunit and may also involved in cell adhesion and establishing epithelial cell polarity.
- Gene Name
- ATP4B
- Uniprot ID
- P51164
- Uniprot Name
- Potassium-transporting ATPase subunit beta
- Molecular Weight
- 33366.95 Da
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Sodium:potassium-exchanging atpase activity
- Specific Function
- Catalyzes the hydrolysis of ATP coupled with the exchange of H(+) and K(+) ions across the plasma membrane. Responsible for acid production in the stomach.
- Gene Name
- ATP4A
- Uniprot ID
- P20648
- Uniprot Name
- Potassium-transporting ATPase alpha chain 1
- Molecular Weight
- 114117.74 Da
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- General Function
- Metal ion binding
- Specific 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.
- Gene Name
- DDAH1
- Uniprot ID
- O94760
- 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
- Unknown
- Actions
- SubstrateInhibitor
- General Function
- Steroid hydroxylase activity
- Specific Function
- 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 im...
- Gene Name
- CYP2C19
- Uniprot ID
- P33261
- Uniprot Name
- Cytochrome P450 2C19
- Molecular Weight
- 55930.545 Da
References
- Goh KL, Choi MG, Hsu PI, Chun HJ, Mahachai V, Kachintorn U, Leelakusolvong S, Kim N, Rani AA, Wong BC, Wu J, Chiu CT, Shetty V, Bocobo JC, Chan MM, Lin JT: Pharmacological and Safety Profile of Dexlansoprazole: A New Proton Pump Inhibitor - Implications for Treatment of Gastroesophageal Reflux Disease in the Asia Pacific Region. J Neurogastroenterol Motil. 2016 Jul 30;22(3):355-66. doi: 10.5056/jnm15150. [Article]
- Li XQ, Andersson TB, Ahlstrom M, Weidolf L: Comparison of inhibitory effects of the proton pump-inhibiting drugs omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole on human cytochrome P450 activities. Drug Metab Dispos. 2004 Aug;32(8):821-7. [Article]
- Dexlanzoprazole FDA label [File]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Substrate
- General Function
- Vitamin d3 25-hydroxylase activity
- Specific Function
- Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation react...
- Gene Name
- CYP3A4
- Uniprot ID
- P08684
- Uniprot Name
- Cytochrome P450 3A4
- Molecular Weight
- 57342.67 Da
Drug created at November 18, 2007 18:24 / Updated at March 21, 2023 17:58