General
Preferred name
DEXLANSOPRAZOLE
Synonyms
(R)-Lansoprazole ()
T 168390, TAK 390,(R)-Lansoprazole ()
Dexlansoprazol ()
NSC-758710 ()
T-168390 ()
Kapidex ()
Lansoprazole, (r)- ()
Dexilant solutab ()
Lansoprazole r-form ()
TAK-390 ()
Dexilant ()
P&D ID
PD001199
CAS
138530-94-6
Tags
available
drug
Approved by
FDA
First approval
2009
Drug indication
NSAID-associated gastric ulcer
Erosive esophagitis
Peptic ulcer
Gastroesophageal reflux disease
Non-erosive gastro-esophageal reflux disease
Drug Status
approved
investigational
Max Phase
4.0
Probe control
Probe control not defined
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
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 (ngâh/mL)[FDA Label].
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.
MOA
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 [A19567]. 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.
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).
DESCRIPTION
In addition to being an approved drug with INN dexlansoprazole, (R)-lansoprazole is also a component of the approved drug lansoprazole, a racemic mixture of (R)- and (S)- stereoisomers. Use this PubChem link to view all 3 isomers.
(GtoPdb)
DESCRIPTION
(R)-Lansoprazole is the R enantiomer of Lansoprazole, Lansoprazole (AG 1749) is an orally active proton pump inhibitor which prevents the stomach from producing acid. Lansoprazole (AG 1749) is a potent brain penetrant neutral sphingomyelinase (N-SMase) inhibitor (exosome inhibitor)[1][2].
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Cell lines
2
Organisms
0
Compound Sets
16
Cayman Chemical Bioactives
ChEMBL Approved Drugs
ChEMBL Drugs
Drug Repurposing Hub
DrugBank
DrugBank Approved Drugs
DrugCentral
DrugCentral Approved Drugs
DrugMAP
DrugMAP Approved Drugs
Guide to Pharmacology
MedChem Express Bioactive Compound Library
NCATS Inxight Approved Drugs
Selleckchem Bioactive Compound Library
The Spectrum Collection
ZINC Tool Compounds
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
34
Molecular Weight
369.08
Hydrogen Bond Acceptors
4
Hydrogen Bond Donors
1
Rotatable Bonds
5
Ring Count
3
Aromatic Ring Count
3
cLogP
3.52
TPSA
67.87
Fraction CSP3
0.25
Chiral centers
1.0
Largest ring
6.0
QED
0.75
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Indication
gastroesophageal reflux disease (GERD), erosive esophagitis (EE)
heartburn
Target
ATP4A, ATP4B
ATP4A
Proton Pump
ATPase,Proton Pump
MOA
ATPase inhibitor
Pathway
Membrane Transporter/Ion Channel
Source data
