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Dexlansoprazole | CAS No: 138530-94-6 | GMP-certified suppliers
A medication that provides acid suppression for healing erosive esophagitis, maintaining remission, and relieving heartburn in gastroesophageal reflux disease patients aged 12 and older.
Therapeutic categories
2-PyridinylmethylsulfinylbenzimidazolesAcid ReducersAlimentary Tract and MetabolismAnti-Ulcer AgentsBenzimidazolesCytochrome P-450 CYP2C19 Inhibitors
Generic name
Dexlansoprazole
Molecule type
small molecule
CAS number
138530-94-6
DrugBank ID
DB05351
Approval status
Approved drug, Investigational drug
ATC code
A02BC06
Primary indications
- Dexlansoprazole is a proton pump inhibitor (PPI) indicated for the:
- Healing of all grades of erosive esophagitis (EE) for up to eight weeks in patients 12 years of age and older
- Maintenance of healed EE and relief of heartburn for up to six months in adults and 16 weeks in patients 12 to 17 years of age
Product Snapshot
- Dexlansoprazole is an oral small molecule proton pump inhibitor available in various tablet and delayed-release capsule formulations
- It is indicated primarily for the treatment and maintenance of erosive esophagitis and symptomatic non-erosive gastroesophageal reflux disease (GERD)
- Dexlansoprazole holds regulatory approval in the US and Canada with both approved and investigational status
Clinical Overview
Dexlansoprazole is a proton pump inhibitor (PPI) indicated primarily for the treatment of gastroesophageal reflux disease (GERD) and erosive esophagitis (EE). Clinically, it is approved for healing all grades of EE in patients aged 12 years and older, maintenance of healed EE and heartburn relief in adults and adolescents, and treatment of symptomatic non-erosive GERD in patients 12 years and older.
Pharmacologically, dexlansoprazole is the R-enantiomer of lansoprazole, delivering acid suppression through inhibition of the gastric H+/K+-ATPase enzyme, the final step in acid secretion by parietal cells. This enzyme exchanges intracellular hydrogen ions (H+) for extracellular potassium ions (K+), facilitating hydrochloric acid release into the gastric lumen. Inhibiting this proton pump results in reduced basal and stimulated gastric acid secretion.
Dexlansoprazole distinguishes itself from earlier-generation PPIs by its dual delayed-release formulation. This delivery system extends plasma concentration duration, mitigating the need for meal-associated dosing and overcoming limitations such as short plasma half-life seen with older PPIs.
Key ADME characteristics include metabolism primarily via CYP2C19 and CYP3A enzymes, with dexlansoprazole acting as a weak inhibitor of CYP2C19. This implicates potential drug-drug interactions in polypharmacy contexts. The compound's pharmacokinetic profile supports twice-daily or once-daily dosing depending on the clinical indication.
Safety considerations include class-related risks such as potential rebound acid hypersecretion following cessation, increased susceptibility to bacterial infections, and nutrient deficiencies (vitamin B12, iron, magnesium, calcium) that may contribute to bone density reduction and fractures. Dexlansoprazole can cause elevated gastrin levels and enterochromaffin-like cell hyperplasia, potentially leading to false positives in neuroendocrine tumor diagnostics due to increased chromogranin A levels. False-positive urine screens for tetrahydrocannabinol can also occur.
Notable commercial formulations include dual-release capsules marketed globally under varying brand names, typically prescribed in gastroenterology settings for comprehensive acid suppression.
For sourcing and quality assurance, procurement of dexlansoprazole API should prioritize compliance with global pharmacopeial standards, stringent control of chiral purity (defined R-enantiomer content), and verification of physicochemical parameters reflecting the unique delayed-release profile. Reliable supply chains and thorough stability data are critical to maintaining formulation consistency and regulatory compliance.
Pharmacologically, dexlansoprazole is the R-enantiomer of lansoprazole, delivering acid suppression through inhibition of the gastric H+/K+-ATPase enzyme, the final step in acid secretion by parietal cells. This enzyme exchanges intracellular hydrogen ions (H+) for extracellular potassium ions (K+), facilitating hydrochloric acid release into the gastric lumen. Inhibiting this proton pump results in reduced basal and stimulated gastric acid secretion.
Dexlansoprazole distinguishes itself from earlier-generation PPIs by its dual delayed-release formulation. This delivery system extends plasma concentration duration, mitigating the need for meal-associated dosing and overcoming limitations such as short plasma half-life seen with older PPIs.
Key ADME characteristics include metabolism primarily via CYP2C19 and CYP3A enzymes, with dexlansoprazole acting as a weak inhibitor of CYP2C19. This implicates potential drug-drug interactions in polypharmacy contexts. The compound's pharmacokinetic profile supports twice-daily or once-daily dosing depending on the clinical indication.
Safety considerations include class-related risks such as potential rebound acid hypersecretion following cessation, increased susceptibility to bacterial infections, and nutrient deficiencies (vitamin B12, iron, magnesium, calcium) that may contribute to bone density reduction and fractures. Dexlansoprazole can cause elevated gastrin levels and enterochromaffin-like cell hyperplasia, potentially leading to false positives in neuroendocrine tumor diagnostics due to increased chromogranin A levels. False-positive urine screens for tetrahydrocannabinol can also occur.
Notable commercial formulations include dual-release capsules marketed globally under varying brand names, typically prescribed in gastroenterology settings for comprehensive acid suppression.
For sourcing and quality assurance, procurement of dexlansoprazole API should prioritize compliance with global pharmacopeial standards, stringent control of chiral purity (defined R-enantiomer content), and verification of physicochemical parameters reflecting the unique delayed-release profile. Reliable supply chains and thorough stability data are critical to maintaining formulation consistency and regulatory compliance.
Identification & chemistry
| Generic name | Dexlansoprazole |
|---|---|
| Molecule type | Small molecule |
| CAS | 138530-94-6 |
| UNII | UYE4T5I70X |
| DrugBank ID | DB05351 |
Pharmacology
| Summary | Dexlansoprazole is a proton pump inhibitor that reduces gastric acid secretion by selectively inhibiting the H+/K+ ATPase enzyme in gastric parietal cells. This inhibition blocks the final step of acid production, suppressing both basal and stimulated acid secretion. Pharmacodynamically, it alters gastric acidity and increases gastrin levels, which may affect related diagnostic markers and carry risks associated with long-term acid suppression. |
|---|---|
| Mechanism of action | Dexlansoprazole suppresses gastric acid secretion by blocking the final step of acid production. It inhibits the H/K ATPase at the secretory surface of the gastric parietal cell, which is involved in the secretion of hydrochloric acid. H/K ATPase is a proton pump responsible for hydrolyzing ATP and exchanging H<sup>+</sup> ions from the cytoplasm for K<sup>+</sup> ions in the secretory canaliculus: this action results in hydrochloric acid secretion into the gastric lumen. |
| Pharmacodynamics | Dexlansoprazole is a proton pump inhibitor (PPI) that suppresses both basal and stimulated gastric acid secretion. PPIs are associated with a risk for a rebound effect and a short-term increase in hypersecretion; thus, such risk cannot be excluded with dexlansoprazole. With long-term use, PPIs are also associated with a risk of increased susceptibility to bacterial infections, vitamin B12 and iron deficiency, and hypomagnesemia and hypocalcemia, possibly leading to osteoporosis and bone fractures. Dexlansoprazole is reported to interfere with the secretin stimulation test and create false positive urine screening tests for tetrahydrocannabinol. Dexlansoprazole can increase gastrin levels, which can cause enterochromaffin-like cell hyperplasia and increase serum CgA levels. Increased CgA levels may cause false positive results in diagnostic investigations for neuroendocrine tumours. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Potassium-transporting ATPase alpha chain 1 | Humans | inhibitor |
| Potassium-transporting ATPase subunit beta | Humans | inhibitor |
| N(G),N(G)-dimethylarginine dimethylaminohydrolase 1 | Humans |
ADME / PK
| Absorption | The dual delayed-release formulation of dexlansoprazole results in a plasma concentration-time profile with two distinct peaks; the first peak occurs one to two hours after administration, followed by a second peak within four to five hours. About 25% of the dose is released at the pH level of 5.5 in the proximal duodenum, while the other 75% is released in the distal small intestine at the pH level of 6.75.[A19567, L48827] After oral administration of dexlansoprazole 30 or 60 mg to healthy subjects and symptomatic GERD patients, mean C<sub>max</sub> and AUC values of dexlansoprazole increased approximately dose-proportionally. Following administration of 30 mg in healthy adults, the mean (%CV) C<sub>max</sub> and AUC were 658 (40%) ng/mL and 3275 (47%) ng x h/mL, respectively. At a dose of 60 mg, the mean (%CV) C<sub>max</sub> and AUC were 1397 (51%) ng/mL and 6529 (60%) ng x h/mL, respectively. In healthy subjects, food increased C<sub>max</sub> by 12 to 55% and AUC by 9 to 37%. The effect of food on Tmax varied, as both an increase and a decrease was observed. |
|---|---|
| Half-life | Dexlansoprazole is eliminated with a half-life of approximately one to two hours.[A19573, L48827] |
| 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. |
| Metabolism | Dexlansoprazole is extensively metabolized in the liver. It undergoes oxidation and reduction, followed by subsequent sulfation, glucuronidation, and glutathione conjugation to form inactive metabolites. Oxidative metabolites are formed from CYP2C19-mediated hydroxylation and CYP3A4-mediated oxidation to the sulfone.[A19575, L48827] CYP2C19 is a polymorphic liver enzyme which exhibits three phenotypes in the metabolism of CYP2C19 substrates: extensive metabolizers (*1/*1), intermediate metabolizers (*1/mutant) and poor metabolizers (mutant/mutant). 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. |
| Route of elimination | Dexlansoprazole does not appear to be eliminated unchanged in the urine.[A19573, L48827] Following the administration of [14C] dexlansoprazole to six healthy male subjects, approximately 50.7% (standard deviation (SD): 9.0%) of the administered radioactivity was excreted in urine and 47.6% (SD: 7.3%) in the feces. |
| Volume of distribution | The apparent volume of distribution (Vz/F) after multiple doses in symptomatic GERD patients was 40 L. |
| 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. |
Formulation & handling
- Dexlansoprazole is formulated primarily for oral administration, including immediate and delayed-release capsules and tablets suitable for nasogastric delivery.
- As a small molecule drug with moderate water solubility and LogP, it does not require peptide or biologic-specific handling conditions.
- The dual delayed-release formulation enables dosing without regard to food intake, though interaction with CYP3A4 inducers like St. John’s Wort should be considered.
Regulatory status
| Lifecycle | The API's key patents in the US expired between 2018 and 2019, while Canadian patents expired in 2011 and 2020, indicating the product has reached market maturity with generic competition likely available in both the US and Canadian markets. |
|---|
| Markets | US, Canada |
|---|
Supply Chain
| Supply chain summary | Dexlansoprazole is marketed primarily in North America, with branded products available in the US and Canada. Multiple patents in these regions indicate protection extending into recent years, suggesting limited generic competition may currently exist but could increase as patents approach expiry. Originator companies play a key role in maintaining market presence through these branded formulations. |
|---|
Safety
| Toxicity | Oral LD<sub>50</sub> value in mice, rats and dogs is reported to be > 5000 mg/kg. There have been no reports of significant overdose with dexlansoprazole. Multiple doses of 120 mg and a single dose of 300 mg did not result in death or other severe adverse events; however, serious adverse events of hypertension have been reported in association with twice daily doses of 60 mg. Nonserious adverse reactions observed with twice daily doses of 60 mg include hot flashes, contusion, oropharyngeal pain, and weight loss. Dexlansoprazole is not expected to be removed from the circulation by hemodialysis. In the event of over-exposure, treatment should be symptomatic and supportive. |
|---|
High Level Warnings:
- Oral LD50 exceeds 5000 mg/kg in mice, rats, and dogs, indicating low acute toxicity
- Overdose cases with doses up to 300 mg have not resulted in fatality or severe adverse effects
- However, hypertension has been reported with repeated 60 mg twice daily dosing
Dexlansoprazole is a type of Gastrointestinal Agents
Gastrointestinal Agents belong to the pharmaceutical API category that focuses on treating disorders and ailments related to the digestive system. These agents play a crucial role in addressing various gastrointestinal conditions, such as acid reflux, ulcers, irritable bowel syndrome (IBS), and inflammatory bowel disease (IBD).
One of the key types of gastrointestinal agents is proton pump inhibitors (PPIs), which work by reducing the production of stomach acid. PPIs help in treating conditions like gastroesophageal reflux disease (GERD) and peptic ulcers. Another essential class of agents is antacids, which neutralize excessive stomach acid, providing relief from heartburn and indigestion.
Gastrointestinal agents also include antispasmodics that alleviate abdominal cramps and spasms associated with conditions like IBS. These drugs work by relaxing the smooth muscles of the digestive tract. Additionally, there are drugs categorized as laxatives that aid in relieving constipation by promoting bowel movements.
Moreover, certain gastrointestinal agents act as antiemetics, effectively reducing nausea and vomiting. These drugs are particularly useful for patients undergoing chemotherapy or experiencing motion sickness.
Pharmaceutical companies develop and manufacture a wide range of gastrointestinal agents in various forms, including tablets, capsules, suspensions, and injections. These agents are typically formulated using active pharmaceutical ingredients (APIs) and other excipients to ensure their efficacy and safety.
In conclusion, gastrointestinal agents form a vital category of pharmaceutical APIs, providing relief from digestive disorders and improving overall gastrointestinal health. The availability of diverse agents catering to different conditions ensures that patients can receive targeted treatment for their specific gastrointestinal needs.
Dexlansoprazole API manufacturers & distributors
Compare qualified Dexlansoprazole API suppliers worldwide. We currently have 1 companies offering Dexlansoprazole API, with manufacturing taking place in 1 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| ACE Japan | Producer | Japan | Japan | CoA | 76 products |
When sending a request, specify which Dexlansoprazole API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
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