Esomeprazole

White to slightly colored crystalline powder. Slightly soluble in water; stability ... is a function of pH; it degrades rapidly in acidic media but has acceptable stability under alkaline conditions; half-lives of 19 and 8 hrs at 25 and 37 °C, respectively /Esomeprazole magnesium/

White to almost white crystalline powder; soluble in water /Esomeprazole strontium/

... for injection is supplied as a sterile, freeze-dried, white to off-white, porous cake or powder. ... The stability of esomeprazole sodium in aqueous solution is strongly pH dependent. /Esomeprazole sodium/

Warning

H312 (100%): Harmful in contact with skin [Warning Acute toxicity, dermal]；H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]；H317 (100%): May cause an allergic skin reaction [Warning Sensitization, Skin]；H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]；H335 (100%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]；H412 (100%): Harmful to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P261, P264, P264+P265, P271, P272, P273, P280, P302+P352, P304+P340, P305+P351+P338, P317, P319, P321, P332+P317, P333+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including esomeprazole magnesium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Esomeprazole magnesium/

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including esomeprazole sodium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Esomeprazole sodium/

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including esomeprazole strontium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Esomeprazole strontium/

In a single-dose study, concomitant administration of omeprazole 20 mg and sucralfate 1 g resulted in delayed absorption of omeprazole and decreased omeprazole bioavailability by 16%. Proton-pump inhibitors should be administered at least 30 minutes before sucralfate.

Pharmacokinetic interaction with omeprazole (decreased plasma concentrations and AUC of rilpivirine).32 343 Concomitant use of other proton-pump inhibitors also may result in decreased plasma concentration of rilpivirine.343 Concomitant use of rilpivirine and proton-pump inhibitors is contraindicated.

Concomitant use of omeprazole 40 mg once daily and atazanavir (with or without low-dose ritonavir) results in a substantial decrease in plasma concentrations of atazanavir and possible loss of the therapeutic effect of the antiretroviral agent or development of drug resistance. Concomitant use of omeprazole 40 mg once daily (administered 2 hours before atazanavir) and atazanavir 400 mg once daily decreased the AUC and peak plasma concentration of atazanavir by 94 and 96%, respectively. The manufacturer of esomeprazole states that concomitant administration with atazanavir is not recommended. If atazanavir is administered in an antiretroviral treatment-naive patient receiving a proton-pump inhibitor, a ritonavir-boosted regimen of 300 mg of atazanavir once daily with ritonavir 100 mg once daily with food is recommended. The dose of the proton-pump inhibitor should be administered approximately 12 hours before ritonavir-boosted atazanavir; the dose of the proton-pump inhibitor should not exceed omeprazole 20 mg daily (or equivalent). Concomitant use of proton-pump inhibitors with atazanavir is not recommended in antiretroviral treatment-experienced patients.

Concomitant use of omeprazole 20 mg once daily and digoxin in healthy individuals increased digoxin bioavailability by 10% (up to 30% in some individuals). Because esomeprazole is an enantiomer of omeprazole, concomitant use of esomeprazole with digoxin is expected to increase systemic exposure to digoxin; therefore, monitoring for manifestations of digoxin toxicity may be required during such concomitant use.

For more Interactions (Complete) data for Esomeprazole (7 total), please visit the HSDB record page.

Blurred vision, confusion, drowsiness, dry mouth, flushing headache, nausea, rapid heartbeat, sweating.

may include bone rebuild interference and B12 vitamin reduction. [Wikipedia]

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1500(SRC), determined from a structure estimation method(2), indicates that esomeprazole is expected to have low mobility in soil(SRC). The estimated pKa of esomeprazole is 4.78(3), indicating that this compound will exist partially in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of neutral esomeprazole from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.1X10-19 atm-cu m/mole(SRC), using a fragment constant estimation method(5). The cation form of esomeprazole will not volatilize(SRC). Esomeprazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.2X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2013).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1500(SRC), determined from a structure estimation method(2), indicates that esomeprazole is expected to adsorb to suspended solids and sediment(SRC). An estimated pKa of 4.78(3) indicates esomeprazole will partially exist in the cation form at pH values of 5 to 9 and, therefore, volatilization from water surfaces of the ion form is not expected to be an important fate process(SRC). Volatilization of the neutral form from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 3.0X10-19 atm-cu m/mole(SRC), developed using a fragment constant estimation method(5). According to a classification scheme(6), an estimated BCF of 14(SRC), from an estimated log Kow of 3.40(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2013).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), esomeprazole, which has an estimated vapor pressure of 1.2X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase esomeprazole may be removed from the air by wet and dry deposition(SRC). Esomeprazole does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to/may be susceptible to direct photolysis by sunlight(SRC).

Oral

The delayed-release capsule are enteric-coated (as omeprazole is acid-labile) so the absorption of omprazole begins once the granules leave the stomach. Absorption is rapid. Peak plasma levels occur within 0.5 - 3.5 hours. The absolute bioavailability (compared with intravenous administration) of the delayed-release capsule is 30-40% at doses of 20 - 40 mg, due to presystemic metabolism. This value increases slightly when given repeatedly. Based on a relative bioavailability study, the AUC and Cmax of PRILOSEC (omeprazole magnesium) for Delayed-Release Oral Suspension were 87% and 88% of those for PRILOSEC Delayed-Release Capsules, respectively. Interestingly, when the 40 mg delayed release capsule is given with or without applesauce, it is bioequivalent. However, when the 20 mg delayed release capsule is given with the same conditions, it is not bioequivalent. When the same capsule is given to the elderly, bioavailability increases. Omeprazole was 76% bioavailable.

Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H⁺/K⁺-ATPase in the gastric parietal cell. By acting specifically on the proton pump, Esomeprazole blocks the final step in acid production, thus reducing gastric acidity.

Omeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H⁺/K⁺-ATPase in the gastric parietal cell. By acting specifically on the proton pump, omeprazole blocks the final step in acid production, thus reducing gastric acidity.

Blurred vision, confusion, drowsiness, dry mouthflushingheadache, nausea, rapid heartbeat, sweating.

Symptoms of overdose include confusion, drowsiness, blurred vision, tachycardia, nausea, diaphoresis, flushing, headache, and dry mouth.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of esomeprazole can be estimated to be 1500(SRC). According to a classification scheme(2), this estimated Koc value suggests that esomeprazole is expected to have low mobility in soil. The estimated pKa of esomeprazole is 4.78(3), indicating that this compound will partially exist in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

No indication of carcinogenicity to humans (not listed by IARC).

No indication of carcinogenicity to humans (not listed by IARC).

An estimated BCF of 14 was calculated in fish for esomeprazole(SRC), using an estimated log Kow of 3.40(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

An estimated pKa of 4.78(1) indicates esomeprazole will partially exist in the cation form at pH values of 5 to 9 and, therefore, volatilization from water and moist soil surfaces of the ion form is not expected to be an important fate process(SRC). The Henry's Law constant for esomeprazole is estimated as 3.0X10-19 atm-cu m/mole(SRC) using a fragment constant estimation method(2). This Henry's Law constant indicates that neutral form of esomeprazole is expected to be essentially nonvolatile from water and moist soil surfaces(3). Esomeprazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.2X10-11 mm Hg(SRC), determined from a fragment constant method(4).

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The carcinogenic potential of NEXIUM was assessed using studies of omeprazole, of which esomeprazole is an enantiomer. In two 24-month oral carcinogenicity studies in rats, omeprazole at daily doses of 1.7, 3.4, 13.8, 44, and 141 mg/kg/day (about 0.7 to 57 times the human dose of 20 mg/day expressed on a body surface area basis) produced gastric ECL cell carcinoids in a dose-related manner in both male and female rats; the incidence of this effect was markedly higher in female rats, which had higher blood levels of omeprazole. Gastric carcinoids seldom occur in the untreated rat. In addition, ECL cell hyperplasia was present in all treated groups of both sexes. In one of these studies, female rats were treated with 13.8 mg omeprazole/kg/day (about 5.6 times the human dose on a body surface area basis) for 1 year, then followed for an additional year without the drug. No carcinoids were seen in these rats. An increased incidence of treatment-related ECL cell hyperplasia was observed at the end of 1 year (94% treated vs. 10% controls). By the second year the difference between treated and control rats was much smaller (46% vs. 26%) but still showed more hyperplasia in the treated group. Gastric adenocarcinoma was seen in one rat (2%). No similar tumor was seen in male or female rats treated for 2 years. For this strain of rat no similar tumor has been noted historically, but a finding involving only one tumor is difficult to interpret. A 78-week mouse carcinogenicity study of omeprazole did not show increased tumor occurrence, but the study was not conclusive.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Reproductive studies have been performed in rats at oral doses up to 280 mg/kg/day (about 57 times the human dose on a body surface area basis) and in rabbits at oral doses up to 86 mg/kg/day (about 35 times the human dose on a body surface area basis) and have revealed no evidence of impaired fertility or harm to the fetus due to esomeprazole.

/GENOTOXICITY/ Esomeprazole was negative in the Ames mutation test, in the in vivo rat bone marrow cell chromosome aberration test, and the in vivo mouse micronucleus test. Esomeprazole, however, was positive in the in vitro human lymphocyte chromosome aberration test.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including esomeprazole magnesium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Esomeprazole magnesium/

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including esomeprazole sodium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Esomeprazole sodium/

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including esomeprazole strontium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Esomeprazole strontium/

A02BC05

A - Alimentary tract and metabolism；A02 - Drugs for acid related disorders；A02B - Drugs for peptic ulcer and gastro-oesophageal reflux disease (gord)；A02BC - Proton pump inhibitors；A02BC05 - Esomeprazole

QA - Alimentary tract and metabolism；QA02 - Drugs for acid related disorders；QA02B - Drugs for peptic ulcer and gastro-oesophageal reflux disease (gord)；QA02BC - Proton pump inhibitors；QA02BC05 - Esomeprazole

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 <i>H. pylori</i> 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 [DB00338], which is a racemate of the S- and R-enantiomer. Esomeprazole has been shown to inhibit acid secretion to a similar extent as [DB00338], 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. 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 osteoporo

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.

Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. This effect is dose-related up to a daily dose of 20 to 40 mg and leads to inhibition of gastric acid secretion.

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. However, the influence of CYP 2C19 polymorphism is less pronounced for esomeprazole than for omeprazole. 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. 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.

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 CYP 2C19 isoenzyme, which forms the hydroxy and desmethyl metabolites. The remaining amount is dependent on CYP 3A4 which forms the sulphone metabolite. CYP 2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15 to 20% of Asians lack CYP 2C19 and are termed Poor Metabolizers. 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.

Esomeprazole has known human metabolites that include Omeprazole sulfone, 5-Hydroxyomeprazole, and 5-O-Desmethylomeprazole.

Mainly hepatic. Esomeprazole is completely metabolized by the cytochrome P450 system via CYP2C19 and CYP3A4. Metabolism produces inactive hydroxy and desmethyl metabolites, which have no effect on gastric acid secretion. Less than 1% of the parent drug is excreted in urine. Route of Elimination: Approximately 80% of the administered dose of esomeprazole is excreted as metabolites in urine and the remaining 20% is excreted in feces. Half Life: 1-1.5 hours

Hepatic. Omeprazole is extensively metabolized by the cytochrome P450 (CYP) enzyme system. The two primary CYP isozymes involved are CYP2C19 and CYP3A4. Metabolism is stereoselective in which the S-isomer is converted to 5'O-desmethylomeprazole via CYP2C19. CYP3A4 converts the S-isomer to 3-hydroxyomeprazole. The R-isomer is converted to 5-hydroxyomeprazole by CYP2C19. CYP3A4 converts the R-isomer to any four different metabolites: 5-hydroxyomeprazole (5-OH OME), omeprazole sulfone (OME sulfone), 5'-O-desmethylomeprazole (5'-desmethyl OME), and 3-hydroxyomeprazole (3-OH OME). Route of Elimination: Urinary excretion is a primary route of excretion of omeprazole metabolites. Little, if any unchanged drug was excreted in the urine. The majority of the dose (about 77%) was eliminated in urine as at least six metabolites. Two were identified as hydroxyomeprazole and the corresponding carboxylic acid. The remainder of the dose was recovered in the feces. Half Life: 0.5-1 hour (healthy subjects, delayed-release capsule); 3 hours (hepatic impairment)

N3PA6559FT

ESOMEPRAZOLE

Established Pharmacologic Class [EPC] - Proton Pump Inhibitor

Mechanisms of Action [MoA] - Proton Pump Inhibitors

Mechanisms of Action [MoA] - Cytochrome P450 2C19 Inhibitors

Esomeprazole is a Proton Pump Inhibitor. The mechanism of action of esomeprazole is as a Proton Pump Inhibitor and Cytochrome P450 2C19 Inhibitor.

Various agents with different action mechanisms used to treat or ameliorate PEPTIC ULCER or irritation of the gastrointestinal tract. This has included ANTIBIOTICS to treat HELICOBACTER INFECTIONS; HISTAMINE H2 ANTAGONISTS to reduce GASTRIC ACID secretion; and ANTACIDS for symptomatic relief.

Compounds that inhibit H(+)-K(+)-EXCHANGING ATPASE. They are used as ANTI-ULCER AGENTS and sometimes in place of HISTAMINE H2 ANTAGONISTS for GASTROESOPHAGEAL REFLUX.

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. _Combination Therapy with Antimicrobials:_ Esomeprazole magnesium 40 mg once daily was given in combination with [DB01211] 500 mg twice daily and [DB01060] 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.

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.

The apparent volume of distribution at steady state in healthy volunteers is approximately 16 L.

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.

Esomeprazole is 97% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 2 to 20 umol/L. The apparent volume of distribution at steady state in healthy volunteers is approximately 16 L.

NEXIUM Delayed-Release Capsules and NEXIUM For Delayed-Release Oral Suspension contain a bioequivalent enteric-coated granule formulation of esomeprazole magnesium. Bioequivalency is based on a single dose (40 mg) study in 94 healthy male and female volunteers under fasting condition. 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 umol*hr/L on Day 1 to 11.2 umol*hr/L on Day 5 after 40 mg once daily dosing.

MEDICATION

Anti-Ulcer Agents; Proton Pump Inhibitors

Use (kg; approx.) in Germany (2009): >1000；Use (kg) in USA (2002): 12000；Consumption (g per capita; approx.) in Germany (2009): 0.0122；Consumption (g per capita) in the USA (2002): 0.0425；Excretion rate: 0.005；Calculated removal (%): 9.8

Used in the treatment of acid-reflux disorders (GERD), peptic ulcer disease, H. pylori eradication, and prevention of gastroinetestinal bleeds with NSAID use. Used in the treatment of dyspepsia, peptic ulcer disease (PUD), gastroesophageal reflux disease (GORD/GERD) and Zollinger-Ellison syndrome. [Wikipedia]

Omeprazole is indicated for the treatment of duodenal ulcers, benign gastric ulcers, gastroesophageal reflux disease (GERD), heartburn and other symptoms associated with GERD, erosive esophagitis, and long-term treatment of pathological hypersecretory conditions like Zollinger-Ellison syndrome, multiple endocrine adenomas, and systemic mastocytosis.

Esomeprazole is available as delayed release capsules containing esomeprazole magnesium trihydrate ... Each capsule contains 20 or 40 mg of esomeprazole present as 22.3 or 44.5 mg of esomeprazole magnesium trihydrate. ... Esomeprazole is marketed under the trade name Nexium (AstraZeneca).

Table: Esomeprazole Magnesium Preparations [Table#8119]

Table: Esomeprazole Magnesium Combination Preparations [Table#8120]

Table: Esomeprazole Sodium Preparations [Table#8121]