Description

Simple

A medication used to improve the symptoms of heartburn, and to treat related conditions such as ulcers, tissue damage and infection with the bacteria called H. pylori.

Clinical

A proton pump inhibitor used to treat GERD associated conditions such as heartburn and gastric acid hypersecretion, and to promote healing of tissue damage and ulcers caused by gastric acid and H. pylori infection.

Overview

Originally approved by the FDA in 1989, omeprazole is a _proton-pump inhibitor_, used to treat gastric acid-related disorders. These disorders may include gastroesophageal reflux disease (GERD), peptic ulcer disease, and other diseases characterized by the oversecretion of gastric acid. This drug was the first clinical useful drug in its class, and its approval was followed by the formulation of many other proton pump inhibitor drugs [6]. Omeprazole is generally effective and well-tolerated, promoting its popular use in children and adults [FDA label].

Pharmacology

Indication

Omeprazole, according to the FDA label [FDA label] is a proton pump inhibitor (PPI) used for the following purposes:

• Treatment of active duodenal ulcer in adults

• Eradication of Helicobacter pylori to reduce the risk of duodenal ulcer
recurrence in adults

• Treatment of active benign... Read more

Pharmacodynamic

**Effects on gastric acid secretion**

This drug decreases gastric acid secretion [FDA label]. After oral administration, the onset of the antisecretory effect of omeprazole is usually achieved within one hour, with the maximum effect occurring by 2 hours after administration. The inhibitory effec... Read more

Mechanism of action

Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump [ Read more

Absorption

Omeprazole delayed-release capsules contain an enteric-coated granule formulation of omeprazole (because omeprazole is acid-labile), so that absorption of omeprazole begins only after the granules exit the stomach [FDA label].

Absorption of omeprazole occurs rapidly, with peak plasma concentrati... Read more

Protein binding

Approximately 95% bound to human plasma proteins [FDA label].

Volume of distribution

Approximately 0.3 L/kg, corresponding to the volume of extracellular water [5].

Clearance

Healthy subject (delayed release capsule), total body clearance 500 - 600 mL/min [FDA label]Geriatric plasma clearance: 250 mL/min [FDA label]Hepatic impairment plasma clearance: 70 mL/min [FDA label]

Half life

0.5-1 hour (healthy subjects, delayed-release capsule) [FDA label]
Approximately 3 hours (hepatic impairment) [FDA label]

Route of elimination

After a single dose oral dose of a buffered solution of omeprazole, negligible (if any) amounts of unchanged drug were excreted in urine. Most of the dose (about 77%) was eliminated in urine as at least six different metabolites. Two metabolites were identified as _hydroxyomeprazole_ and the corresp... Read more

Toxicity

**Oral acute (LD50)**: 4000 mg/kg (mouse), 2210 mg/kg (rat) [MSDS].

**Overdose**

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

**Carcinogenesis and mutagenesis**

In 24-month studies in rats, a dos... Read more

Adverse Effects

Contraindications

  • Regions: US
  • Patient Conditions:
      • Name: Patients with known hypersensitivity to any component of the formulation or any substituted benzimidazole
      • Drugbank Id: DBCOND0117161
  • Route:
    • Oral
  • Regions: US
  • With Drugs:
      • Name: Rilpivirine
      • Drugbank Id: DB08864

Food Interactions

  • Avoid alcohol.
  • Take 30-60 minutes before meals.

Interactions

Type in a drug name to check for interaction with Omeprazole
Type a drug name in the box above to get started
  • Paracetamol(acetaminophen)
  • Paxil(paroxetine)
  • Pamelor(nortriptyline)
  • Panadol(acetaminophen)
  • Patanol(olopatadine ophthalmic)
  • Pataday(olopatadine ophthalmic)
  • Parnate(tranylcypromine)
  • Pazeo(olopatadine ophthalmic)
(R)-warfarin
The metabolism of (R)-warfarin can be increased when combined with Omeprazole.
(S)-Warfarin
The metabolism of (S)-Warfarin can be increased when combined with Omeprazole.
4-hydroxycoumarin
The metabolism of 4-hydroxycoumarin can be increased when combined with Omeprazole.
4-Methoxyamphetamine
The metabolism of 4-Methoxyamphetamine can be decreased when combined with Omeprazole.
5-methoxy-N,N-dimethyltryptamine
The metabolism of 5-methoxy-N,N-dimethyltryptamine can be decreased when combined with Omeprazole.
6-O-benzylguanine
The metabolism of 6-O-benzylguanine can be decreased when combined with Omeprazole.
8-azaguanine
The metabolism of 8-azaguanine can be decreased when combined with Omeprazole.
8-chlorotheophylline
The metabolism of 8-chlorotheophylline can be decreased when combined with Omeprazole.
9-aminocamptothecin
The metabolism of 9-aminocamptothecin can be increased when combined with Omeprazole.
9-Deazaguanine
The metabolism of 9-Deazaguanine can be decreased when combined with Omeprazole.
9-Methylguanine
The metabolism of 9-Methylguanine can be decreased when combined with Omeprazole.
Abatacept
The metabolism of Omeprazole can be increased when combined with Abatacept.
Abemaciclib
The serum concentration of Abemaciclib can be increased when it is combined with Omeprazole.
Abiraterone
The metabolism of Omeprazole can be decreased when combined with Abiraterone.
Acebutolol
The serum concentration of Acebutolol can be increased when it is combined with Omeprazole.
Acefylline
The metabolism of Acefylline can be decreased when combined with Omeprazole.
Acenocoumarol
The metabolism of Acenocoumarol can be increased when combined with Omeprazole.
Acetaminophen
The serum concentration of Omeprazole can be increased when it is combined with Acetaminophen.
Acetohexamide
The metabolism of Acetohexamide can be decreased when combined with Omeprazole.
Acetyl sulfisoxazole
The metabolism of Omeprazole can be decreased when combined with Acetyl sulfisoxazole.
16 References
  1. 1 . Yang YX, Lewis JD, Epstein S, Metz DC: Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006 Dec 27;296(24):2947-53.PubMed: 17190895
  2. 2 . Castell D: Review of immediate-release omeprazole for the treatment of gastric acid-related disorders. Expert Opin Pharmacother. 2005 Nov;6(14):2501-10. doi: 10.1517/14656566.6.14.2501 .PubMed: 16259581
  3. 3 . Higuera-de-la-Tijera F: Efficacy of omeprazole/sodium bicarbonate treatment in gastroesophageal reflux disease: a systematic review. Medwave. 2018 Mar 14;18(2):e7179. doi: 10.5867/medwave.2018.02.7179.PubMed: 29547594
  4. 4 . Welage LS, Berardi RR: Evaluation of omeprazole, lansoprazole, pantoprazole, and rabeprazole in the treatment of acid-related diseases. J Am Pharm Assoc (Wash). 2000 Jan-Feb;40(1):52-62; quiz 121-3.PubMed: 10665250
  5. 5 . Cederberg C, Andersson T, Skanberg I: Omeprazole: pharmacokinetics and metabolism in man. Scand J Gastroenterol Suppl. 1989;166:33-40; discussion 41-2.PubMed: 2690330
  6. 6 . Strand DS, Kim D, Peura DA: 25 Years of Proton Pump Inhibitors: A Comprehensive Review. Gut Liver. 2017 Jan 15;11(1):27-37. doi: 10.5009/gnl15502.PubMed: 27840364
  7. 7 . McTavish D, Buckley MM, Heel RC: Omeprazole. An updated review of its pharmacology and therapeutic use in acid-related disorders. Drugs. 1991 Jul;42(1):138-70. doi: 10.2165/00003495-199142010-00008.PubMed: 1718683
  8. 8 . Langtry HD, Wilde MI: Omeprazole. A review of its use in Helicobacter pylori infection, gastro-oesophageal reflux disease and peptic ulcers induced by nonsteroidal anti-inflammatory drugs. Drugs. 1998 Sep;56(3):447-86. doi: 10.2165/00003495-199856030-00012.PubMed: 9777317
  9. 9 . Lewin MJ: Cellular mechanisms and inhibitors of gastric acid secretion. Drugs Today (Barc). 1999 Oct;35(10):743-52.PubMed: 12973369
  10. 10 . Sachs G, Wallmark B: The gastric H+,K+-ATPase: the site of action of omeprazole. Scand J Gastroenterol Suppl. 1989;166:3-11.PubMed: 2557669
  11. 11 . Sachs G, Shin JM, Howden CW: Review article: the clinical pharmacology of proton pump inhibitors. Aliment Pharmacol Ther. 2006 Jun;23 Suppl 2:2-8. doi: 10.1111/j.1365-2036.2006.02943.x.PubMed: 16700898
  12. 12 . Sung JJ, Kuipers EJ, El-Serag HB: Systematic review: the global incidence and prevalence of peptic ulcer disease. Aliment Pharmacol Ther. 2009 May 1;29(9):938-46. doi: 10.1111/j.1365-2036.2009.03960.x.PubMed: 19220208
  13. 13 . Vcev A, Stimac D, Vceva A, Takac B, Pezerovic D, Ivandic A: High dose omeprazole plus amoxicillin and azithromycin in eradication of Helicobacter pylori in duodenal ulcers. Helicobacter. 1999 Mar;4(1):54-7.PubMed: 10352088
  14. 14 . Scott DR, Sachs G, Marcus EA: The role of acid inhibition in Helicobacter pylori eradication. F1000Res. 2016 Jul 19;5. doi: 10.12688/f1000research.8598.1. eCollection 2016.PubMed: 30023042
  15. 15 . Mobley HL: The role of Helicobacter pylori urease in the pathogenesis of gastritis and peptic ulceration. Aliment Pharmacol Ther. 1996 Apr;10 Suppl 1:57-64.PubMed: 8730260
  16. 16 . FDA Approved Drugs: Talicia® delayed-release oral capsules Link