Omeprazole chemical structure (PPI), 2D skeletal formula, C17H19N3O3S

Omeprazole Chemical Structure

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1. Identification

Summary
Omeprazole is a proton-pump inhibitor (PPI) used to reduce gastric acid secretion, treating GERD, peptic ulcer disease, erosive esophagitis, and hypersecretory states; it is supplied as a racemic mixture and often dosed before meals.

Brand Names
Prilosec, Losec, Zegerid (omeprazole/sodium bicarbonate); numerous generics (region-dependent)

Name
Omeprazole

Background
A benzimidazole sulfoxide first approved in the late 1980s; acid-activated in parietal cells to a reactive sulfenamide that irreversibly inhibits the gastric H⁺/K⁺-ATPase. Available as delayed-release capsules/tablets, suspensions/granules, and certain IV/lyophilized products (jurisdiction-dependent).

Modality
Small molecule

Groups
Approved; OTC/Rx (region-dependent)

Structure

Omeprazole 2D chemical structure (benzimidazole sulfoxide). Formula C17H19N3O3S; IUPAC long name; CAS 73590-58-6.
Omeprazole chemical structure (PPI), 2D skeletal formula, C17H19N3O3S

Weight
≈ 345.42 g/mol

Chemical Formula
C₁₇H₁₉N₃O₃S

Synonyms
5-Methoxy-2-[(4-methoxy-3,5-dimethylpyridin-2-yl)methylsulfinyl]-1H-benzimidazole; Prilosec (trade)

External IDs
CAS: 73590-58-6; PubChem CID: 4594; UNII: KG60484QX9; ATC: A02BC01; KEGG: D00455; ChEMBL: 1503; ChEBI: 7772

2. Pharmacology

Indication
Short- and long-term management of GERD, erosive esophagitis, peptic/duodenal ulcers (including H. pylori eradication regimens), and Zollinger–Ellison syndrome; maintenance of healing where indicated.

Associated Conditions
Heartburn/acid reflux, NSAID-associated ulcer prevention (per label), hypersecretory states.

Associated Therapies
Triple therapy for H. pylori (e.g., omeprazole + amoxicillin + clarithromycin or bismuth-based regimens). Combination with sodium bicarbonate to expedite absorption (Zegerid).

Contraindications & Blackbox Warnings
Hypersensitivity to omeprazole/PPIs or formulation components. (Class has no boxed warning; labels include precautions such as bone fracture risk with long-term/high-dose use, acute interstitial nephritis, C. difficile–associated diarrhea, lupus erythematosus, B₁₂ deficiency, hypomagnesemia, and masking of gastric malignancy—evaluate alarm symptoms.)

Pharmacodynamics
Marked and sustained suppression of basal and stimulated gastric acid secretion; duration exceeds plasma half-life due to irreversible pump inhibition.

Mechanism of action
A prodrug that accumulates in the acidic canaliculi of parietal cells and converts to a sulfenamide that forms covalent bonds with cysteine residues on the H⁺/K⁺-ATPase, irreversibly blocking acid secretion until new pumps are synthesized.

Absorption
Delayed-release forms protect against acid degradation; food can delay absorption. Oral bioavailability varies and may increase on repeated dosing.

Volume of distribution
Approx. ~0.4 L/kg (literature values vary by source/formulation).

Protein binding
High (~95%).

Metabolism
Extensively hepatic via CYP2C19 and CYP3A4 to inactive metabolites; CYP2C19 phenotype influences exposure.

Route of elimination
Metabolites excreted predominantly in urine (major fraction) and in feces (biliary).

Half-life
Typically ~0.5–1 hour in healthy adults (prolonged in hepatic impairment); pharmacodynamic effect lasts much longer.

Clearance
Apparent oral clearance influenced by CYP2C19 activity and drug interactions (inducers/inhibitors).

Adverse Effects
Common: headache, abdominal pain, nausea/diarrhea, flatulence. Serious but uncommon: C. difficile infection, fractures (long-term/high dose), hypomagnesemia, B₁₂ deficiency, AIN, cutaneous/systemic lupus, and rare severe skin reactions.

Toxicity
Overdose is uncommon; management is supportive. Chronic over-suppression risks are addressed in labeling (e.g., infections, micronutrient effects).

Pathways
Acid-activation → covalent H⁺/K⁺-ATPase inhibition; downstream suppression of gastric acid.

Pharmacogenomic Effects/ADRs
CYP2C19 poor metabolizers show increased exposure and effect; potent enzyme inducers (e.g., rifampin, St. John’s wort) may reduce efficacy.

3. Interactions

Drug Interactions

  • Clopidogrel: avoid co-administration—omeprazole inhibits CYP2C19, reducing clopidogrel activation and antiplatelet effect (label caution).
  • Drugs needing acidic pH for absorption (e.g., ketoconazole, itraconazole, erlotinib, some HIV protease inhibitors/atazanavir): decreased exposure—consider alternatives/timing per label.
  • CYP inducers/inhibitors: rifampin/St. John’s wort (↓ levels/efficacy); strong inhibitors may ↑ exposure.
  • High-dose methotrexate: PPIs may reduce clearance—consider temporary interruption (per institutional/label guidance where applicable).

Food Interactions
Administer before meals (commonly 30–60 minutes) to optimize effect; food may slow absorption but not necessarily reduce total exposure.

4. Categories

ATC Codes
A02BC01 (proton-pump inhibitors)

Drug Categories
Proton-pump inhibitor; Anti-ulcer agent; Small molecule

Chemical Taxonomy
Benzimidazole sulfoxide; weak base; racemate (R/S-omeprazole)

Affected organisms
Humans (therapeutic use)

5. Chemical Identifiers

UNII
KG60484QX9

CAS number
73590-58-6

InChI Key
SUBDBMMJDZJVOS-UHFFFAOYSA-N

InChI
InChI=1S/C17H19N3O3S/c1-10-8-18-15(11(2)16(10)23-4)9-24(21)17-19-13-6-5-12(22-3)7-14(13)20-17/h5-8H,9H2,1-4H3,(H,19,20)

IUPAC Name
5-Methoxy-2-[(4-methoxy-3,5-dimethylpyridin-2-yl)methylsulfinyl]-1H-benzimidazole

SMILES
COc1ccc2nc(Nc2c1)S(=O)Cc1ncc(c(c1C)OC)C (canonical forms vary across sources; confirm per chosen database.)

6. References

  1. FDA/GSRS UNII — Omeprazole: UNII KG60484QX9, formula C17H19N3O3S, InChIKey SUBDBMMJDZJVOS-UHFFFAOYSA-N. precisionFDA+1
  2. ATC/DDD Index (WHO/NCMP, Norway/FHI) — A02BC01 omeprazole; DDD routes. atcddd.fhi.no+1
  3. DailyMed — Omeprazole labels: clopidogrel interaction warning; precautions (fracture, C. difficile, AIN, lupus). DailyMed+2DailyMed+2
  4. StatPearls (NCBI Bookshelf) — PK/PD overview: short plasma half-life (~0.5–1 h), metabolism via CYP2C19/3A4, urinary excretion of metabolites. NCBI+1
  5. KEGG DRUG — Entry D00455 (omeprazole), cross-refs and classification. genome.jp+1
  6. PubChem — Omeprazole/Prilosec pages (CID 4594): identifiers and chemical data. PubChem+1
  7. Tocris / Fisher — CAS 73590-58-6, molecular weight 345.42 g/mol, and identifier confirmations. Tocris Bioscience+1
  8. IUPHAR Guide to Pharmacology — Ligand entry notes (PPI class; racemic mixture). guidetopharmacology.org

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