Pantoprazole 40mg powder for solution for injection vials
Prescription only
Requires a prescription from a doctor or prescriber
Active ingredients:
Pantoprazole
1 safety notice
Safety information for pregnancy and breastfeeding
Category B
Animal studies show no risk; no adequate human studiesPregnancy
The relevance of these findings to tumor development in humans is unknown at this time.F3202
Teratogenic Effects
This drug falls under pregnancy category B category.
Teratogenic Effects
This drug falls under pregnancy category B category.
Reproduction studies have been performed in rats at oral doses up to 88 times the recommended human dose (RHD), as well as in rabbits at oral doses up to 16 times the RHD, and have shown no evidence of impaired fertility or harm to the fetus caused by pantoprazole.
No adequate and well-controlled studies in pregnant women have been completed.
Because animal reproduction studies are not always predictive of human response, this drug should only be used during pregnancy if clearly required.F3202
Nursing Mothers
Pantoprazole and its metabolites have been found to be excreted in the milk of rats.
Nursing Mothers
Pantoprazole and its metabolites have been found to be excreted in the milk of rats.
Breastfeeding
Because animal reproduction studies are not always predictive of human response, this drug should only be used during pregnancy if clearly required.F3202
Nursing Mothers
Pantoprazole and its metabolites have been found to be excreted in the milk of rats.
Nursing Mothers
Pantoprazole and its metabolites have been found to be excreted in the milk of rats.
Pantoprazole excretion in human milk has been found in a study performed with a single nursing mother after one 40 mg oral dose.
The clinical relevance of this finding is not known, however, it is advisable to take note of this finding when considering pantoprazole use during nursing.
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 6 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Pantoprazole
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Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
EMA
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Pantoprazole
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
14 branded products available
14 products
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Protium I.V. 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
Pantoprazole 40mg powder for solution for injection vials
£5.00indicative price
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
40 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
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Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 5 · Randomised trials: 14 · 1993–2025
Showing the 50 most relevant studies, sorted by most relevant.
Withholding Pantoprazole for Stress Ulcer Prophylaxis in Critically Ill Patients: A Pilot Randomized Clinical Trial and Meta-Analysis* (opens in a new tab)
Waleed Alhazzani, Gordon Guyatt, Mohammed Alshahrani, et al.
Critical Care Medicine, 2017
Meta-analysis
Highly cited for its field
Cited by 110- Critical Illness
- Pantoprazole
- Clostridium Infections
Pantoprazole to Prevent Gastroduodenal Events in Patients Receiving Rivaroxaban and/or Aspirin in a Randomized, Double-Blind, Placebo-Controlled Trial (opens in a new tab)
Paul Moayyedi, John W. Eikelboom, Jackie Bosch, et al.
Gastroenterology, 2019
Randomised trial
Highly cited for its field
Cited by 153- Rivaroxaban
- Pantoprazole
- Anticoagulants
Healing and relapse rates in gastroesophageal reflux disease treated with the newer proton-pump inhibitors lansoprazole, rabeprazole, and pantoprazole compared with omeprazole, ranitidine, and placebo: evidence from randomized clinical trials (opens in a new tab)
J. Jaime
Clinical Therapeutics, 2001
Randomised trial
Highly cited for its field
Cited by 133- Pantoprazole
- Anti-Ulcer Agents
- Benzimidazoles
Pantoprazole in Patients at Risk for Gastrointestinal Bleeding in the ICU (opens in a new tab)
Mette Krag, Søren Marker, Anders Perner, et al.
New England Journal of Medicine, 2018
Highly cited for its field
Cited by 341- Pantoprazole
- Gastrointestinal Hemorrhage
- Injections, Intravenous
Oral pantoprazole for erosive esophagitis: a placebo-controlled, randomized clinical trial (opens in a new tab)
Joel E. Richter, Wieslaw Bochenek
The American Journal of Gastroenterology, 2000
Randomised trial
Highly cited for its field
Cited by 103- Pantoprazole
- Anti-Ulcer Agents
- Benzimidazoles
Meta-analysis of the efficacy and safety of pantoprazole in the treatment and symptom relief of patients with gastroesophageal reflux disease – PAN-STAR (opens in a new tab)
Andrzej Dąbrowski, B. Štabuc, L. Lazebnik
Przegla̜d Gastroenterologiczny, 2018
Meta-analysis
Cited by 13High-dose amoxicillin and pantoprazole regimen for <i>Helicobacter pylori</i> eradication: a multi-center, multinational randomized controlled trial. (opens in a new tab)
Alavinejad P, Mohamadi S, Rezaei MJ, et al.
2025
Randomised trial
Comparison of safety and efficacy of pantoprazole alone with pantoprazole plus amitriptyline in functional dyspepsia patients: a randomized control trial (opens in a new tab)
Neelam Kumari, Atal Sood, Swatantara Gupta, et al.
International Journal of Basic & Clinical Pharmacology, 2025
Randomised trial
Pantoprazole Does Not Reduce the Antiplatelet Effect of Clopidogrel: A Randomized Controlled Trial in Korea (opens in a new tab)
Y. J. Choi, Nayoung Kim, I. Jang, et al.
Gut and Liver, 2017
Randomised trial
Cited by 29Comparison of efficacy of pantoprazole alone versus pantoprazole plus mosapride in therapy of gastroesophageal reflux disease: a randomized trial (opens in a new tab)
Karan Madan, Vineet Ahuja, Purna Kashyap, et al.
Diseases of the Esophagus, 2004
Randomised trial
Cited by 67- Pantoprazole
- Anti-Ulcer Agents
- Benzamides
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
1 hour
Mechanism
Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
2 – 3 hours
Pantoprazole is absorbed after oral administration as an enteric-coated tablet with maximum plasma concentrations attained within 2 – 3 hours…
Half-life
1 hour
About 1 hourF3202
Protein binding
98%
Approximately 98%[FDA label]
Volume of distribution
11.0-23.6 L
The apparent volume of distribution of pantoprazole is approximately 11.0-23.6 L, distributing mainly in the extracellular fluid.[FDA label]
Metabolism
80%
Pantoprazole is heavily metabolized in the liver by the cytochrome P450 (CYP) system.…
Elimination
71%
After a single oral or intravenous (IV) dose of 14C-labeled pantoprazole to healthy, normal metabolizing subjects, about 71% of the dose was…
Clearance
7.6-14.0 L/h
Adults: With intravenous administration of pantoprazole to extensive metabolizers, total clearance is 7.6-14.0…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Pantoprazole is a first-generation proton pump inhibitor (PPI) used for the management of gastroesophageal reflux disease (GERD), for gastric protection to prevent recurrence of stomach ulcers or gastric damage from chronic use of NSAIDs, and for the treatment of pathological hypersecretory conditions including Zollinger-Ellison (ZE) Syndrome. It can also be found in quadruple regimens for the treatment of H. pylori infections along with other antibiotics including [amoxicillin], [clarithromycin], and [metronidazole], for example.[A177271]F4498 Its efficacy is considered similar to other medications within the PPI class including [omeprazole], [esomeprazole], [lansoprazole], [dexlansoprazole], and [rabeprazole].
Pantoprazole 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 cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of pantoprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, pantoprazole's duration of antisecretory effect persists longer than 24 hours.[FDA Label]
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 pantoprazole have 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 osteoporosis and bone fractures later in life.[A177571]
PPIs such as pantoprazole 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.[A177577][A177580]
Pantoprazole doses should be slowly lowered, or tapered, before discontinuing as rapid discontinuation of PPIs such as pantoprazole may cause a rebound effect and a short term increase in hypersecretion.[A177574]
Pantoprazole 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 cell. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of pantoprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, pantoprazole's duration of antisecretory effect persists longer than 24 hours.[FDA Label]
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 pantoprazole have 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 osteoporosis and bone fractures later in life.[A177571]
PPIs such as pantoprazole 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.[A177577][A177580]
Pantoprazole doses should be slowly lowered, or tapered, before discontinuing as rapid discontinuation of PPIs such as pantoprazole may cause a rebound effect and a short term increase in hypersecretion.[A177574]
Properties:
View FDA drug labelsolid
Avg. mass: 383.37 Da
DrugBank indication
Pantoprazole Injection:
Treatment of gastroesophageal reflux disease associated with a history of erosive esophagitis
Pantoprazole for injection is indicated for short-term treatment (7-10 days) of patients having gastroesophageal reflux disease (GERD) with a history of erosive esophagitis, as an alternative to oral medication in patients who are unable to continue taking pantoprazole delayed-release tablets. Safety and efficacy of pantoprazole injection as the initial treatment of patients having GERD with a history of erosive esophagitis have not been demonstrated at this time.[FDA label]
Pathological Hypersecretion Associated with Zollinger-Ellison Syndrome
Pantoprazole for injection is indicated for the treatment of pathological hypersecretory conditions associated with Zollinger-Ellison Syndrome or other neoplastic conditions.[FDA label]
Pantoprazole delayed-release oral suspension:
Short-Term Treatment of erosive esophagitis associated with gastroesophageal reflux disease (GERD)
Indicated in adults and pediatric patients five years of age and above for the short-term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For adult patients who have not healed after 8 weeks of treatment, an additional 8-week course of pantoprazole may be considered. Safety of treatment beyond 8 weeks in pediatric patients has not been determined.F3202
Maintenance of healing of erosive esophagitis
Indicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in adult patients with GERD.F3202
Pathological hypersecretory conditions including Zollinger-Ellison syndrome
Indicated for the long-term treatment of the above conditions.F3202
Treatment of gastroesophageal reflux disease associated with a history of erosive esophagitis
Pantoprazole for injection is indicated for short-term treatment (7-10 days) of patients having gastroesophageal reflux disease (GERD) with a history of erosive esophagitis, as an alternative to oral medication in patients who are unable to continue taking pantoprazole delayed-release tablets. Safety and efficacy of pantoprazole injection as the initial treatment of patients having GERD with a history of erosive esophagitis have not been demonstrated at this time.[FDA label]
Pathological Hypersecretion Associated with Zollinger-Ellison Syndrome
Pantoprazole for injection is indicated for the treatment of pathological hypersecretory conditions associated with Zollinger-Ellison Syndrome or other neoplastic conditions.[FDA label]
Pantoprazole delayed-release oral suspension:
Short-Term Treatment of erosive esophagitis associated with gastroesophageal reflux disease (GERD)
Indicated in adults and pediatric patients five years of age and above for the short-term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For adult patients who have not healed after 8 weeks of treatment, an additional 8-week course of pantoprazole may be considered. Safety of treatment beyond 8 weeks in pediatric patients has not been determined.F3202
Maintenance of healing of erosive esophagitis
Indicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in adult patients with GERD.F3202
Pathological hypersecretory conditions including Zollinger-Ellison syndrome
Indicated for the long-term treatment of the above conditions.F3202
Also known as(60)
Pantoprazol
Pantoprazole
Pantoprazolum
7.2.2.19
Gastric H(+)/K(+) ATPase subunit alpha
Proton pump
Gastric H(+)/K(+) ATPase subunit beta
Proton pump beta chain
Molecular properties(19)
Drug interactions(1115)
Known interactions with other medications. Always consult a healthcare professional.
Cilostazol
Unknown severity
The serum concentration of Cilostazol can be increased when it is combined with Pantoprazole.
Dabrafenib
Unknown severity
The serum concentration of Pantoprazole can be decreased when it is combined with Dabrafenib.
Amphetamine
Moderate
Pantoprazole can cause an increase in the absorption of Amphetamine resulting in an increased serum concentration and potentially a worsening of adverse effects.
Pantoprazole can cause a decrease in the absorption of Bosutinib resulting in a reduced serum concentration and potentially a decrease in efficacy.
Cefditoren
Unknown severity
The serum concentration of Cefditoren can be decreased when it is combined with Pantoprazole.
Clopidogrel
Moderate
The serum concentration of the active metabolites of Clopidogrel can be reduced when Clopidogrel is used in combination with Pantoprazole resulting in a loss in efficacy.
Dabigatran etexilate
Moderate
Pantoprazole can cause a decrease in the absorption of Dabigatran etexilate resulting in a reduced serum concentration and potentially a decrease in efficacy.
Pantoprazole can cause a decrease in the absorption of Dasatinib resulting in a reduced serum concentration and potentially a decrease in efficacy.
Delavirdine
Moderate
Pantoprazole can cause a decrease in the absorption of Delavirdine resulting in a reduced serum concentration and potentially a decrease in efficacy.
Dextroamphetamine
Moderate
Pantoprazole can cause an increase in the absorption of Dextroamphetamine resulting in an increased serum concentration and potentially a worsening of adverse effects.
Pantoprazole can cause a decrease in the absorption of Erlotinib resulting in a reduced serum concentration and potentially a decrease in efficacy.
Fluconazole
Moderate
The metabolism of Pantoprazole can be decreased when combined with Fluconazole.
Pantoprazole can cause a decrease in the absorption of Gefitinib resulting in a reduced serum concentration and potentially a decrease in efficacy.
Pantoprazole can cause a decrease in the absorption of Indinavir resulting in a reduced serum concentration and potentially a decrease in efficacy.
Itraconazole
Moderate
Pantoprazole can cause a decrease in the absorption of Itraconazole resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ledipasvir
Moderate
Pantoprazole can cause a decrease in the absorption of Ledipasvir resulting in a reduced serum concentration and potentially a decrease in efficacy.
Methotrexate
Unknown severity
The excretion of Methotrexate can be decreased when combined with Pantoprazole.
Methylphenidate
Moderate
Pantoprazole can cause an increase in the absorption of Methylphenidate resulting in an increased serum concentration and potentially a worsening of adverse effects.
Dexmethylphenidate
Moderate
Pantoprazole can cause an increase in the absorption of Dexmethylphenidate resulting in an increased serum concentration and potentially a worsening of adverse effects.
The serum concentration of Nilotinib can be decreased when it is combined with Pantoprazole.
Pantoprazole can cause a decrease in the absorption of Pazopanib resulting in a reduced serum concentration and potentially a decrease in efficacy.
Posaconazole
Moderate
Pantoprazole can cause a decrease in the absorption of Posaconazole resulting in a reduced serum concentration and potentially a decrease in efficacy.
Raltegravir
Moderate
Pantoprazole can cause an increase in the absorption of Raltegravir resulting in an increased serum concentration and potentially a worsening of adverse effects.
Pantoprazole can cause a decrease in the absorption of Riociguat resulting in a reduced serum concentration and potentially a decrease in efficacy.
Risedronic acid
Moderate
Pantoprazole can cause an increase in the absorption of Risedronic acid resulting in an increased serum concentration and potentially a worsening of adverse effects.
Voriconazole
Moderate
The metabolism of Pantoprazole can be decreased when combined with Voriconazole.
Luliconazole
Unknown severity
The serum concentration of Pantoprazole can be increased when it is combined with Luliconazole.
Succinic acid
Unknown severity
The excretion of Succinic acid can be decreased when combined with Pantoprazole.
Citrulline
Unknown severity
The excretion of Citrulline can be decreased when combined with Pantoprazole.
Aminohippuric acid
Unknown severity
The excretion of Aminohippuric acid can be decreased when combined with Pantoprazole.
The excretion of Cefdinir can be decreased when combined with Pantoprazole.
Leucovorin
Unknown severity
The excretion of Leucovorin can be decreased when combined with Pantoprazole.
Fluorescein
Unknown severity
The excretion of Fluorescein can be decreased when combined with Pantoprazole.
The excretion of Quinapril can be decreased when combined with Pantoprazole.
Dinoprostone
Unknown severity
The excretion of Dinoprostone can be decreased when combined with Pantoprazole.
Famotidine
Unknown severity
The excretion of Famotidine can be decreased when combined with Pantoprazole.
Benzylpenicillin
Unknown severity
The excretion of Benzylpenicillin can be decreased when combined with Pantoprazole.
Tazobactam
Unknown severity
The excretion of Tazobactam can be decreased when combined with Pantoprazole.
Cyclic adenosine monophosphate
Unknown severity
The excretion of Cyclic adenosine monophosphate can be decreased when combined with Pantoprazole.
Cholic Acid
Unknown severity
The excretion of Cholic Acid can be decreased when combined with Pantoprazole.
Glutaric Acid
Unknown severity
The excretion of Glutaric Acid can be decreased when combined with Pantoprazole.
Oxalic Acid
Unknown severity
The excretion of Oxalic Acid can be decreased when combined with Pantoprazole.
Ellagic acid
Unknown severity
The excretion of Ellagic acid can be decreased when combined with Pantoprazole.
The excretion of Avibactam can be decreased when combined with Pantoprazole.
The excretion of Silibinin can be decreased when combined with Pantoprazole.
Relebactam
Unknown severity
The excretion of Relebactam can be decreased when combined with Pantoprazole.
The excretion of Cefotiam can be decreased when combined with Pantoprazole.
Tenofovir disoproxil
Unknown severity
The excretion of Tenofovir disoproxil can be decreased when combined with Pantoprazole.
Cephalexin
Unknown severity
The excretion of Cephalexin can be decreased when combined with Pantoprazole.
Valaciclovir
Unknown severity
The excretion of Valaciclovir can be decreased when combined with Pantoprazole.
Showing 50 of 1115 interactions
Food & lifestyle interactions
Advice
Take with or without food. The absorption is unaffected by food.
Toxicity & overdose
Rat Oral LD 50 747 mg/kgF3196
Tumorigenicity
Because of the chronic nature of GERD, there may be a potential for long-term administration of pantoprazole. In long-term rodent studies, pantoprazole was carcinogenic and its administration lead to rare types of gastrointestinal tumors. The relevance of these findings to tumor development in humans is unknown at this time.F3202
Teratogenic Effects
This drug falls under pregnancy category B category.
Reproduction studies have been performed in rats at oral doses up to 88 times the recommended human dose (RHD), as well as in rabbits at oral doses up to 16 times the RHD, and have shown no evidence of impaired fertility or harm to the fetus caused by pantoprazole. No adequate and well-controlled studies in pregnant women have been completed. Because animal reproduction studies are not always predictive of human response, this drug should only be used during pregnancy if clearly required.F3202
Nursing Mothers
Pantoprazole and its metabolites have been found to be excreted in the milk of rats.
Pantoprazole excretion in human milk has been found in a study performed with a single nursing mother after one 40 mg oral dose. The clinical relevance of this finding is not known, however, it is advisable to take note of this finding when considering pantoprazole use during nursing. Many drugs excreted in human breastmilk have a risk for serious adverse effects in nursing infants.F3202
Tumorigenicity
Because of the chronic nature of GERD, there may be a potential for long-term administration of pantoprazole. In long-term rodent studies, pantoprazole was carcinogenic and its administration lead to rare types of gastrointestinal tumors. The relevance of these findings to tumor development in humans is unknown at this time.F3202
Teratogenic Effects
This drug falls under pregnancy category B category.
Reproduction studies have been performed in rats at oral doses up to 88 times the recommended human dose (RHD), as well as in rabbits at oral doses up to 16 times the RHD, and have shown no evidence of impaired fertility or harm to the fetus caused by pantoprazole. No adequate and well-controlled studies in pregnant women have been completed. Because animal reproduction studies are not always predictive of human response, this drug should only be used during pregnancy if clearly required.F3202
Nursing Mothers
Pantoprazole and its metabolites have been found to be excreted in the milk of rats.
Pantoprazole excretion in human milk has been found in a study performed with a single nursing mother after one 40 mg oral dose. The clinical relevance of this finding is not known, however, it is advisable to take note of this finding when considering pantoprazole use during nursing. Many drugs excreted in human breastmilk have a risk for serious adverse effects in nursing infants.F3202
How it works
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, expressed in high quantities by the parietal cells of the stomach.[A174295] ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid).
Proton pump inhibitors such as pantoprazole are substituted benzimidazole derivatives, weak bases, which accumulate in the acidic space of the parietal cell before being converted in the canaliculi (small canal) of the gastric parietal cell, an acidic environment, to active sulfenamide derivatives. This active form then makes disulfide bonds with important cysteines on the gastric acid pump, inhibiting its function.[A174247] Specifically, pantoprazole binds to the sulfhydryl group of H+, K+-ATPase, which is an enzyme implicated in accelerating the final step in the acid secretion pathway. The enzyme is inactivated, inhibiting gastric acid secretion.[A174253] The inhibition of gastric acid secretion is stronger with proton pump inhibitors such as pantoprazole and lasts longer than with the H(2) antagonists.[A174295]
Proton pump inhibitors such as pantoprazole are substituted benzimidazole derivatives, weak bases, which accumulate in the acidic space of the parietal cell before being converted in the canaliculi (small canal) of the gastric parietal cell, an acidic environment, to active sulfenamide derivatives. This active form then makes disulfide bonds with important cysteines on the gastric acid pump, inhibiting its function.[A174247] Specifically, pantoprazole binds to the sulfhydryl group of H+, K+-ATPase, which is an enzyme implicated in accelerating the final step in the acid secretion pathway. The enzyme is inactivated, inhibiting gastric acid secretion.[A174253] The inhibition of gastric acid secretion is stronger with proton pump inhibitors such as pantoprazole and lasts longer than with the H(2) antagonists.[A174295]
Pharmacodynamics
This drug acts to decrease gastric acid secretion, which reduces stomach acidity. Pantoprazole administration leads to long-lasting inhibition of gastric acid secretion.F3193
General Effects
Pantoprazole has been shown to reduce acid reflux-related symptoms, heal inflammation of the esophagus, and improve patient quality of life more effectively than histamine-2 receptor antagonists (H2 blockers). This drug has an excellent safety profile and a low incidence of drug interactions. It can be used safely in various high-risk patient populations, including the elderly and those with renal failure or moderate hepatic dysfunction.[A174226]
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 pantoprazole have 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 osteoporosis and bone fractures later in life.[A177571]
PPIs such as pantoprazole 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 [A177577][A177580].
A note on laboratory testing abnormalities
During treatment with antisecretory medicinal products such as pantoprazole, serum gastrin (a peptide hormone that stimulates secretion of gastric acid) increases in response to the decreased acid secretion caused by proton pump inhibition. The increased gastrin level may interfere with investigations for neuroendocrine tumors. Published evidence suggests that proton pump inhibitors should be stopped 14 days before chromogranin A (CgA) measurements. This permits chromogranin A levels, that might be falsely elevated after proton pump inhibitor treatment, to return to the normal reference range.F3217
Reports have been made of false-positive results in urine screening tests for tetrahydrocannabinol (THC) in patients receiving the majority of proton pump inhibitors, including pantoprazole. A confirmatory method should be used.F3217
General Effects
Pantoprazole has been shown to reduce acid reflux-related symptoms, heal inflammation of the esophagus, and improve patient quality of life more effectively than histamine-2 receptor antagonists (H2 blockers). This drug has an excellent safety profile and a low incidence of drug interactions. It can be used safely in various high-risk patient populations, including the elderly and those with renal failure or moderate hepatic dysfunction.[A174226]
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 pantoprazole have 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 osteoporosis and bone fractures later in life.[A177571]
PPIs such as pantoprazole 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 [A177577][A177580].
A note on laboratory testing abnormalities
During treatment with antisecretory medicinal products such as pantoprazole, serum gastrin (a peptide hormone that stimulates secretion of gastric acid) increases in response to the decreased acid secretion caused by proton pump inhibition. The increased gastrin level may interfere with investigations for neuroendocrine tumors. Published evidence suggests that proton pump inhibitors should be stopped 14 days before chromogranin A (CgA) measurements. This permits chromogranin A levels, that might be falsely elevated after proton pump inhibitor treatment, to return to the normal reference range.F3217
Reports have been made of false-positive results in urine screening tests for tetrahydrocannabinol (THC) in patients receiving the majority of proton pump inhibitors, including pantoprazole. A confirmatory method should be used.F3217
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Pantoprazole is absorbed after oral administration as an enteric-coated tablet with maximum plasma concentrations attained within 2 – 3 hours and a bioavailability of 77% that does not change with multiple dosing .
[A174247]
Following an oral dose of 40mg, the Cmax is approximately 2.5 μg/mL with a tmax of 2 to 3 hours. The AUC is approximately 5 μg.h/mL. There is no food effect on AUC (bioavailability) and Cmax.F4486
Delayed-release tablets are prepared as enteric-coated tablets so that absorption of pantoprazole begins only after the tablet leaves the stomach.
[A174247]
Following an oral dose of 40mg, the Cmax is approximately 2.5 μg/mL with a tmax of 2 to 3 hours. The AUC is approximately 5 μg.h/mL. There is no food effect on AUC (bioavailability) and Cmax.F4486
Delayed-release tablets are prepared as enteric-coated tablets so that absorption of pantoprazole begins only after the tablet leaves the stomach.
Half-life
About 1 hourF3202
Protein binding
Approximately 98%[FDA label]
Volume of distribution
The apparent volume of distribution of pantoprazole is approximately 11.0-23.6 L, distributing mainly in the extracellular fluid.[FDA label]
Metabolism
Pantoprazole is heavily metabolized in the liver by the cytochrome P450 (CYP) system. Pantoprazole metabolism is independent of the route of administration (intravenous or oral). The main metabolic pathway is demethylation, by CYP2C19 hepatic cytochrome enzyme, followed by sulfation; other metabolic pathways include oxidation by CYP3A4.
There is no evidence that any of the pantoprazole metabolites are pharmacologically active.F3202
After hepatic metabolism, almost 80% of an oral or intravenous dose is excreted as metabolites in urine; the remainder is found in feces and originates from biliary secretion.
[A174256]
There is no evidence that any of the pantoprazole metabolites are pharmacologically active.F3202
After hepatic metabolism, almost 80% of an oral or intravenous dose is excreted as metabolites in urine; the remainder is found in feces and originates from biliary secretion.
[A174256]
Route of elimination
After a single oral or intravenous (IV) dose of 14C-labeled pantoprazole to healthy, normal metabolizing subjects, about 71% of the dose was excreted in the urine, with 18% excreted in the feces by biliary excretion. There was no kidney excretion of unchanged pantoprazole.F3202
Clearance
Adults: With intravenous administration of pantoprazole to extensive metabolizers, total clearance is 7.6-14.0 L/h.F3193
In a population pharmacokinetic analysis, the total clearance increased with increasing body weight in a non-linear fashion.F3193
Children: clearance values in the children 1 to 5 years old with endoscopically proven GERD had a median value of 2.4 L/h.F3202
In a population pharmacokinetic analysis, the total clearance increased with increasing body weight in a non-linear fashion.F3193
Children: clearance values in the children 1 to 5 years old with endoscopically proven GERD had a median value of 2.4 L/h.F3202
Drug targets(3)
Proteins and enzymes this drug interacts with in the body
Potassium-transporting ATPase alpha chain 1
ATP4A
inhibitor
Specific functionATP binding
Cellular location
Apical cell membrane
General function & pharmacology
The catalytic subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Uses ATP as an energy source to pump H(+) ions to the gastric lumen while transporting K(+) ion from the lumen into the cell (By similarity). Remarkably generates a million-fold proton gradient across the gastric parietal cell membrane, acidifying the gastric juice down to pH 1 (By similarity).
Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). The release of the H(+) ion in the stomach lumen is followed by binding of K(+) ion converting the pump conformation back to the E1 state (By similarity)
Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2). The release of the H(+) ion in the stomach lumen is followed by binding of K(+) ion converting the pump conformation back to the E1 state (By similarity)
Potassium-transporting ATPase subunit beta
ATP4B
modulator
Specific functionATPase activator activity
Cellular location
Apical cell membrane
General function & pharmacology
The beta subunit of the gastric H(+)/K(+) ATPase pump which transports H(+) ions in exchange for K(+) ions across the apical membrane of parietal cells. Plays a structural and regulatory role in the assembly and membrane targeting of a functionally active pump (By similarity). Within a transport cycle, the transfer of a H(+) ion across the membrane is coupled to ATP hydrolysis and is associated with a transient phosphorylation of the alpha subunit that shifts the pump conformation from inward-facing (E1) to outward-facing state (E2).
Interacts with the phosphorylation domain of the alpha subunit and functions as a ratchet, stabilizing the lumenal-open E2 conformation and preventing the reverse reaction of the transport cycle (By similarity)
Interacts with the phosphorylation domain of the alpha subunit and functions as a ratchet, stabilizing the lumenal-open E2 conformation and preventing the reverse reaction of the transport cycle (By similarity)
N(G),N(G)-dimethylarginine dimethylaminohydrolase 1
DDAH1
inhibitor
Specific functionamino acid binding
General function & pharmacology
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation
Metabolizing enzymes(2)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP2C19Cytochrome P450 2C19
substrate
inhibitor
CYP3A4Cytochrome P450 3A4
substrate
Transporters(3)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Organic anion transporter 3
SLC22A8
inhibitor
Specific functionorganic anion transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Functions as an organic anion/dicarboxylate exchanger that couples organic anion uptake indirectly to the sodium gradient .
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
Biological pathways(2)
Scientific references(15)
Mathews S., Reid A., Tian C., Cai Q.
An update on the use of pantoprazole as a treatment for gastroesophageal reflux disease. Clinical and Experimental Gastroenterology. 2010;:11. doi: 10.
2147/ceg
s6355
Dabrowski A., Stabuc B., Lazebnik L.
Meta-analysis of the efficacy and safety of pantoprazole in the treatment and symptom relief of patients with gastroesophageal reflux disease - PAN-STAR.
Prz Gastroenterol
201813(1):6-15. doi: 10.5114/pg.2018.74556. Epub 2018 Mar 26
Strand D.S., Kim D., Peura D.A.
25 Years of Proton Pump Inhibitors: A Comprehensive Review.
Gut Liver
2017 Jan 1511(1):27-37. doi: 10.5009/gnl15502
Jungnickel P.W.
Pantoprazole: A new proton pump inhibitor.
Clinical Therapeutics
200022(11):1268-1293. doi: 10.1016/s0149-2918(00)83025-8
Shin J.M., Kim N.
Pharmacokinetics and pharmacodynamics of the proton pump inhibitors.
Journal Neurogastroenterol Motil
2013 Jan19(1):25-35. doi: 10.5056/jnm.2013.19.1.25. Epub 2013 Jan 8
Bardou M., Martin J.
Pantoprazole: from drug metabolism to clinical relevance.
Expert Opinion Drug Metabolism Toxicology
2008 Apr4(4):471-83. doi: 10.1517/17425255.4.4.471
Shin J.M., Sachs G.
Differences in binding properties of two proton pump inhibitors on the gastric H+,K+-ATPase in vivo.
Biochemical Pharmacology
2004 Dec 168(11):2117-27. doi: 10.1016/j.bcp.2004.07.035
Huber R., Hartmann M., Bliesath H., Luhmann R., Steinijans V.W., Zech K.
Twenty‐four‐hour intragastric pH profiles and pharmacokinetics following single and repeated oral administration of the proton pump inhibitor pantoprazole in comparison to omeprazole..
Alimentary Pharmacology & Therapeutics
199610(3):359-366. doi: 10.1111/j.0953-0673.1996.00359.x
Lewin M.J.
Cellular mechanisms and inhibitors of gastric acid secretion.
Drugs of Today
199935(10):743. doi: 10.1358/dot.1999.35.10.561693
Fallone C.A., Chiba N., van Zanten S.V., Fischbach L., Gisbert J.P., Hunt R.H., Jones N.L., Render C., Leontiadis G.I., Moayyedi P., Marshall J.K.
The Toronto Consensus for the Treatment of Helicobacter pylori Infection in Adults.
Gastroenterology
2016 Jul151(1):51-69.e14. doi: 10.1053/j.gastro.2016.04.006. Epub 2016 Apr 19
Tanus-Santos J.E., Pinheiro L.C.
Proton pump inhibitors: new mechanisms of action. Basic Clin Pharmacol Toxicol. 2019 Apr 13. doi: 10.
1111/bcpt
13237
Haastrup P.F., Thompson W., Sondergaard J., Jarbol D.E.
Side Effects of Long-Term Proton Pump Inhibitor Use: A Review.
Basic & Clinical Pharmacology & Toxicology
2018 Aug123(2):114-121. doi: 10.1111/bcpt.13023. Epub 2018 May 24
Reimer C., Sondergaard B., Hilsted L., Bytzer P.
Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy.
Gastroenterology
2009 Jul137(1):80-7, 87.e1. doi: 10.1053/j.gastro.2009.03.058. Epub 2009 Apr 10
Ghebremariam Y.T., LePendu P., Lee J.C., Erlanson D.A., Slaviero A., Shah N.H., Leiper J., Cooke J.P.
Unexpected effect of proton pump inhibitors: elevation of the cardiovascular risk factor asymmetric dimethylarginine.
Circulation
2013 Aug 20128(8):845-53. doi: 10.1161/CIRCULATIONAHA.113.003602. Epub 2013 Jul 3
Tommasi S., Elliot D.J., Hulin J.A., Lewis B.C., McEvoy M., Mangoni A.A.
Human dimethylarginine dimethylaminohydrolase 1 inhibition by proton pump inhibitors and the cardiovascular risk marker asymmetric dimethylarginine: in vitro and in vivo significance.
Science Reports
2017 Jun 67(1):2871. doi: 10.1038/s41598-017-03069-1
ATC classification(3 codes)
ATC A02BD04
ATC A02BD11
ATC A02BC02
Affected organisms(1)
Humans and other mammals
Salt forms(4)
Pantoprazole magnesium(DBSALT000853)
Pantoprazole magnesium dihydrate(DBSALT002977)
Pantoprazole magnesium hemipentahydrate(DBSALT001960)
Pantoprazole sodium(DBSALT000386)
Experimental properties(5)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Pantoprazole
Additional database identifiers
Drugs Product Database (DPD)
11086
ChemSpider
4517
BindingDB
50241342
HUGO Gene Nomenclature Committee (HGNC)
HGNC:819
GenAtlas
ATP4A
GeneCards
ATP4A
GenBank Gene Database
J05451
GenBank Protein Database
561634
Guide to Pharmacology
849
UniProt Accession
ATP4A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:820
GenAtlas
ATP4B
GeneCards
ATP4B
GenBank Gene Database
M75110
GenBank Protein Database
184105
UniProt Accession
ATP4B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2715
GenAtlas
DDAH1
GeneCards
DDAH1
GenBank Gene Database
AB001915
GenBank Protein Database
4160666
Guide to Pharmacology
1247
UniProt Accession
DDAH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
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Source: go.drugbank.comCC BY-NC 4.0
Updated 4 months ago(8 Mar 2026)Structured knowledge from the free knowledge base
WHO INN:pantoprazole
International Nonproprietary Name
ATC classifications (Wikidata)
Linked open data from Wikidata (Q286846), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.