General
Preferred name
PANTOPRAZOLE
Synonyms
Pantoprazole (sodium hydrate) ()
BY1023 (sodium hydrate) ()
SKF96022 (sodium hydrate) ()
SKF96022 sodium hydrate ()
Pantecta ()
SKF96022 sodium ()
SKF96022 (sodium) ()
BY1023 (sodium) ()
BY-1023 sodium ()
Pantoloc ()
SKF96022 ()
BY1023 ()
Pantoprazole Sodium Hydrate ()
PANTOPRAZOLE SODIUM ()
SKF96022 (sodium)BY1023 (sodium)SKF96022 sodium ()
SKF96022 (sodium hydrate)BY1023 (sodium hydrate)SKF96022 sodium hydrate ()
Pantoprazole (Protonix) ()
Protonix / Pantozol ()
Pantoprazole (sodium) ()
SKF96022 sodium, BY-1023 sodium ()
SKFSKF96022, BY-1023 ()
Protonix, BY1023 sodium hydrate, SKF96022 sodium hydrate ()
Pantoprazole ()
SK&F-96022 ()
Zovanta ()
Altopan ()
BY 1023 ()
SK&F 96022 ()
SKF-96022 ()
Protium ()
Pantocid ()
NSC-759257 ()
Protium i.v. ()
Pantoprazol ()
BY-1023 ()
SK-96022 ()
Pantozol ()
Pantecta control ()
Pantoprazole sodium hydrate ()
Controloc control ()
Pantozol control ()
Somac control ()
Pantoprazole (as sodium) ()
Pantoloc Control ()
Protonix Iv ()
Pantoprazole sodium sesquihydrate ()
Protonix ()
Pantoprazole-d6 ()
P&D ID
PD000711
CAS
922727-65-9
164579-32-2
138786-67-1
102625-70-7
Tags
available
drug
Approved by
FDA
First approval
2000
Drug indication
Gastroesophageal reflux disease
Drug Status
approved
Max Phase
4.0
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
HALF-LIFE About 1 hour [F3202].
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]. **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].
ROE 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].
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].
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].
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]. Delayed-release tablets are prepared as enteric-coated tablets so that absorption of pantoprazole begins only after the tablet leaves the stomach.
TOXICITY **Rat Oral LD 50** 747 mg/kg [F3196] ; ; **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].; ;
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].
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.
DESCRIPTION Pantoprazole is a proton pump inhibitor.
Marketed formulations may contain pantoprazole sodium (PubChem CID 15008962) or pantoprazole sodium sesquihydrate (PubChem CID 23690067). (GtoPdb)
MOA 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].
TOXICITY **Rat Oral LD 50** 747 mg/kg [F3196] **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].
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].
MOA 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].
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].
PRICE 29
DESCRIPTION Pantoprazole (BY10232) is an orally active and potent proton pump inhibitor (PPI)[1]. Pantoprazole, a substituted benzimidazole, is a potent H+/K+-ATPase inhibitor with an IC50 of 6.8 ¦ÌM. Pantoprazole improves pH stability and has anti-secretory, anti-ulcer activities. Pantoprazole significantly increased tumor growth delay combined with Doxorubicin (HY-15142)[3][4].
PRICE 29
DESCRIPTION Pantoprazole sodium (BY10232 sodium) is an orally active and potent proton pump inhibitor (PPI)[1]. Pantoprazole sodium, a substituted benzimidazole, is a potent H+/K+-ATPase inhibitor with an IC50 of 6.8 ¦ÌM. Pantoprazole sodium improves pH stability and has anti-secretory, anti-ulcer activities. Pantoprazole sodium significantly increased tumor growth delay combined with Doxorubicin (HY-15142)[3][4].
PRICE 29
DESCRIPTION Pantoprazole, an irreversible protonpump inhibitor, inhibits the final step of the production ofgastric acid by binding to the sites of H+/K+ ATPase system in gastric parietal cells. (BOC Sciences Bioactive Compounds)
DESCRIPTION Pantoprazole (BY1023) is a proton pump inhibitor used for short-term treatment of erosion and ulceration of the esophagus caused by gastroesophageal reflux disease. (TargetMol Bioactive Compound Library)
DESCRIPTION Pantoprazole sodium (Pantecta) is the sodium salt form of a substituted benzimidazole with proton pump inhibitor activity. Pantoprazole sodium is a lipophilic, weak base that crosses the parietal cell membrane and enters the acidic parietal cell canaliculus where it becomes protonated, producing the active metabolite sulfenamide, which forms an irreversible covalent bond with two sites of the H+/K+-ATPase enzyme located on the gastric parietal cell, thereby inhibiting both basal and stimulated gastric acid production. (TargetMol Bioactive Compound Library)
DESCRIPTION Pantoprazole Sodium Hydrate (BY1023 (sodium hydrate)) is a proton pump inhibitor drug, used for short-term treatment of erosion and ulceration of the esophagus caused by gastroesophageal reflux disease. (TargetMol Bioactive Compound Library)
Cell lines
0
Organisms
4
Compound Sets
26
AdooQ Bioactive Compound Library
A11696
Axon Medchem Screening Library
3161
BOC Sciences Bioactive Compounds
pantoprazole-cas-102625-70-7-item-331793
Cayman Chemical Bioactives
21345
28483
ChEMBL Approved Drugs
CHEMBL1502
CHEMBL3989559
ChEMBL Drugs
CHEMBL1502
CHEMBL3989559
DrugBank
DB00213
DrugBank Approved Drugs
DB00213
DrugCentral
2054
DrugCentral Approved Drugs
2054
DrugMAP
DMSVOCZ
DrugMAP Approved Drugs
DMSVOCZ
DrugMatrix
EU-OPENSCREEN Bioactive Compound Library
EOS101284
Guide to Pharmacology
7260
MedChem Express Bioactive Compound Library
HY-17507
HY-17507A
Natural product-based probes and drugs
NCATS Inxight Approved Drugs
D8TST4O562
NIH Clinical Collections (NCC)
NPC Screening Collection
Other bioactive compounds
Prestwick Chemical Library
ReFrame library
Selleckchem Bioactive Compound Library
pantoprazole-protonix
pantoprazole-sodium
pantoprazole-sodium-hydrate
TargetMol Bioactive Compound Library
T6928
T6929
T0161
The Spectrum Collection
External IDs
105
Properties
(calculated by RDKit )
Molecular Weight
383.08
Hydrogen Bond Acceptors
6
Hydrogen Bond Donors
1
Rotatable Bonds
7
Ring Count
3
Aromatic Ring Count
3
cLogP
2.88
TPSA
86.33
Fraction CSP3
0.25
Chiral centers
1.0
Largest ring
6.0
QED
0.68
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Target
Proton Pump
Potassium-transporting ATPase
PPI
Bacterial
ATPase,Proton Pump
HIF-1α
Pronton Pump
Pathway
Membrane Transporter/Ion Channel
Apoptosis
Autophagy
Angiogenesis
Chromatin/Epigenetic
Anti-infection
MOA
Potassium Channel agonist
Proton Pump inhibitor
Therapeutic Indication
Antiulcer
Therapeutic Class
Antiulcer Agents
Solubility
10 mM in DMSO
Source data