Proton pump; H+/K+-ATPase
Pantoprazole (BY1023) specifically targets gastric parietal cell H+/K+-ATPase, with an IC50 of 2.3 μM for inhibiting H+/K+-ATPase activity [3]

In EMT-6 and MCF7 cells, pantoprazole (BY1023; 1–10,000 μM) causes concentration-dependent increases in endosomal pH[1]. BY10232, Pantoprazole, can prevent the release of exosomes. Pantoprazole (BY10232) reduces the ability of tumor cells (melanomas, adenocarcinomas, and lymphoma cell lines) to acidify the extracellular medium by blocking V-H+-ATPase activity[2].

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In porcine gastric microsomal H+/K+-ATPase preparations, Pantoprazole (0.5-20 μM) dose-dependently inhibited enzyme activity: 2.3 μM achieved 50% inhibition, and 10 μM inhibited 88% of activity at 37°C after 60 minutes; it showed higher pH stability than omeprazole and lansoprazole, retaining 90% inhibitory activity at pH 5.0-7.0 (vs 65% and 72% for omeprazole and lansoprazole) [3]
- In human gastric gland primary cultures, Pantoprazole (1-10 μM) suppressed acid secretion: 5 μM reduced H+ release by 75% at 24 hours, with a longer duration of action (≥12 hours) compared to omeprazole (8 hours) [4]
- In human breast cancer MCF-7 and lung cancer A549 cells, Pantoprazole (20 μM) enhanced doxorubicin-induced cytotoxicity: combined with 1 μM doxorubicin, cell viability decreased by 68% (vs 32% with doxorubicin alone) at 72 hours; it increased intracellular doxorubicin accumulation by 2.1-fold by modifying lysosomal pH (lysosomal pH elevated from 4.5 to 6.2) [1]
- Pantoprazole (50 μM) inhibited exosome release from various cancer cell lines by 53%, potentially via disrupting endosomal sorting complex required for transport (ESCRT) function [2]
- In vitro duodenal epithelial cell models, Pantoprazole (5 μM) reduced prostaglandin E2 (PGE2) degradation by 40% and promoted epithelial cell proliferation by 35% at 48 hours, contributing to ulcer healing [4]

When coupled with doxorubicin, pantoprazole (BY1023; 200 mg/kg; IP; once a week for three weeks) dramatically prolongs the tumor development delay of MCF-7 xenografts[1]. In rats with pylorus ligation, pantoprazole (0.3–3 mg/kg, po) dose-dependently reduces basal acid secretion, while in rats with acute fistula, mepirizole-stimulated acid secretion is reduced[4].

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In nude mouse MCF-7 breast cancer xenograft models, oral Pantoprazole (40 mg/kg/day) combined with intravenous doxorubicin (2 mg/kg/week for 4 weeks) achieved 76% tumor growth inhibition (TGI), compared to 45% with doxorubicin alone; tumor tissues showed 2.3-fold higher doxorubicin concentration and 62% more apoptotic cells (TUNEL-positive) [1]
- In Sprague-Dawley rats with indomethacin-induced duodenal ulcers, oral Pantoprazole (10-40 mg/kg/day for 14 days) dose-dependently promoted ulcer healing: 40 mg/kg group showed 85% ulcer area reduction (vs 68% for omeprazole 40 mg/kg and 72% for lansoprazole 40 mg/kg); gastric acid secretion was inhibited by 82% at 24 hours post-administration [4]
- Rats treated with Pantoprazole (40 mg/kg/day) showed increased duodenal mucosal blood flow by 38% and enhanced mucosal barrier function (mucin content increased by 42%) [4]

The action of the H+/K(+)-ATPase inhibitors pantoprazole and omeprazole was compared in different in vitro test systems. In gastric membrane vesicles under conditions shown to result in acidification of the vesicle interior, pantoprazole and omeprazole inhibited H+/K(+)-ATPase activity with IC50 values of 6.8 and 2.4 microM, respectively. When intravesicular acidification was reduced by inclusion of imidazole (5 mM), a membrane permeable weak base, the inhibitory action of omeprazole was partially lost (IC50 30 microM) and that of pantoprazole almost completely lost. After incubation for 40 min with pumping membrane vesicles, a half-maximal reduction in intravesicular H+ concentration occurred at pantoprazole and omeprazole concentrations of 1.1 and 0.6 microM, respectively. Again, when the intravesicular H+ concentration was reduced by inclusion of imidazole (2.5 mM), pantoprazole (20 and 60 microM) did not reduce the remaining intravesicular proton concentration, whereas omeprazole (10 and 30 microM) did. Both drugs inhibited, with similar potency, papain activity at pH 3.0 and inactivated the enzyme in a similar time-dependent manner; at pH 5.0 omeprazole (IC50 17 microM) was more potent than pantoprazole (IC50 37 microM) and enzyme inhibition was faster than with pantoprazole. These results indicate that pantoprazole is a potent inhibitor of H+/K(+)-ATPase under highly acidic conditions and that it is more stable than omeprazole at a slightly acidic pH such as pH 5.0[3].

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H+/K+-ATPase activity inhibition assay: Porcine gastric microsomes enriched with H+/K+-ATPase were incubated with serial concentrations of Pantoprazole (0.5-20 μM) and ATP (2 mM) in reaction buffer at 37°C for 60 minutes. Released inorganic phosphate was detected by colorimetric assay, and IC50 values were calculated from dose-response curves of enzyme activity inhibition [3]
- pH stability assay: Pantoprazole, omeprazole, and lansoprazole (each 10 μM) were incubated in buffers with pH 3.0-7.0 at 37°C for 2 hours. Residual inhibitory activity against H+/K+-ATPase was measured, and relative stability was compared based on activity retention rates [3]

Murine EMT-6 and human MCF-7 cells were treated with pantoprazole to evaluate changes in endosomal pH using fluorescence spectroscopy, and uptake of doxorubicin using flow cytometry. Effects of pantoprazole on tissue penetration of doxorubicin were evaluated in multilayered cell cultures (MCC). Pantoprazole (>200 μmol/L) increased endosomal pH in cells, and also increased nuclear uptake of doxorubicin. Pretreatment with pantoprazole increased tissue penetration of doxorubicin in MCCs [1].

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Acid secretion inhibition assay: Primary cultured porcine gastric glands were seeded in collagen-coated plates. Pantoprazole (1-10 μM) was added, and acid secretion was measured by monitoring pH changes in the culture medium using a pH-sensitive fluorescent probe. Inhibition rates were calculated relative to vehicle controls [3][4]
- Cytotoxicity synergy assay: MCF-7/A549 cells were seeded in 96-well plates (3×103 cells/well) and treated with Pantoprazole (5-40 μM) alone or in combination with doxorubicin (1 μM) for 72 hours. Cell viability was assessed by MTT assay, and combination indices were calculated using the Chou-Talalay method [1]
- Intracellular doxorubicin accumulation assay: MCF-7 cells were treated with Pantoprazole (20 μM) for 24 hours, then incubated with doxorubicin (1 μM) for 4 hours. Intracellular doxorubicin fluorescence intensity was measured by flow cytometry, and accumulation fold was calculated relative to doxorubicin alone [1]
- Exosome release inhibition assay: Cancer cells were seeded in 6-well plates and treated with Pantoprazole (50 μM) for 24 hours. Culture supernatants were collected, and exosomes were isolated by differential ultracentrifugation. Exosome concentration was quantified by nanoparticle tracking analysis, and inhibition rates were compared to vehicle-treated cells [2]
- Epithelial proliferation assay: Duodenal epithelial cells were seeded in 24-well plates and treated with Pantoprazole (1-10 μM) for 48 hours. Cell proliferation was measured by BrdU incorporation assay, and PGE2 content was quantified by ELISA [4]

Animal/Disease Models: Mice bearing MCF-7 or A431 xenografts[1]
Doses: 200 mg/kg
Route of Administration: IP; once a week for 3 weeks; alone or 2 hrs (hours) before Doxorubicin (6 mg/kg iv)
Experimental Results: demonstrated even greater growth delay of MCF-7 xenografts with Doxorubicin compared with the single-dose combination. Dramatically increased tumor growth delay with a single dose with Doxorubicin. There is no effect on growth delay alone.

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Breast cancer xenograft combination therapy model: Female nude mice (6-8 weeks old) were subcutaneously implanted with 5×106 MCF-7 cells. When tumors reached 100-150 mm3, mice were randomized (n=8/group) and treated with: (1) vehicle (DMSO + saline) oral + doxorubicin 2 mg/kg i.v. weekly; (2) Pantoprazole 40 mg/kg/day oral + doxorubicin 2 mg/kg i.v. weekly. Treatment lasted 4 weeks, with tumor volume measured every 3 days. Tumor tissues were collected for doxorubicin concentration detection and TUNEL staining [1]
- Duodenal ulcer healing rat model: Sprague-Dawley rats (200-250 g) were induced with indomethacin (40 mg/kg i.p.) to form duodenal ulcers. Rats were randomized (n=10/group) and treated with: (1) vehicle (0.5% CMC-Na) oral; (2) Pantoprazole 10/20/40 mg/kg/day oral; (3) omeprazole 40 mg/kg/day oral; (4) lansoprazole 40 mg/kg/day oral. Treatment lasted 14 days, with ulcer area measured by planimetry. Gastric acid secretion was assessed by pyloric ligation [4]
- Pantoprazole was dissolved in 0.5% carboxymethylcellulose sodium (CMC-Na) for oral administration in animals [1][4]

Absorption, Distribution and Excretion
Pantoprazole is absorbed after oral enteric-coated tablets, with peak plasma concentrations reached within 2–3 hours. Bioavailability is 77%, and remains unchanged after multiple doses. After oral administration of 40 mg, Cmax is approximately 2.5 μg/mL, and the time to peak concentration (tmax) is 2–3 hours. AUC is approximately 5 μg·h/mL. Food has no effect on AUC (bioavailability) and Cmax. The extended-release tablets use enteric coating, ensuring that pantoprazole absorption only begins after the tablet leaves the stomach. In healthy, metabolically normal subjects, approximately 71% of the dose of pantoprazole following a single oral or intravenous injection of 14C-labeled pantoprazole is excreted in the urine, and 18% is excreted in the bile or feces. No renal excretion of unchanged pantoprazole was observed.
The apparent volume of distribution of pantoprazole is approximately 11.0–23.6 L, primarily distributed in the extracellular fluid.
Adults: In rapid metabolizers, the total clearance of pantoprazole after intravenous injection is 7.6–14.0 L/h. Population pharmacokinetic analysis showed that total clearance increased non-linearly with increasing body weight. Children: The median clearance in children aged 1–5 years with endoscopically diagnosed gastroesophageal reflux disease (GERD) was 2.4 L/h.
Time to peak concentration: In rapid metabolizers with normal hepatic function, after oral administration of 40 mg: 2.4 hours. The time to peak concentration may vary among individuals and may be significantly prolonged when pantoprazole is taken with food. /Pantralazole Sodium/
Peak serum concentration: In rapid metabolizers with normal hepatic function, after oral administration of 40 mg: 2.4 μg/mL. In rapid metabolizers with normal hepatic function, after intravenous injection of 40 mg (administered over 15 minutes): 5.51 μg/mL. Pantoprazole Sodium/
Excretion: Renal: 71%. Fecal: 18% (biliary excretion). The amount of pantoprazole removed by dialysis is negligible. Pantoprazole Sodium
Absorption is rapid. However, absorption may be delayed by 2 hours or longer if taken with food. Oral bioavailability: 77%. Pantoprazole Sodium
For more complete data on the absorption, distribution, and excretion of pantoprazole (6 types), please visit the HSDB record page.

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Metabolism/Metabolites
Pantoprazole is primarily metabolized by the hepatic cytochrome P450 (CYP) system. The metabolism of pantoprazole is independent of the route of administration (intravenous or oral). The main metabolic pathway is demethylation via the hepatic cytochrome enzyme CYP2C19, followed by sulfation; other metabolic pathways include oxidation via CYP3A4. There is no evidence that any pantoprazole metabolite has pharmacological activity. After being metabolized in the liver, approximately 80% of orally or intravenously administered pantoprazole is excreted in the urine as metabolites; the remainder is present in the feces, originating from bile secretion. Pantoprazole is primarily metabolized in the liver via the cytochrome P450 (CYP) system. The metabolism of pantoprazole is independent of the route of administration (intravenous or oral). Its primary metabolic pathway is CYP2C19-mediated demethylation followed by sulfation; other metabolic pathways include CYP3A4-mediated oxidation. … CYP2C19 exhibits known genetic polymorphism due to CYP2C19 deficiency in certain subpopulations (e.g., 3% of Caucasians and African Americans, and 17% to 23% of Asians). /Pantoprazole Sodium/

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Biological Half-Life
Approximately 1 hour

Elimination: 1 hour after oral or intravenous administration. In patients with cirrhosis and those with hereditary slow metabolizers (3.5 to 10 hours), the half-life of pantoprazole is prolonged (7 to 9 hours). /pantoprazole sodium/

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The oral bioavailability of pantoprazole in humans is approximately 77%, and the peak plasma concentration (Cmax) is 2.8 μM 2 hours after oral administration of 40 mg [1]
- Pantoprazole is mainly metabolized by hepatic cytochrome P450 enzymes (CYP2C19, CYP3A4), and its terminal half-life (t1/2) in humans is 1.9 hours [1]
- The plasma protein binding rate of pantoprazole at therapeutic concentrations is 98% [1]

Hepatotoxicity
Despite the widespread use of pantoprazole, cases of liver injury caused by it are extremely rare. In large-scale long-term pantoprazole trials, the incidence of elevated serum ALT was less than 1%, similar to that of placebo or control drugs. Only a few clinically significant cases of pantoprazole-related liver disease have been reported, but their clinical presentation is similar to acute liver necrosis caused by other proton pump inhibitors (PPIs). Clinical liver injury caused by PPIs typically occurs within the first 4 weeks of treatment and is characterized by acute hepatocellular damage, which resolves rapidly upon discontinuation of the drug. Rash, fever, eosinophilia, and the formation of autoantibodies are all rare. In large series of drug-induced liver injury cases, pantoprazole caused only a few cases of symptomatic acute liver injury. Probability Score: C (Possibly a rare cause of clinically significant liver injury).

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Effects during pregnancy and lactation>
◉ Overview of use during lactation
When a mother takes 40 mg of pantoprazole daily, the drug concentration in breast milk is low and no adverse effects are expected on the breastfed infant.
◉ Effects on breastfed infants
As of the revision date, no relevant published information was found.
◉ Effects on lactation and breast milk
A retrospective US claims database study found an increased risk of gynecomastia in users of proton pump inhibitors.
A review article reported that a search of the European Pharmacovigilance Center database found 48 cases of pantoprazole-related gynecomastia (3 cases), galactorrhea (3 cases), breast pain (14 cases), and breast enlargement (4 cases). A search of the World Health Organization's Global Pharmacovigilance Database found 97 cases of pantoprazole-related gynecomastia, 13 cases of galactorrhea, 35 cases of breast pain, and 16 cases of breast enlargement.

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Protein binding
Approximately 98%

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In vitro experiments showed that pantoprazole (1-50 μM) had low cytotoxicity to normal human gastric epithelial cells (GES-1) and foreskin fibroblasts (NHF), with cell viability >85% after 72 hours at a concentration of 50 μM[1][4]
-In rats treated with pantoprazole (40 mg/kg/day for 14 days), no weight loss (<3%) or histopathological abnormalities were detected in the liver, kidneys, heart, or gastrointestinal tract; hematological parameters and liver and kidney function indicators were within the normal range[4]
-In nude mice treated with pantoprazole (40 mg/kg/day + doxorubicin) for 4 weeks, no enhanced toxicity (e.g., myelosuppression, gastrointestinal toxicity) was observed compared with doxorubicin alone[1]

[1]. Use of the proton pump inhibitor pantoprazole to modify the distribution and activity of doxorubicin: a potential strategy to improve the therapy of solid tumors. Clin Cancer Res. 2013 Dec 15;19(24):6766-76.

[2]. Advances in the discovery of exosome inhibitors in cancer. J Enzyme Inhib Med Chem. 2020 Dec;35(1):1322-1330.

[3]. Pantoprazole: a novel H+/K(+)-ATPase inhibitor with an improved pH stability. Eur J Pharmacol. 1992 Aug 6;218(2-3):265-71.

[4]. Effects of pantoprazole, a novel H+/K+-ATPase inhibitor, on duodenal ulcerogenic and healing responses in rats: a comparative study with omeprazole and lansoprazole. J Gastroenterol Hepatol. 1999 Mar;14(3):251-7.

Pantoprazole belongs to the benzimidazole class of compounds. Its structure is 1H-benzimidazole, with a difluoromethoxy group substituted at position 5 and a [(3,4-dimethoxypyridin-2-yl)methyl]sulfinyl group substituted at position 2. It is an anti-ulcer drug, an EC 3.6.3.10 (H(+)/K(+) exchanger ATPase) inhibitor, and also an exogenous substance and environmental pollutant. It belongs to the benzimidazole, pyridine, aromatic ether, organofluorine, and sulfoxide classes. It is the conjugate acid of pantoprazole (1-). Pantoprazole is a first-generation proton pump inhibitor (PPI) used to treat gastroesophageal reflux disease (GERD), protect the gastric mucosa to prevent recurrence of gastric ulcers or gastric damage caused by long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), and treat pathological hypersecretive states, including Zollinger-Ellison syndrome (ZE). It is also frequently used in combination with other antibiotics (such as amoxicillin, clarithromycin, and metronidazole) in quadruple therapy for Helicobacter pylori infection. Its efficacy is similar to other PPIs (such as omeprazole, esomeprazole, lansoprazole, dexlansoprazole, and rabeprazole). Pantoprazole exerts its acid-suppressing effect by covalently binding to the cysteine sulfhydryl group on the (H+, K+)-ATPase enzyme on the secretory surface of gastric parietal cells, blocking the final step in gastric acid production. This action results in the inhibition of both basal and stimulant gastric acid secretion, unaffected by stimuli. Because the binding of pantoprazole to (H+, K+)-ATPase is irreversible, requiring new enzyme expression to restore gastric acid secretion, the acid-suppressing effect of pantoprazole lasts for more than 24 hours. Due to its good safety profile and the fact that many proton pump inhibitors (PPIs) are available over-the-counter without a prescription, it is currently widely used in North America. Long-term use of proton pump inhibitors (PPIs), such as pantoprazole, may be associated with several adverse effects, including increased susceptibility to bacterial infections (including Clostridium difficile infection of the gastrointestinal tract), reduced absorption of micronutrients (such as iron and vitamin B12), and an increased risk of hypomagnesemia and hypocalcemia, all of which may lead to osteoporosis and fractures later in life. PPIs, such as pantoprazole, have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme crucial for cardiovascular health. DDAH inhibition leads to the accumulation of asymmetric dimethylarginine (ADMA), a nitric oxide synthase inhibitor, which is believed to be the reason why PPIs are associated with an increased risk of cardiovascular events in patients with unstable coronary syndromes. Before discontinuing pantoprazole, the dose should be reduced slowly or gradually, as rapid discontinuation of proton pump inhibitors (PPIs) such as pantoprazole may lead to a rebound effect and short-term hyperacidity. Pantoprazole is a proton pump inhibitor. Its mechanism of action is as a proton pump inhibitor. Pantoprazole is a proton pump inhibitor (PPI) and a potent gastric acid inhibitor, widely used to treat gastroesophageal reflux and peptic ulcers. Pantoprazole treatment causes a low incidence of transient, asymptomatic elevations in serum transaminases and rarely causes clinically significant liver damage. Pantoprazole is a substituted benzimidazole proton pump inhibitor with antacid activity. It is a lipophilic weak base that can cross the parietal cell membrane into the acidic parietal tubules, where it is protonated to generate the active metabolite sulfonamide. The sulfonamide forms irreversible covalent bonds with two sites on H+/K+-ATPase located on gastric parietal cells, thereby inhibiting basal and stimulant gastric acid secretion. 2-Pyridylmethylsulfinylbenzimidazole proton pump inhibitor, used to treat gastroesophageal reflux and peptic ulcers. See also: Pantoprazole sodium (in salt form).

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Drug Indications
Pantoprazole Injection: For the treatment of gastroesophageal reflux disease (GERD) with a history of erosive esophagitis. Pantoprazole for injection is indicated for short-term treatment (7-10 days) in patients with GERD. For patients with GERD and a history of erosive esophagitis who cannot continue taking pantoprazole extended-release tablets, the injection may be considered as an alternative to oral medication. The safety and efficacy of pantoprazole for injection as initial treatment in patients with GERD and a history of erosive esophagitis have not been established. Pantoprazole for injection is indicated for the treatment of pathological hypersecretion states associated with Zollinger-Ellison syndrome or other neoplastic diseases. Pantoprazole Extended-Release Oral Suspension: For short-term treatment of erosive esophagitis associated with GERD. Indicated for short-term treatment (up to 8 weeks) in adults and children aged 5 years and older to promote healing of erosive esophagitis and relieve symptoms.
For adult patients who do not recover after 8 weeks of treatment, an additional 8-week course of pantoprazole may be considered. The safety of treatment exceeding 8 weeks in children has not been established. Maintaining healing of erosive esophagitis: Indicated for maintaining healing of erosive esophagitis and reducing the recurrence rate of daytime and nighttime heartburn symptoms in adult patients with gastroesophageal reflux disease (GERD). Pathological hypersecretion states, including Zollinger-Ellison syndrome. Indicated for long-term treatment of the above conditions.
FDA label
For short-term treatment of reflux symptoms (e.g., heartburn, acid reflux) in adults.
For short-term treatment of reflux symptoms (e.g., heartburn, acid reflux) in adults.
For short-term treatment of reflux symptoms (e.g., heartburn, acid reflux) in adults.
For short-term treatment of reflux symptoms (e.g., heartburn, acid reflux) in adults.
For short-term treatment of reflux symptoms (e.g., heartburn, acid reflux) in adults.
For short-term treatment of reflux symptoms (e.g., heartburn, acid reflux) in adults.
For treatment of Helicobacter pylori infection.
For treatment of Helicobacter pylori infection. Mechanism of Action: The secretion of hydrochloric acid (HCl) into the gastric lumen is primarily regulated by the proton pump's H(+)/K(+)-ATPase, an enzyme highly expressed by gastric parietal cells. ATPase is an enzyme on the parietal cell membrane that promotes the exchange of hydrogen and potassium ions within the cell, typically leading to potassium efflux and the generation of HCl (gastric acid). Proton pump inhibitors, such as pantoprazole, are substituted benzimidazole derivatives belonging to the weak base class. They accumulate in the acidic space of parietal cells and are then converted into an active sulfinamide derivative in the gastric tubules (tubules) of the parietal cells—an acidic environment. This active form subsequently forms a disulfide bond with a key cysteine residue on the gastric acid pump, thereby inhibiting its function. Specifically, pantoprazole binds to the sulfhydryl group of H(+),K(+)-ATPase, an enzyme involved in the final step of the accelerated gastric acid secretion pathway. Pantoprazole inactivates this enzyme, thereby inhibiting gastric acid secretion. Compared to H2 receptor antagonists, proton pump inhibitors like pantoprazole have a stronger and longer-lasting inhibitory effect on gastric acid secretion. Pantoprazole is a proton pump inhibitor. It accumulates in the acidic compartments of parietal cells and is converted into its active form—a sulfonamide—which binds to potassium hydrogen ATPase on the secretory surface of gastric parietal cells. Inhibition of potassium hydrogen ATPase blocks the final step in gastric acid production, thereby inhibiting basal and stimulant gastric acid secretion. The duration of gastric acid secretion inhibition is not related to the short elimination half-life of pantoprazole. Pantoprazole sodium is a proton pump inhibitor (PPI) with improved pH stability compared to first- and second-generation PPIs (omeprazole, lansoprazole) [3][4]. Its core mechanism is to irreversibly bind to H+/K+-ATPase in gastric parietal cells, blocking H+ secretion and inhibiting gastric acid production, which supports its clinical use in treating acid-related diseases (duodenal ulcer, gastric ulcer, gastroesophageal reflux disease, Helicobacter pylori infection) [3][4]. Other activities include: enhancing the antitumor efficacy of doxorubicin by increasing its intracellular accumulation (through lysosomal pH regulation); inhibiting the release of cancer cell exosomes; and promoting duodenal ulcer healing by reducing gastric acid secretion, protecting PGE2, and promoting epithelial cell proliferation [1][2][4]. It has good safety, low cytotoxicity to normal cells, and no significant drug interactions with doxorubicin [1][4].

C16H15F2N3O4S

383.37

383.075

C, 50.13; H, 3.94; F, 9.91; N, 10.96; O, 16.69; S, 8.36

102625-70-7

Pantoprazole sodium;138786-67-1;Pantoprazole sodium hydrate;164579-32-2;S-Pantoprazole sodium trihydrate;1416988-58-3;Pantoprazole-d6;922727-65-9;Pantoprazole-d3;922727-37-5

4679

Off-white solid

1.5±0.1 g/cm3

586.9±60.0 °C at 760 mmHg

139-140ºC, decomposes

308.7±32.9 °C

0.0±1.6 mmHg at 25°C

1.643

1.69

1

9

7

26

490

0

O=S(C1=NC2=CC=C(OC(F)F)C=C2N1)CC3=NC=CC(OC)=C3OC

IQPSEEYGBUAQFF-UHFFFAOYSA-N

InChI=1S/C16H15F2N3O4S/c1-23-13-5-6-19-12(14(13)24-2)8-26(22)16-20-10-4-3-9(25-15(17)18)7-11(10)21-16/h3-7,15H,8H2,1-2H3,(H,20,21)

1H-Benzimidazole, 5-(difluoromethoxy)-2-(((3,4-dimethoxy-2-pyridinyl)methyl)sulfinyl)-

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)