Proton pump
In EMT-6 and MCF7 cells, pantoprazole sodium hydrate (BY1023 sodium hydrate; 1–10,000 μM) raises endosomal pH in a concentration-dependent manner [1]. Pantoprazole sodium hydrate prevents exosome release. Pantoprazole sodium hydrate prevents tumor cells (melanoma, adenocarcinoma, and lymphoma cell lines) from acidifying the extracellular medium by inhibiting V-H+-ATPase activity [2].

In EMT-6 and MCF7 cells, pantoprazole sodium hydrate (BY1023 sodium hydrate; 1–10,000 μM) raises endosomal pH in a concentration-dependent manner [1]. Pantoprazole sodium hydrate prevents exosome release. Pantoprazole sodium hydrate prevents tumor cells (melanoma, adenocarcinoma, and lymphoma cell lines) from acidifying the extracellular medium by inhibiting V-H+-ATPase activity [2].

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Pantoprazole, at concentrations above 200 µmol/L, increased endosomal pH in both murine EMT-6 and human MCF-7 cancer cells. The effect was concentration-dependent and was enhanced in the presence of doxorubicin. [1]
Pretreatment with pantoprazole (1 mmol/L) altered the intracellular distribution of doxorubicin in MCF-7 and EMT-6 cells, reducing doxorubicin fluorescence in punctuate cytoplasmic compartments (indicative of endosomal sequestration) while retaining it in the nucleus. [1]
Flow cytometry analysis showed that pretreatment with pantoprazole (1 mmol/L) significantly increased the net cellular uptake of doxorubicin in EMT-6 cells but decreased it by 24% in MCF-7 cells and 36% in A431 cells. At a lower concentration (100 µmol/L), similar trends were observed but were not statistically significant. [1]
Pretreatment of multilayered cell cultures (MCCs) derived from EMT-6 and MCF-7 cells with pantoprazole (1 mmol/L) significantly increased the penetration of doxorubicin through the tissue. The increase was more than 2-fold in EMT-6 MCCs and approximately 1.3-fold in MCF-7 MCCs. Fluorescence microscopy confirmed increased doxorubicin signal in cells distal from the drug source in pretreated MCCs. [1]

In MCF-7 xenografts, the combination of pantoprazole sodium hydrate (BY1023 sodium hydrate; 200 mg/kg; IP; once weekly for 3 weeks) and doxorubicin significantly prolonged the tumor growth delay [1]. Oral pantoprazole sodium hydrate (0.3–3 mg/kg) decreases mepizole-induced stimulated acid secretion in acute fistula rats and basal acid secretion in pyloric ligation rats in a dose-dependent manner [4].

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In mice bearing MCF-7 xenograft tumors, pretreatment with pantoprazole (200 mg/kg, i.p.) 2 hours before doxorubicin administration led to a significant increase in doxorubicin fluorescence within the tumor tissue compared to doxorubicin alone, indicating improved drug distribution. Quantitative analysis showed a shallower gradient of decreasing doxorubicin intensity with distance from functional blood vessels in the pantoprazole-pretreated group. This effect was not observed in EMT-6 tumors. [1]
Pretreatment with a single dose of pantoprazole (200 mg/kg, i.p.) before a single dose of doxorubicin (8 mg/kg, i.v.) significantly increased tumor growth delay in MCF-7 xenografts compared to doxorubicin alone or control groups. Pantoprazole alone had no effect on tumor growth. [1]
In A431 xenograft tumors (relatively resistant to doxorubicin), pretreatment with pantoprazole before a single dose of doxorubicin resulted in a small, marginally significant increase in growth delay. However, when administered weekly for three weeks in combination with doxorubicin, no significant growth delay was observed in this model. [1]
Weekly administration of pantoprazole (200 mg/kg, i.p.) before doxorubicin (6 mg/kg, i.v.) for three weeks led to an even greater growth delay in MCF-7 xenografts compared to the single-dose combination regimen. [1]

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].

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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To measure endosomal pH, EMT-6 or MCF-7 cells were treated with varying concentrations of pantoprazole (and other agents for comparison) for 3 hours in the presence of a fluorescent pH-sensitive dextran conjugate (FITC/TMR-dextran) that is taken up into endosomes. After a 2-hour incubation in media, fluorescence was measured using flow cytometry. The ratio of pH-dependent (FITC) to pH-independent (TMR) fluorescence was calibrated using the ionophore nigericin in buffers of known pH to determine endosomal pH. [1]
To evaluate doxorubicin distribution within cells, cells grown on chambered cover glass were pretreated with pantoprazole (1 mmol/L) for 2 hours, then incubated with media containing doxorubicin (2 µg/mL) for 1 hour. After washing, intracellular doxorubicin fluorescence was visualized using fluorescence microscopy with specific excitation/emission filters. To visualize endosomes, cells were co-stained with the pH-sensitive dye LysoSensor Yellow/Blue. [1]
To measure net cellular uptake of doxorubicin by flow cytometry, cells were treated with saline or pantoprazole (1 mmol/L) for 2 hours, followed by incubation with doxorubicin (1.8 µmol/L) for 1 hour. Cells were washed, and mean doxorubicin fluorescence was measured using a flow cytometer equipped with a 530 nm emission filter. [1]
To assess drug penetration in an in vitro tumor-like environment, multilayered cell cultures (MCCs) were established by growing EMT-6 or MCF-7 cells on collagen-coated membranes for 6-8 days. MCCs were pretreated with or without pantoprazole (1 mmol/L) for 2 hours. The penetration of radiolabeled doxorubicin (10 µmol/L, mixed with agar to prevent convection) through the MCC into a receiving compartment was monitored over time by liquid scintillation counting. The penetration of a non-cell-penetrating tracer (³H-sucrose) was used as an internal standard to control for MCC thickness variations. Parallel MCCs were exposed to doxorubicin and frozen sections were imaged by fluorescence microscopy to visualize drug distribution. [1]

Animal/Disease Models: Mice bearing MCF-7 or A431 xenografts [1]
Doses: 200 mg/kg
Route of Administration: IP; once weekly for 3 weeks; alone or in combination with doxorubicin (6 mg/kg iv) First 2 hour
Experimental Results: The growth delay of MCF-7 xenografts with doxorubicin was even greater compared to the single dose combination. A single dose of doxorubicin Dramatically increased tumor growth delay. alone had no effect on growth delay.

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For tumor growth delay studies, female athymic nude mice bearing subcutaneous MCF-7 or A431 xenografts (or syngeneic Balb/C mice bearing EMT-6 tumors) were used. When tumors reached 5-8 mm in diameter, mice were randomized into treatment groups. Pantoprazole was administered intraperitoneally (i.p.) at a dose of 200 mg/kg, dissolved in 0.9% saline. Doxorubicin was administered intravenously (i.v.) at a dose of 8 mg/kg (single-dose study) or 6 mg/kg (multiple-dose study). For combination therapy, pantoprazole was given i.p. 2 hours before doxorubicin injection. Tumor volumes and body weights were measured regularly until endpoints were reached. [1]
For studying doxorubicin distribution in tumors, mice bearing EMT-6 or MCF-7 tumors (8-12 mm mean diameter) were treated. They received pantoprazole (200 mg/kg, i.p.) or vehicle 2 hours before a high dose of doxorubicin (25 mg/kg, i.v.) to facilitate fluorescence detection. To mark functional vasculature and hypoxia, mice also received intravenous DIOC7 (1 mg/kg) and intraperitoneal EF5 respectively, shortly before sacrifice. Mice were sacrificed 10 minutes after doxorubicin injection, tumors were excised, frozen, sectioned, and analyzed by fluorescence microscopy and immunohistochemistry for drug distribution relative to blood vessels. [1]
For toxicity studies, mice were treated with pantoprazole at doses of 100, 150, 200, 250, or 300 mg/kg (i.p.), alone or 2 hours before doxorubicin (8 mg/kg, i.v.). Body weight was monitored every other day. [1]
For pharmacokinetic analysis, Balb/C mice were treated with a single i.p. dose of pantoprazole (200 mg/kg). Blood was collected via cardiac puncture at various time points, plasma was isolated, and pantoprazole concentration was determined using a validated HPLC-MS/MS method. [1]

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 administration 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. When pantoprazole is taken with food, the time to peak concentration may vary among individuals and may be significantly prolonged. /Pantralazole Sodium/
Peak serum concentration: In rapid metabolizers with normal hepatic function, after oral administration of 40 mg: 2.4 μg/mL. In rapidly metabolizing individuals with normal liver function, after intravenous administration of 40 mg (dose 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, if taken with food, absorption may be delayed for up to 2 hours or longer. Oral bioavailability: 77%. /Pantoprazole Sodium/
For more complete data on the absorption, distribution, and excretion of pantoprazoles (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 primary metabolic pathway is demethylation via the hepatic cytochrome P450 enzyme CYP2C19, followed by sulfation; other metabolic pathways include oxidation via CYP3A4. There is no evidence that any pantoprazole metabolites are pharmacologically active. After hepatic metabolism, approximately 80% of orally or intravenously administered pantoprazole is excreted in the urine as metabolites; the remainder is present in the feces, derived 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 deficiencies 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 (half-life of 3.5 to 10 hours), the half-life of pantoprazole is prolonged (7 to 9 hours). /Pantoprazole sodium/

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In mice, after a single intraperitoneal injection of pantoprazole (200 mg/kg), the peak plasma concentration is approximately 300 µmol/L, occurring within 1 hour of injection. [1]
Two hours after injection, the plasma concentration decreases to approximately 150 µmol/L. [1]
Five hours after injection, the plasma concentration has decreased to less than 1% of the peak concentration. [1]
Twenty-four hours after injection, the detectable concentration of pantoprazole in plasma is less than 0.01 µmol/L. [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). Clinically significant PPI-induced liver injury 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 autoantibody formation 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 is not expected to have any adverse effects on breastfed infants.
◉ 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 gynecomastia, of which 3 cases were associated with pantoprazole, including 14 cases of galactorrhea, 14 cases of breast pain, and 4 cases of breast enlargement. A search of the World Health Organization Global Pharmacovigilance Database found 97 cases of gynecomastia, 13 cases of galactorrhea, 35 cases of breast pain, and 16 cases of breast enlargement associated with pantoprazole.

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Protein binding rate
Approximately 98%Drug interactions
Pantralazole can cause long-term inhibition of gastric acid secretion, which may interfere with the absorption of drugs such as ampicillin, iron salts, or ketoconazole, as well as other drugs whose bioavailability is affected by gastric pH. (Pantralazole sodium)
Although pantoprazole is metabolized by the hepatic cytochrome P450 system, it does not appear to inhibit or induce cytochrome P450 enzyme activity. To date, no clinically significant interactions have been found between commonly used drugs such as diazepam, phenytoin sodium, nifedipine, theophylline, digoxin, warfarin, or oral contraceptives and pantoprazole sodium. Pantoprazole sodium can affect the bioavailability of any pH-dependent drug by increasing gastric pH. Furthermore, pantoprazole sodium may inhibit the degradation of acid-labile drugs. In other in vivo studies, no clinically significant interactions were found between pantoprazole sodium and ethanol, glibenclamide, caffeine, antipyrine, metronidazole, and amoxicillin. In mice, the maximum tolerated dose of pantoprazole sodium in combination with doxorubicin (8 mg/kg) was 200 mg/kg. At this dose, combination therapy resulted in a transient decrease in body weight (approximately 15%) in mice over the first 5–8 days, followed by recovery. [1] When pantoprazole was used at higher doses (250 or 300 mg/kg) in combination with doxorubicin, body weight in mice continued to decrease after 20 days. [1] Treatment with pantoprazole alone (up to 300 mg/kg) or doxorubicin alone (8 mg/kg) resulted in minimal weight gain, similar to the saline control group. [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.

Therapeutic Uses
Pantoprazole extended-release tablets are indicated for short-term (up to 8 weeks) treatment of heartburn and other symptoms associated with gastroesophageal reflux disease (GERD). Pantoprazole injection is indicated for short-term (7 to 10 days) GERD treatment in patients who cannot continue taking pantoprazole extended-release tablets. Pantoprazole injection is not indicated for initial treatment of GERD. /Included on US product label/ /Pantralazole Sodium/
Pantralazole is indicated for the prevention of recurrence in patients with reflux esophagitis. /Not included on US product label/ /Pantralazole Sodium/
Pantralazole is indicated for short-term (up to 4 weeks) treatment in patients with active duodenal ulcers to relieve symptoms and promote healing. /Not included on US product label/ /Pantralazole Sodium/
Pantralazole, used in combination with clarithromycin and amoxicillin or metronidazole, is indicated for the treatment of patients with Helicobacter pylori-positive active duodenal ulcers. /Not included in US product label/ /Pantralazole Sodium/
For more complete data on the therapeutic uses of pantoprazole (6 types), please visit the HSDB record page.

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Drug Warnings
There have been reports of allergic reactions to intravenous pantoprazole sodium. If an allergic reaction or other serious hypersensitivity reaction occurs, immediate medical intervention and discontinuation of the medication are necessary. /Pantralazole Sodium/
Adverse reactions occurring in more than 1% of patients receiving oral pantoprazole for up to 8 weeks, and higher than in the placebo group, include diarrhea and hyperglycemia. Adverse reactions occurring in 1% or more of patients receiving oral pantoprazole for up to 12 months (higher than in patients receiving ranitidine) include headache, abdominal pain, and abnormal liver function. Adverse reactions occurring in 4% or more of patients receiving intravenous pantoprazole (probably, likely, or definitely related to treatment) include abdominal pain, chest pain, rash, and pruritus. Adverse reactions occurring in more than 1% of patients receiving intravenous pantoprazole (often unrelated to the drug) include headache, injection site reaction, dyspepsia, diarrhea, vomiting, dizziness, and rhinitis. /Pantralazole Sodium/
Spontaneously reported adverse events include: angioedema (Quinck's edema); anterior ischemic optic neuropathy; severe skin reactions, including erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis (TEN, fatal in some cases). Hepatocellular damage can lead to cholestasis and liver failure; pancreatitis; pancytopenia; and rhabdomyolysis. In addition, confusion, bradykinesia, speech disturbances, increased salivation, dizziness, nausea, tinnitus, and blurred vision have been observed. /Pantralazole Sodium/
FDA Pregnancy Risk Classification: B / No evidence of risk in humans. Although adverse reactions have been observed in animal studies, adequately controlled studies in pregnant women have not shown an increased risk of fetal malformations; or, in the absence of adequate human studies, animal studies have shown no fetal risk. The possibility of fetal harm is small, but still exists. /Pantoprazole Sodium/
For more complete data on pantoprazole (8 of 8), please visit the HSDB record page.

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Pharmacodynamics
This drug reduces gastric acid secretion. Pantoprazole can inhibit gastric acid secretion for a long period. General Actions Studies have shown that pantoprazole is more effective than histamine H2 receptor antagonists (H2 receptor blockers) in reducing symptoms associated with acid reflux, curing esophagitis, and improving patients' quality of life. This drug has an excellent safety profile with a low incidence of drug interactions. It is safe for use in a variety of high-risk patient groups, including the elderly, patients with renal failure, or patients with moderate hepatic impairment. Due to its good safety profile and the availability of many proton pump inhibitors (PPIs) without a prescription, it is currently widely used in North America. However, long-term use of PPIs such as pantoprazole may have some adverse effects, including an increased risk of 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. Proton pump inhibitors (PPIs), such as pantoprazole, have 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 thought to be the reason why PPIs are associated with an increased risk of cardiovascular events in patients with unstable coronary syndromes. Note on Laboratory Abnormalities During treatment with acid-suppressing drugs such as pantoprazole, serum gastrin (a peptide hormone that stimulates gastric acid secretion) levels may increase due to the reduced gastric acid secretion caused by proton pump inhibitors. Elevated gastrin levels may interfere with the detection of neuroendocrine tumors. Published evidence suggests that proton pump inhibitors (PPIs) should be discontinued 14 days prior to chromogranin A (CgA) testing. This allows falsely elevated CgA levels, which may occur after PPI treatment, to return to the normal reference range. False-positive results have been reported in urine tetrahydrocannabinol (THC) screening tests in patients taking most PPIs, including pantoprazole. Confirmatory methods should be used. Pantoprazole is a PPI that inhibits vacuolar H⁺-ATPase (VH⁺-ATPase). In this cancer study, pantoprazole was not investigated for its antacid effect, but rather as a tumor microenvironment modulator. It inhibits the isolation of weakly basic chemotherapeutic drugs, such as doxorubicin, by increasing the pH of acidic intracellular compartments, such as endosomes and lysosomes. This mechanism is thought to increase drug binding to nuclear targets and enhance drug distribution from blood vessels to deeper tumor tissues, potentially overcoming resistance mechanisms associated with poor drug penetration. [1] The study concluded that pantoprazole pretreatment could improve the therapeutic index of doxorubicin in certain solid tumors by enhancing its distribution and cytotoxicity. These preclinical findings led to the initiation of a clinical trial evaluating high-dose pantoprazole in combination with chemotherapy. [1]

2(C16H14F2N3NAO4S).3(H2O)

864.75

864.145

164579-32-2

Pantoprazole;102625-70-7;Pantoprazole sodium;138786-67-1;S-Pantoprazole sodium trihydrate;1416988-58-3

4679

Off-white solid

149-150
139-140 °C, decomposes
Mol wt: 405.36. White to off-white solid; mp: >130 °C (dec); UV max (methanol): 289 (E=1.64X10+4) /Sodium salt/

2.4

1

9

7

26

490

0

VNKNFEINTHUQGZ-UHFFFAOYSA-N

InChI=1S/2C16H14F2N3O4S.2Na.3H2O/c2*1-23-13-5-6-19-12(14(13)24-2)8-26(22)16-20-10-4-3-9(25-15(17)18)7-11(10)21-16;;;;;/h2*3-7,15H,8H2,1-2H3;;;3*1H2/q2*-1;2*+1;;;

disodium;5-(difluoromethoxy)-2-[(3,4-dimethoxypyridin-2-yl)methylsulfinyl]benzimidazol-1-ide;trihydrate

BY1023 sodium hydrate; SKF96022 sodium hydrate; BY1023; SKF96022; Protonix; BY 1023; BY-1023; SKF 96022; Pantoprazole sodium sesquihydrate; 164579-32-2; Protonix; Pantoprazole Sodium [USAN]; Somac Control; disodium;5-(difluoromethoxy)-2-[(3,4-dimethoxypyridin-2-yl)methylsulfinyl]benzimidazol-1-ide;trihydrate; Pantoloc Control; SKF-96022

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

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

H2O : ~250 mg/mL (~578.21 mM)
DMSO : ~100 mg/mL (~231.28 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.78 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 (5.78 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 (5.78 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.)