Pantoprazole(SKF96022; Protonix) is a proton pump inhibitor drug used for short-term treatment of erosion and ulceration of the esophagus caused by gastroesophageal reflux disease.IC50 value:Target: proton pump inhibitor
Bafilomycin A1, a macrolide antibiotic isolated from the Streptomyces species, is a specific inhibitor of vacuolar-type H+ ATPase.
(±)-Vasicine is the racemate of Vasicine. Vasicine (Peganine), isolated from Peganum harmala seeds, significantly inhibits H+-K+-ATPase activity in vitro with an IC50 of 73.47 μg/mL. Anti-ulcer activity. Vasicine shows significant anti-secretory, antioxidant and cytoprotective effect[1].
Manzamine A, an orally active beta-carboline alkaloid, inhibits specifically GSK-3β and CDK-5 with IC50s of 10.2 μM and 1.5 μM, respectively. Manzamine A targets vacuolar ATPases and inhibits Autophagy in pancreatic cancer cells. Manzamine A has antimalarial and anticancer activities. Manzamine A also shows potent activity against HSV-1[1][2][3][4].
Esomeprazole sodium is a proton pump inhibitor which reduces acid secretion through inhibition of the H+ / K+ ATPase in gastric parietal cells.IC50 value:Target: proton pumpEsomeprazole sodium (Nexium) is the S-isomer of omeprazole and acts as a proton pump inhibitor and gastric antisecretory agent indicated for the short-term treatment of gastroesophageal reflux disease in patients with a history of erosive esophagitis. Esomeprazole 0.4 and 0.8 mg/mL as the sodium salt in the infusion solutions tested is chemically and physically stable for at least 2 days at room temperature and 5 days under refrigeration.
Esomeprazole magnesium salt is a proton pump inhibitor which reduces acid secretion through inhibition of the H+ / K+ ATPase in gastric parietal cells.IC50 value:Target: proton pumpEsomeprazole magnesium salt is a proton pump inhibitor and gastric antisecretory agent indicated for the short-term treatment of gastroesophageal reflux disease in patients with a history of erosive esophagitis.
Pantoprazole sodium salt(SKF96022; Protonix) is a proton pump inhibitor drug used for short-term treatment of erosion and ulceration of the esophagus caused by gastroesophageal reflux disease.IC50 value:Target: proton pump inhibitor
Rabeprazole D4 (LY307640 D4) is a deuterium labeled Rabeprazole. Rabeprazole is a second-generation proton pump inhibitor (PPI) that irreversibly inactivates gastric H+/K+-ATPase. Rabeprazole induces apoptosis. Rabeprazole acts as an uridine nucleoside ribohydrolase (UNH) inhibitor with an IC50 of 0.3 μM. Rabeprazole can be used for the research of gastric ulcerations and gastroesophageal reflux[1][2][3].
Esomeprazole magnesium is an inhibitor of H+, K+-ATPase, effectively used in the research of upper intestinal disorder.
Pantoprazole-d6 is deuterium labeled Pantoprazole. 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 μM. Pantoprazole improves pH stability and has anti-secretory, anti-ulcer activities. Pantoprazole significantly increased tumor growth delay combined with Doxorubicin (HY-15142)[3][4].
Chebulinic acid is a potent natural inhibitor of M. tuberculosis DNA gyrase, also can inhibit SMAD-3 phosphorylation, inhibit H+ K+-ATPase activity.
Soraprazan is a reversible, and fast-acting inhibitor of gastric H+/K+ ATPase.
Pantoprazole 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.IC50 value:Target: proton pump inhibitor
TAK-438 (free base) is a novel P-CAB (potassium-competitive acid blocker) that reversibly inhibits H+/K+ ATPase with IC50 of 19 nM (pH 6.5), controls gastric acid secretion.IC50 value: 19 nM [1]Target: H+/K+ ATPasein vitro: TAK-438 is a pyrrole derivative with a chemical structure that is completely different from the P-CABs developed to date. TAK-438 inhibits gastric H+/K+ ATPase activity in a concentration-dependent manner. Under neutral conditions (pH 7.5), the inhibitory activity of TAK-438 is almost the same as that under weakly acidic conditions (pH 6.5). TAK-438 does not inhibit Na+/K+ ATPase activity even at concentration 500 times higher than their IC50 values against gastric H+/K+ ATPase activity. TAK-438 inhibits gastric H+/K+ ATPase in a K+ competitive manner with Ki of 3 nM [2]. in vivo: TAK-438 inhibits basal gastric acid secretion in a dose-dependent manner, and the ID50 value is 1.26 mg/kg. Intravenous administration of TAK-438 dose-dependently increases the pH of the gastric perfusate, and the increase in pH is sustained for 5 h after administration. At the 1 mg/kg dose, the pH plateaues 90 min after administration, and the highest pH value reached is 5.9 [2]. In addition, TAK-438 shows a potent and longer-lasting inhibitory effect on the histamine-stimulated gastric acid secretion in rats and dogs. TAK-438 shows significant antisecretory activity through high accumulation and slow clearance from the gastric tissue. TAK-438 is unaffected by the gastric secretory state, unlike PPIs [3].
Rabeprazole sodium(LY307640 sodium) is an antiulcer drug in the class of proton pump inhibitors.Target: Proton PumpRabeprazole belongs to a class of antisecretory compounds (substituted benzimidazole proton-pump inhibitors) that do not exhibit anticholinergic or histamine H2-receptor antagonist properties, but suppress gastric acid secretion by inhibiting the gastric H+/K+ATPase (hydrogen-potassium adenosine triphosphatase) at the secretory surface of the gastric parietal cell. Because this enzyme is regarded as the acid (proton) pump within the parietal cell, rabeprazole has been characterized as a gastric proton-pump inhibitor. Rabeprazole blocks the final step of gastric acid secretion. In gastric parietal cells, rabeprazole is protonated, accumulates, and is transformed to an active sulfenamide. When studied in vitro, rabeprazole is chemically activated at pH 1.2 with a half-life of 78 seconds.
Tenatoprazole sodium (TU-199 sodium) is a proton pump inhibitor; inhibits hog gastric H+/K+-ATPase with an IC50 of 6.2 μM.
Diphyllin is an arylnaphthalene lignan isolated from Justicia procumbens and is a potent HIV-1 inhibitor with an IC50 of 0.38 μM. Diphyllin is active against vesicular stomatitis virus (VSV) and influenza virus[1]. Diphyllin is a vacuolar type H+-ATPase (V-ATPase) inhibitor with an IC50 value of 17 nM and inhibits lysosomal acidification in human osteoclasts[2]. Diphyllin inhibits NO production with an IC50 of 50 μM and has anticancer and anti-inflammatory activities[3].
Pantoprazole-d3 is deuterium labeled Pantoprazole. 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 μM. Pantoprazole improves pH stability and has anti-secretory, anti-ulcer activities. Pantoprazole significantly increased tumor growth delay combined with Doxorubicin (HY-15142)[3][4].
Esomeprazole ((S)-Omeprazole) is a potent and orally active proton pump inhibitor and reduces acid secretion through inhibition of the H+, K+-ATPase in gastric parietal cells. Esomeprazole has the potential for symptomatic gastroesophageal reflux disease research[1][2][3].
Omeprazole D3 is deuterium labeled Omeprazole, which is a proton pump inhibitor used in the treatment of dyspepsia.
Lansoprazole D4 (AG-1749 D4) is a deuterium labeled Lansoprazole. Lansoprazole is a proton pump inhibitor which prevents the stomach from producing acid[1].
Caloxin 2A1 is an extracellular plasma membrane Ca2+-ATPase (PMCA) peptide inhibitor. Caloxin 2A1 does not affect basal Mg2+-ATPase or Na+-K+-ATPase[1].
Verucopeptin is a potent HIF-1 (IC50=0.22 μM) inhibitor and decreases the expression of HIF-1 target genes and HIF-1α protein levels[1][2]. Verucopeptin strongly inhibits v-ATPase activity by directly targeting the v-ATPase ATP6V1G subunit but not ATP1V1B2 or ATP6V1D. Verucopeptin exhibits antitumor activity against multidrug resistance (MDR) cancers and can be used for cancer research[3].
Tiludronate (Tiludronic Acid), an orally active bisphosphonate, can act an osteoregulator. Tiludronate is used for the research of the metabolic bone disorders. Tiludronate is a potent inhibitor of the osteoclast vacuolar H(+)-ATPase. Antiresorptive and anti-inflammatory properties[1][2][3][4].
WY-47766, a proton pump inhibitor, is used potentially for the treatment of postmenopausal osteoporosis.
Esomeprazole-d6 sodium is the deuterium labeled Esomeprazole. Esomeprazole ((S)-Omeprazole) is a potent and orally active proton pump inhibitor and reduces acid secretion through inhibition of the H+, K+-ATPase in gastric parietal cells. Esomeprazole has the potential for symptomatic gastroesophageal reflux disease research[1][2][3].
Manzamine A hydrochloride, an orally active beta-carboline alkaloid, inhibits specifically GSK-3β and CDK-5 with IC50s of 10.2 and 1.5μM, respectively. Manzamine A hydrochloride targets vacuolar ATPases and inhibits autophagy in pancreatic cancer cells. Manzamine A hydrochloride has antimalarial and anticancer activities. Manzamine A hydrochloride also shows potent activity against HSV-1[1][2][3][4].
EN6 is a small-molecule in vivo activator of autophagy that covalently targets cysteine 277 in the ATP6V1A subunit of the lysosomal the vacuolar H+ ATPase (v-ATPase). EN6-mediated ATP6V1A modification decouples the v-ATPase from the Rags, leading to inhibition of mTORC1 signaling, increased lysosomal acidification and activation of autophagy. EN6 clears TDP-43 aggregates, a causative agent in frontotemporal dementia, in a lysosome-dependent manner[1].
Esomeprazole ((S)-Omeprazole) hemistrontium is a potent and orally active proton pump inhibitor and reduces acid secretion through inhibition of the H+, K+-ATPase in gastric parietal cells. Esomeprazole hemistrontium has the potential for symptomatic gastroesophageal reflux disease research[1][2][3].
Omeprazole(Prilosec) is a proton pump inhibitor used in the treatment of dyspepsia.Target: Proton PumpOmeprazole is a proton pump inhibitor used in the treatment of dyspepsia, peptic ulcer disease, gastroesophageal reflux disease, laryngopharyngeal reflux, and Zollinger-Ellison syndrome. Omeprazole virtually eliminated intragastric acidity in all patients: the median 24 hour intragastric pH rose from 1.4 to 5.3 and the mean hourly hydrogen ion activity fell from 38.50 to 1.95 mmol(mEq)/1 (p less than 0.001). This inhibition of 24 hour intragastric acidity is more profound than that previously reported with either cimetidine 1 g daily or ranitidine 300 mg daily [1]. The pharmacokinetics of omeprazole were studied in a group of healthy male subjects after single and repeated oral doses of 30 and 60 mg. Absorption of omeprazole from its enteric-coated formulation was unpredictable. There was a highly significant increase in the area under the plasma concentration time curve (AUC) after repeated dosing. Omeprazole increases its own relative availability following repeated dosing. This may be due to inhibition of gastric acid secretion by omeprazole which is an acid-labile compound [2].Clinical indications: Duodenal ulcer; Endocrine tumor; Esophagitis; Gastroesophageal reflux; Helicobacter pylori infection; Stomach ulcer; Zollinger-Ellison syndromeToxicity: Symptoms of overdose include confusion, drowsiness, blurred vision, tachycardia, nausea, diaphoresis, flushing, headache, and dry mouth.