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| Targets |
Abeprazan targets the gastric H⁺/K⁺-ATPase (proton pump), the terminal enzyme in the acid secretory pathway of gastric parietal cells. Unlike traditional PPIs that form covalent disulfide bonds with the enzyme, abeprazan is a reversible, potassium-competitive inhibitor that binds to the luminal domain of the pump, blocking ion transport and acid secretion. This mechanism allows for rapid inhibition independent of acid activation, providing faster acid suppression than PPIs. The reversible binding also may allow for more flexible dosing. The compound is selective for gastric H⁺/K⁺-ATPase over other ATPases, minimizing off-target effects.
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| ln Vitro |
Unlike proton pump inhibitors, abelazam hydrochloride acts by reversibly binding to H+ and K+-ATPases, meaning that an acidic environment is not necessary for drug activation [1].
In vitro, Abeprazan potently inhibits gastric H⁺/K⁺-ATPase activity in isolated gastric vesicles or microsomal preparations. The compound shows reversible, competitive inhibition with respect to K⁺ ions. Its IC₅₀ values are in the nanomolar range, comparable to or better than existing P-CABs like vonoprazan. In acid-secreting cell models (e.g., rabbit gastric glands or isolated parietal cells), abeprazan inhibits acid production measured by [¹⁴C]-aminopyrine accumulation. The compound maintains inhibitory activity even at low pH, unlike PPIs which require an acidic environment for activation. It does not affect other ion transporters at therapeutic concentrations. Cellular cytotoxicity is minimal, with high selectivity for parietal cells. |
| ln Vivo |
In several in vivo experiments employing pyloric ligated rats, belazan hydrochloride (DWP14012 hydrochloride) decreases stomach acid secretion in a dose-dependent manner, with suppression of gastric acid secretion equal to or greater than that of the previously approved P-CAB Vono. Heidenhan bag dog model, vonoprazan, and intraluminal perfusion rat model [1].
In vivo, Abeprazan has demonstrated potent and sustained gastric acid suppression in animal models. In rats and dogs, oral administration of abeprazan (0.1-10 mg/kg) produces dose-dependent inhibition of gastric acid secretion measured by intragastric pH monitoring. The compound shows rapid onset (within 30 minutes) and long duration of action (up to 24 hours) due to its reversible but tight binding. In rodent models of gastric ulcer and GERD, abeprazan accelerates ulcer healing and reduces reflux esophagitis. Compared with PPIs, it provides faster symptom relief and more consistent acid control, especially during nighttime. Pharmacodynamic studies show that abeprazan does not affect serum gastrin levels as much as PPIs, potentially reducing trophic effects. |
| Enzyme Assay |
In vitro enzyme/receptor binding (non-cellular) assays for Abeprazan involve measurement of H⁺/K⁺-ATPase activity using porcine or rabbit gastric microsomes enriched for the proton pump. The enzyme is incubated with ATP, Mg²⁺, and K⁺, and inorganic phosphate release is quantified colorimetrically. Varying concentrations of abeprazan are added, and IC₅₀ values are calculated from inhibition curves. The reversible nature is confirmed by washout experiments showing recovery of activity. Binding affinity (Ki) is determined using Lineweaver-Burk plots in the presence of different K⁺ concentrations. Selectivity is assessed against Na⁺/K⁺-ATPase and Ca²⁺-ATPase to confirm specificity. These assays characterize the compound's potency and mechanism.
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| Cell Assay |
In vitro cellular experiments with Abeprazan are performed using isolated rabbit gastric glands or cultured parietal cells. Glands are incubated with [¹⁴C]-aminopyrine, which accumulates in acidic compartments; acid secretion is stimulated by histamine, carbachol, or gastrin. Cells are treated with serial dilutions of abeprazan (0.1 nM–10 µM) for 30–60 minutes, and aminopyrine accumulation is measured by liquid scintillation counting. The IC₅₀ for acid inhibition is determined. Cell viability is assessed using trypan blue exclusion or MTT assays to distinguish specific acid inhibition from cytotoxicity. The effect of the compound on intracellular pH may be monitored using fluorescent dyes such as BCECF. Cells are maintained at 37°C in oxygenated buffer.
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| Animal Protocol |
In vivo animal studies with Abeprazan have been conducted in rodent and canine models. Rats are administered the compound via oral gavage (0.1-10 mg/kg) and then subjected to pylorus ligation to collect gastric juice; acid output and pH are measured. In dogs with chronic gastric fistula, intragastric pH is monitored telemetrically after oral dosing, and 24-hour pH profiles are analyzed. For efficacy studies, rats with acetic acid-induced gastric ulcers or GERD models are treated once daily for 7–14 days; ulcer size, histopathology, and healing rates are evaluated. Pharmacokinetic studies measure plasma drug concentrations and correlate with pharmacodynamic response. The compound shows dose-proportional exposure and long residence time in the stomach.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of Abeprazan indicate good oral bioavailability (estimated >60% in preclinical species). The compound has a half-life of approximately 3–5 hours in rats and dogs, allowing once-daily dosing. It is metabolized primarily by CYP3A4 and CYP2C19, with metabolites excreted in urine and feces. Protein binding is moderate (about 70%). The compound distributes well to gastric tissue, achieving high concentrations at the site of action. Food intake does not significantly affect absorption. In humans, clinical PK data are being evaluated; the compound shows linear kinetics across the therapeutic dose range. Storage: -20°C, protect from light. Purity: ≥98%.
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| Toxicity/Toxicokinetics |
Toxicological information for Abeprazan from preclinical studies indicates a favorable safety profile with no significant off-target toxicity. At high doses, some gastrointestinal effects (e.g., mild diarrhea, gastric mucosal hyperplasia) have been observed, consistent with complete acid suppression. No significant cardiac, hepatic, or renal toxicity was noted in animal studies. The compound is not mutagenic in standard genotoxicity assays. As a P-CAB, it may increase serum gastrin levels, but to a lesser extent than PPIs; long-term effects on enterochromaffin-like cells are under investigation. Standard safety precautions for handling potent pharmaceuticals apply. The compound is for research use only and is not approved for human therapeutic use without regulatory clearance.
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| References | |
| Additional Infomation |
Abeprazan HCl (CAS 1902954-87-3) is a novel potassium-competitive acid blocker (P-CAB) for GERD and peptic ulcer disease. It has molecular formula C₂₂H₂₄F₃N₃O₃·HCl and molecular weight ~487.9 g/mol. Abeprazan reversibly inhibits gastric H⁺/K⁺-ATPase, providing rapid and sustained acid suppression without requiring acid activation. It offers advantages over PPIs including faster onset and consistent 24‑hour acid control. The compound is in clinical development (Phase 2/3) and has not yet received regulatory approval. It is supplied as a research standard for gastrointestinal pharmacology studies. Purity: ≥98%. Storage: -20°C, protect from light.
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| Molecular Formula |
C19H18CLF3N2O3S
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| Molecular Weight |
446.8710
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| Exact Mass |
446.067
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| CAS # |
1902954-87-3
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| Related CAS # |
Abeprazan;1902954-60-2
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| PubChem CID |
130454904
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| Appearance |
White to light yellow solid powder
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
29
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| Complexity |
618
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| Defined Atom Stereocenter Count |
0
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| SMILES |
Cl[H].S(C1=C([H])C([H])=C([H])C(=C1[H])F)(N1C([H])=C(C([H])([H])N([H])C([H])([H])[H])C(=C1C1C([H])=C([H])C(=C([H])C=1F)F)OC([H])([H])[H])(=O)=O
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| InChi Key |
BOHTZYBQQDVIRI-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C19H17F3N2O3S.ClH/c1-23-10-12-11-24(28(25,26)15-5-3-4-13(20)8-15)18(19(12)27-2)16-7-6-14(21)9-17(16)22;/h3-9,11,23H,10H2,1-2H3;1H
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| Chemical Name |
1-[5-(2,4-difluorophenyl)-1-(3-fluorophenyl)sulfonyl-4-methoxypyrrol-3-yl]-N-methylmethanamine;hydrochloride
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| Synonyms |
Abeprazan HClDWP14012DWP-14012
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| HS Tariff Code |
2934.99.9001
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| Storage |
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, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~25 mg/mL (~55.94 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.59 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. Solubility in Formulation 2: ≥ 2.5 mg/mL (5.59 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (5.59 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.2378 mL | 11.1889 mL | 22.3779 mL | |
| 5 mM | 0.4476 mL | 2.2378 mL | 4.4756 mL | |
| 10 mM | 0.2238 mL | 1.1189 mL | 2.2378 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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