| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
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| Other Sizes |
| Targets |
Linaprazan glurate targets the gastric H⁺/K⁺-ATPase (proton pump) in a potassium-dependent manner. It selectively inhibits acid formation from gastric H⁺/K⁺-ATPase with an IC50 of 436.2 nM. As a potassium-competitive acid blocker (P-CAB), it competes with potassium ions for binding to the enzyme, thereby inhibiting acid secretion. Unlike traditional proton pump inhibitors that require acid activation, P-CABs provide rapid and sustained acid suppression. The compound inhibits both exogenously and endogenously stimulated gastric acid secretion. Its target is the final common pathway of gastric acid secretion, making it effective for acid-related disorders.
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| ln Vitro |
In vitro studies have demonstrated that Linaprazan glurate selectively inhibits acid formation from gastric H⁺/K⁺-ATPase with an IC50 of 436.2 nM. The inhibition is potassium-dependent, consistent with its mechanism as a potassium-competitive acid blocker. The compound inhibits both exogenously and endogenously stimulated gastric acid secretion in cell-based and tissue-based assays. Its prodrug nature allows for improved pharmacokinetic properties compared to the active parent compound. These in vitro findings support its potential as a therapeutic agent for acid-related gastrointestinal disorders including gastroesophageal reflux disease (GERD) and peptic ulcer diseases.
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| ln Vivo |
In vivo studies have demonstrated that Linaprazan glurate exhibits high in vivo potency, rapid onset of action, and long duration of action. The compound inhibits both exogenously and endogenously stimulated gastric acid secretion in animal models. As a prodrug for linaprazan, it provides favorable pharmacokinetic properties that translate to effective acid suppression in vivo. Studies have evaluated its effects on gastrointestinal inflammatory diseases and peptic ulcer diseases. The compound's potassium-competitive acid blocker mechanism provides advantages over traditional proton pump inhibitors, including rapid onset and sustained acid suppression. Further clinical studies are needed to fully establish its therapeutic profile.
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| Enzyme Assay |
In vitro enzyme assays for Linaprazan glurate involve testing its inhibitory activity against gastric H⁺/K⁺-ATPase. Enzyme activity is measured by monitoring proton transport or ATP hydrolysis in the presence of varying concentrations of the compound. IC50 values are determined from dose-response curves, with a reported IC50 of 436.2 nM for inhibition of acid formation. The potassium-dependent nature of inhibition is assessed by performing assays at different potassium concentrations. For prodrug characterization, the conversion of Linaprazan glurate to linaprazan is monitored using analytical methods such as high-performance liquid chromatography-mass spectrometry. All assays are performed with appropriate controls and standardized protocols to ensure reproducibility of results.
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| Cell Assay |
In vitro cell-based assays for Linaprazan glurate involve culturing gastric parietal cells to evaluate its effects on acid secretion. Cells are treated with varying concentrations of the compound and stimulated with secretagogues such as histamine, gastrin, or carbachol to induce acid secretion. Acid production is measured using pH-sensitive dyes, [¹⁴C]-aminopyrine accumulation, or other methods. The compound's ability to inhibit both exogenous and endogenous stimulation is assessed. Cell viability is assessed using MTT or similar colorimetric assays to ensure that observed effects are not due to cytotoxicity. All experiments are performed in triplicate with appropriate controls (vehicle control, positive control with known P-CAB) to ensure statistical reliability.
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| Animal Protocol |
In vivo animal experiments for Linaprazan glurate utilize rodent or other animal models to evaluate its effects on gastric acid secretion. Animals are administered the compound orally or intravenously, and gastric acid secretion is measured using various methods including gastric fistula, pylorus ligation, or intragastric pH monitoring. The compound's ability to inhibit both exogenously (e.g., histamine-stimulated) and endogenously stimulated acid secretion is assessed. For efficacy studies in gastrointestinal inflammatory diseases and peptic ulcer diseases, animal models of these conditions are used. Parameters assessed include gastric acid output, gastric pH, ulcer formation, and inflammation markers. Control groups receiving vehicle alone are included for comparison. All procedures must comply with institutional animal care and use committee guidelines.
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| ADME/Pharmacokinetics |
The pharmacokinetic properties of Linaprazan glurate reflect its nature as a prodrug. It has a molecular weight of 480.56 and the molecular formula C26H32N4O5. As a prodrug, it is designed to improve the pharmacokinetic properties of the active compound linaprazan. The compound displays favorable properties such as rapid onset of action, high in vivo potency, and long duration of action. Its prodrug nature allows for improved oral bioavailability and distribution. The compound is metabolized to the active linaprazan, which then inhibits gastric H⁺/K⁺-ATPase. Complete pharmacokinetic profiling including half-life, clearance, and bioavailability would require further systematic studies using appropriate analytical methods such as high-performance liquid chromatography-mass spectrometry.
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| Toxicity/Toxicokinetics |
The toxicity profile of Linaprazan glurate has been evaluated in the context of its development as a therapeutic agent for acid-related disorders. As a potassium-competitive acid blocker, it has a different safety profile compared to traditional proton pump inhibitors. The compound's selectivity for gastric H⁺/K⁺-ATPase suggests a favorable safety profile with minimal off-target effects. However, as with all pharmaceuticals, comprehensive toxicology studies including acute, subchronic, and chronic toxicity, genotoxicity, and reproductive toxicity would be required for regulatory approval. The compound is intended for research purposes and is not approved for human use. Proper handling procedures including use of personal protective equipment are recommended.
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| References |
[1]. Mikael Dahlström, et al. Imidazopyridine derivatives which inhibit the secretion of gastric acid. Patent WO2010063876A1.
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| Additional Infomation |
Linaprazan Glurate is a small molecule drug. Its International Nonproprietary Name (INN) stem "-prazan" indicates that linaprazan gluconate is a proton pump inhibitor that is not acid-dependent. Linaprazan gluconate is currently being investigated in the clinical trial NCT07037875 (a study comparing the efficacy and safety of linaprazan gluconate versus lansoprazole in patients with erosive esophagitis (EE) caused by gastroesophageal reflux disease (GERD)). The monoisotopic molecular weight of linaprazan gluconate is 480.24 Da.
Linaprazan glurate (X842, CAS# 1228559-81-6) is a next-generation therapeutic agent for acid-related disorders, functioning as a prodrug for the potent potassium-competitive acid blocker linaprazan. It has the molecular formula C26H32N4O5 and a molecular weight of 480.56. The compound is a proton pump inhibitor not dependent on acid activation. It inhibits both exogenously and endogenously stimulated gastric acid secretion. The compound selectively inhibits acid formation from gastric H⁺/K⁺-ATPase in a potassium-dependent manner with an IC50 of 436.2 nM. It can be utilized in studies on gastrointestinal inflammatory diseases and peptic ulcer diseases. The compound displays favorable properties including rapid onset of action, high in vivo potency, and long duration of action. It is intended for research use only. |
| Molecular Formula |
C26H32N4O5
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|---|---|
| Molecular Weight |
480.556086540222
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| Exact Mass |
480.237
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| CAS # |
1228559-81-6
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| PubChem CID |
46208366
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| Appearance |
White to off-white solid powder
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| LogP |
3.7
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
12
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| Heavy Atom Count |
35
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| Complexity |
725
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CC1=C(C(=CC=C1)C)CNC2=CC(=CN3C2=NC(=C3C)C)C(=O)NCCOC(=O)CCCC(=O)O
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| InChi Key |
GPHPBXRKAJSSIC-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C26H32N4O5/c1-16-7-5-8-17(2)21(16)14-28-22-13-20(15-30-19(4)18(3)29-25(22)30)26(34)27-11-12-35-24(33)10-6-9-23(31)32/h5,7-8,13,15,28H,6,9-12,14H2,1-4H3,(H,27,34)(H,31,32)
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| Chemical Name |
5-[2-[[8-[(2,6-dimethylphenyl)methylamino]-2,3-dimethylimidazo[1,2-a]pyridine-6-carbonyl]amino]ethoxy]-5-oxopentanoic acid
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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 |
| 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) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.0809 mL | 10.4045 mL | 20.8091 mL | |
| 5 mM | 0.4162 mL | 2.0809 mL | 4.1618 mL | |
| 10 mM | 0.2081 mL | 1.0405 mL | 2.0809 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.
Link: https://clinicaltrials.gov/ct2/show/NCT07313774
Conditions:GERD (Gastroesophageal Reflux Disease)Link: https://clinicaltrials.gov/ct2/show/NCT07294846
Conditions:Healthy Volunteers|PatientsLink: https://clinicaltrials.gov/ct2/show/NCT07079540
Conditions:Reflux Esophagitis
Title:Study to Evaluate the Safety and Efficacy of X842 in Patients With Reflux Esophagitis
Status:Completed
updateDate:2025-07-17
Ctid:NCT04531475
Link: https://clinicaltrials.gov/ct2/show/NCT04531475
Conditions:Reflux EsophagitisLink: https://clinicaltrials.gov/ct2/show/NCT05627518
Conditions:Safety|Bioavailability|PharmacokineticsLink: https://clinicaltrials.gov/ct2/show/NCT05633147
Conditions:Safety Issues|Pharmacokinetics|Drug Interaction|TolerabilityLink: https://clinicaltrials.gov/ct2/show/NCT05469854
Conditions:Pharmacokinetics|Cardiodynamic ECG|Safety, and Tolerability|GERDLink: https://clinicaltrials.gov/ct2/show/NCT05055128
Conditions:Erosive EsophagitisProducts are for research use only; We do not sell to patients
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