2. Membrane Transporter/Ion Channel Apoptosis Anti-infection
  3. Proton Pump Apoptosis Bacterial
  4. Rabeprazole

Rabeprazole (LY307640) 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.

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Rabeprazole Chemical Structure

Rabeprazole Chemical Structure

CAS No. : 117976-89-3

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Based on 2 publication(s) in Google Scholar

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Rabeprazole Related Antibodies

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Description

Rabeprazole (LY307640) 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].

IC50 & Target

Pump inhibitor (PPI)[1]
IC50: 0.3 μM (UNH)[1]
H+/K+-ATPase[2]
Apoptosis[2]
In Vitro

Rabeprazole attenuates the cell viability of the human gastric cancer cells following treatment with 0.2 mM for 16 hours[2].
Rabeprazole completely inhibits the phosphorylation of ERK1/2 in the MKN-28 cells. The gastric cancer cell line MKN-28 is cultured in acidic culture media (pH 5.4) for 2 hours. Pretreatment with Rabeprazole (0.2 mM for 2 hours) leads to strong inhibition of ERK1/2 phosphorylation in the MKN-28 cells[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Rabeprazole Related Antibodies

Cell Viability Assay[2]

Cell Line: Three gastric cancer cell lines KATO III, MKN-28 and MKN-45
Concentration: 0.2 mM
Incubation Time: 16 hours
Result: Treatment resulted in the attenuation of viability in all cancer cell lines tested, the cell viability of the MKN-28 cells significantly decreased compared with the KATO III and MKN-45 cells, respectively.

Cell Viability Assay[2]

Cell Line: Three gastric cancer cell lines (KATO III, MKN-28 and MKN-45)[2]
Concentration: 0.2 mM
Incubation Time: Pretreatment for 2 hours
Result: Led to strong inhibition of ERK 1/2 phosphorylation in the MKN-28 cells, but a similar effect was not observed in the KATO III and MKN-45 cells.
In Vivo

Rabeprazole (10 mg/kg; P.O.; every 48 h for 18 weeks) course leads to a significant decline in bone mineral density (BMD) and decreases serum calcium level and produces secondary hyperparathyroidism in female mice[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female Swiss albino mice (body weight equals 18-26 g)[3]
Dosage: 10 mg/kg
Administration: Oral administration; every 48 h for 18 weeks
Result: Showed significantly lower serum calcium level compared to the vehicle treated group (5.5±2.07 vs. 9.68±2.77).
Clinical Trial
Molecular Weight

359.44

Formula

C18H21N3O3S
CAS No.
SMILES

O=S(C1=NC2=CC=CC=C2N1)CC3=NC=CC(OCCCOC)=C3C
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Storage

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Solvent & Solubility

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In Vivo:

The following protocol is derived from the literature and is for reference only. It is recommended to first try a small sample.

  • Protocol 1

    Rabeprazole was dissolved in distilled water[3].

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Purity & Documentation
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Rabeprazole Related Classifications

Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Rabeprazole117976-89-3LY307640LY 307640LY-307640Proton PumpApoptosisBacterialprotonpumpPPIgastricATPaseuridinenucleosideribohydrolaseUNHulcerationsgastroesophagealrefluxInhibitorinhibitorinhibit

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