GPR4 antagonist 2
GPR4 antagonist 2 is a selective GPR4 antagonist with an IC50 of 67 nM. GPR4 antagonist 2 inhibits pH-dependent GPR4 activation and CRE-driven transcriptional activity. GPR4 antagonist 2 prolongs the survival of mice in a myocardial infarction model. GPR4 antagonist 2 can be used for research on myocardial infarction.
For research use only. We do not sell to patients.
- CAS No.: 1883333-94-5
- Formula: C31H37N5
- Molecular Weight:479.67
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | IC50 |
>10 μM
Compound: 3b
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Antagonist activity at N-terminal HA-tagged OGR1 (unknown origin) expressed in HEK293 cells assessed as inhibition of pH dependent nuclear factor of activated T-cell activity at pH 7.2 incubated for 6 hrs by dual luciferase reporter gene assay
Antagonist activity at N-terminal HA-tagged OGR1 (unknown origin) expressed in HEK293 cells assessed as inhibition of pH dependent nuclear factor of activated T-cell activity at pH 7.2 incubated for 6 hrs by dual luciferase reporter gene assay
|
[PMID: 27190599] |
| HEK293 | IC50 |
67 nM
Compound: 3b
|
Antagonist activity at N-terminal HA-tagged GPR4 (unknown origin) expressed in HEK293 cells assessed as inhibition of pH dependent cAMP response element-driven transcriptional activity at pH 7.2 incubated for 6 hrs by dual luciferase reporter gene assay
Antagonist activity at N-terminal HA-tagged GPR4 (unknown origin) expressed in HEK293 cells assessed as inhibition of pH dependent cAMP response element-driven transcriptional activity at pH 7.2 incubated for 6 hrs by dual luciferase reporter gene assay
|
[PMID: 27190599] |
In Vitro
GPR4 antagonist 2 (compound 3b) (10 μM) is a potent antagonist of pH-dependent GPR4 activation in HEK293 cells expressing GPR4, with a CRE activity ratio of 0.39 and an IC50 of 67 nM[1].
GPR4 antagonist 2 (10 μM) shows no activity against TDAG8 or OGR1 in HEK293 cells expressing these receptors[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mice were subjected to permanent left anterior descending coronary artery ligation under anesthetized conditions[1]
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Dosage:6.7 mg/kg/day
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Administration:i.p.; twice a day; from 1 day before to 7 days after the operation
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Result:Achieved 100% survival (7/7) in mice with myocardial infarction, compared to 1/7 survival in controls.
Chemical Information
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CAS No. 1883333-94-5
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Molecular Weight 479.67
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Formula C31H37N5
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SMILES
N=1C(=CC(=C2N=C(N(C12)CC3=CC=C4NC5=CC=C(C=C5CCC4=C3)CN6CCCCC6)CC)C)C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Dual Luciferin reporter gene assay
Luciferin reporter gene assay is a reporting system to detect the activity of Firefly Luciferase using luciferin as a substrate, which is often used in the research of miRNA target gene verification and promoter transcriptive activity regulation. Dual luciferase usually refers to Firefly luciferase and Renilla luciferase.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)