MRS542
MRS542 is a nucleoside A3 AR antagonist with a pKi of 8.74. MRS542 also acts as a partial agonist (pEC50 = 7.76) in promoting β-arrestin translocation. MRS542 can be converted into an agonist by LUF6000 (HY-13236). MRS542 can be used for cardiovascular disease research.
For research use only. We do not sell to patients.
- CAS No.: 163152-31-6
- Formula: C17H17ClIN5O4
- Molecular Weight:517.71
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[2]|
A3 8.76 (pKi) |
Chemical Information
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CAS No. 163152-31-6
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Molecular Weight 517.71
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Formula C17H17ClIN5O4
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SMILES
N(CC1=CC(I)=CC=C1)C2=C3C(N(C=N3)[C@@H]4O[C@H](CO)[C@@H](O)[C@H]4O)=NC(Cl)=N2
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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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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
[1]. Gao ZG, et al. Translocation of arrestin induced by human A(3) adenosine receptor ligands in an engineered cell line: comparison with G protein-dependent pathways. Pharmacol Res. 2008 Apr;57(4):303-11. [Content Brief]
[2]. Gao ZG, et al. Flexible modulation of agonist efficacy at the human A3 adenosine receptor by the imidazoquinoline allosteric enhancer LUF6000. BMC Pharmacol. 2008 Dec 12;8:20. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MRS542 Related Classifications
HY-153157 Related Classifications
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