3-MPPI
3-MPPI is a GPCR ligand with high selectivity for α1-adrenergic receptor, with a Ki value of 0.21 nM for α1-adrenergic receptor and 50 nM for 5-HT1A receptor. 3-MPPI modulates the α1-adrenergic receptor signaling cascade. 3-MPPI is applicable to research related to hypertension, stress-induced anxiety-like behavioral responses, and levodopa-induced dyskinesia.
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- CAS. Nr.: 133399-65-2
- Formel: C23H25N5O3
- Molecular Weight:419.49
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| Caco-2 | Inhibition |
9.14 %
Compound: 3-MPPI
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Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells at 10 uM after 48 hours by high content imaging
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells at 10 uM after 48 hours by high content imaging
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10.21203/rs.3.rs-23951/v1 |
In Vitro
3-MPPI (compound RN5) derivatives exhibit exceptional α1-adrenoceptor (α1-AR) affinity (Ki = 2.71 nM) and selectivity over 5-HT1A receptors (5-HT1A/α1 ratio > 3500)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS. Nr. 133399-65-2
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Molecular Weight 419.49
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Formel C23H25N5O3
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SMILES
O=C1NC=2C=3C=CC=CC3NC2C(=O)N1CCN4CCN(C=5C=CC=CC5OC)CC4
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
3-MPPI Related Classifications
HY-101008 Related Classifications
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Keywords
- 3-MPPI
- 133399-65-2
- Adrenergic Receptor
- G protein-coupled Bile Acid Receptor 1
- benign prostatic hyperplasia
- stress-induced anxiety-like behavioral responses
- l-dopa-induced dyskinesia
- GPCR ligand
- α1-adrenoceptor
- lower urinary tract symptoms
- hypertension
- myocardial hypertrophy
- 5-HT1A receptor
- human α1?-AR
- Inhibitor
- inhibitor
- inhibit