Brefonalol (hydrochloride)
Based on 1 Customer Validation
Brefonalol (Brefanolol) hydrochloride is an orally active, non-selective β-adrenergic receptor blocker with vasodilatory properties. Brefonalol hydrochloride exhibits an optimal balance between β-blockade and vasodilatory effects at low doses: it reduces blood pressure and slows heart rate, while increasing stroke volume instead of decreasing it, causing no significant elevation in peripheral resistance and increasing reactive hyperemia; at high doses, the β-blockade effect dominates. Brefonalol hydrochloride can be used in the research of arterial hypertension.
For research use only. We do not sell to patients.
- CAS No.: 3026677-28-8
- Formula: C22H29ClN2O2
- Molecular Weight:388.93
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
All Adrenergic Receptor Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
β-adrenoceptor |
In Vitro
Brefonalol hydrochloride exhibits balanced β-receptor blocking and vasodilatory effects at a dose of 50 mg, while at a dose of 100 mg, it primarily exerts β-receptor blocking effects[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 No. 3026677-28-8
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Appearance Solid
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Molecular Weight 388.93
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Formula C22H29ClN2O2
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SMILES
O=C1NC2=C(C=C(C(O)CNC(C)(C)CCC3=CC=CC=C3)C=C2)CC1.Cl
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Synonyms
Brefanolol hydrochloride
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)