Etafenone
Etafenone is an antiarrhythmic agent and vasodilator. Etafenone exerts β-adrenergic agonistic effects. Etafenone inhibits the automaticity of sinoatrial nodes, atrioventricular junctions and Purkinje fibers, prolongs action potential duration and refractory period, slows the rising rate of action potentials, and prolongs conduction time. Etafenone enhances collateral circulation after coronary occlusion and suppresses ventricular premature beats. Etafenone delays ischemic myocardial energy imbalance, improves the recovery of high-energy phosphates after ischemia, and reduces myocardial oxygen consumption. Etafenone can be used in research related to ischemic heart disease, arrhythmia and angina pectoris.
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- CAS. Nr.: 90-54-0
- Formel: C21H27NO2
- Molecular Weight:325.44
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Speicherung:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biologische Aktivität
Beschreibung
IC50 & Target
[3]|
β-adrenoceptor |
In Vitro
Etafenone (0.5-3 mg/L) dose-dependently reduces membrane responsiveness in canine Purkinje fibers, as evidenced by a rightward shift of the membrane responsiveness curve at 0.5 mg/L and an exaggerated shift at 3 mg/L[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Cmax | Tmax |
|---|---|---|---|---|
| Dog[1] | 20 mg/kg | p.o. | 20 mg/L | 1 h |
In Vivo
Etafenone (0.3-3 mg/kg; i.v.) dose-dependently decreases systemic blood pressure and heart rate, increases venous return, cardiac output, and right atrial pressure at doses up to 3 mg/kg in anesthetized open-chest mongrel dogs, while higher doses above 3 mg/kg induce cardiodepressant effects with reduced venous return and cardiac output[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mongrel dogs (both sexes, 20-39 kg, starved for 24 h, anaesthetized)[3]
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Dosage:0.1 mg/kg/min; 0.5 mg/kg/min; 0.5 mg/kg/min (following propranolol pretreatment)
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Administration:i.v.; infusion over 10 min
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Result:Produced non-significant slight increases in heart rate, coronary conductance, femoral conductance, expiratory CO2, and non-significant slight decreases in arterial and left ventricular blood pressure; no change in dp/dt at 0.1 mg/kg/min.
Produced significant increases in heart rate, coronary conductance (significant only at 6-12 min), femoral conductance, left ventricular dp/dt, expiratory CO2, and myocardial oxygen consumption (significant only at 2-4 min); caused a significant fall in systemic blood pressure throughout the infusion; peak left ventricular blood pressure was unchanged; all parameters returned to preinfusion values 5-10 min post-infusion except heart rate and femoral conductance at 0.5 mg/kg/min.
Completely abolished increases in heart rate and dp/dt seen without β-blockade, with dp/dt showing a significant reduction from 10 min onwards; significant increases in coronary conductance, femoral conductance, and expiratory CO2 persisted but were significantly reduced compared to pre-β-blockade levels; systemic and left ventricular blood pressure decreased significantly throughout the infusion and remained lowered during the observation period at 0.5 mg/kg/min after propranolol pretreatment.
Chemical Information
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CAS. Nr. 90-54-0
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Appearance Solid
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Molecular Weight 325.44
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Formel C21H27NO2
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Color White to off-white
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SMILES
O=C(C1=CC=CC=C1OCCN(CC)CC)CCC2=CC=CC=C2
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protokoll
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Cardiac voltage-sensitive optical mapping
Cardiac voltage-sensitive optical mapping records changes in transmembrane potential from cardiac tissue by staining the preparation with a voltage-sensitive dye and imaging fluorescence changes during electrical activation; the resulting optical action potentials can be used to map activation time, action potential duration, conduction velocity, wavefront propagation, and arrhythmia dynamics. The optical signal represents a relative fluorescence change from a tissue volume rather than a single-cell intracellular recording, so spatial resolution, sampling rate, voltage resolution, optical magnification, light penetration, and motion control must be considered together when interpreting optical action potentials.
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Neuronal voltage-sensitive dye imaging
Neuronal voltage-sensitive dye imaging detects membrane-potential-dependent optical changes from dyes associated with neuronal membranes, enabling optical recording of electrical activity from single neurons, dendrites, axons, spines, or neuronal populations in brain slices and cultured neurons. VSD signals are typically reported as fractional fluorescence or absorbance changes over baseline, such as ΔF/F or ΔI/I, and published protocols use high-speed cameras or photodiode arrays because neuronal voltage signals occur on millisecond time scales. Fast VSD imaging can be applied at two common scales: bulk staining of brain slices to measure circuit-level spatiotemporal activity, and single-cell loading or biolistic delivery to record membrane-potential transients from individual neuronal compartments. Optical signals should be interpreted as membrane-potential-related readouts, and validation by simultaneous electrophysiology or pharmacological controls is recommended when the experimen
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Acute brain-slice whole-cell patch-clamp recording
Acute brain-slice whole-cell patch-clamp recording measures membrane voltage or ionic current from visually targeted cells in living brain slices; after giga-seal formation, the membrane under the pipette is ruptured to provide low-resistance electrical access to the cell interior, enabling current-clamp analysis of excitability and voltage-clamp analysis of synaptic or membrane currents. Acute slices preserve local tissue architecture better than dissociated preparations and allow visually guided recording from defined brain regions or fluorescently labeled cells; however, whole-cell access also permits exchange between pipette solution and cytoplasm, so intracellular dialysis must be considered when interpreting signaling-dependent phenomena.
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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
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Data Sheet (276 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)