Dexnafenodone

Dexnafenodone ((S)-Nafenodone) inhibits potassium chloride- and norepinephrine-induced contractions of isolated rat aortic strips with equal potency; it possesses voltage-sensitive Ca²⁺ channel blocking activity, with an IC₅₀ of 2.5×10^‑6 M for inhibiting Ca²⁺-induced contractions of potassium-depolarized aortas. It also inhibits norepinephrine-induced phasic contractions mediated by intracellular calcium stores in a calcium-free environment, and suppresses spontaneous myogenic activity of rat portal veins with an IC₅₀ of 1.4×10^‑6 M^[1].

Dexnafenodone inhibits ⁴⁵Ca²⁺ influx in isolated rat aortic strips stimulated by potassium chloride and norepinephrine, but does not alter ⁴⁵Ca²⁺ influx under resting conditions. The I₅₀ value of this compound for inhibiting potassium chloride-induced calcium influx is 2.1×10^‑5 M^[1].

Dexnafenodone exerts concentration-dependent negative chronotropic and negative inotropic effects in isolated spontaneously beating guinea pig right atria, and prolongs the sinus node recovery time. Its IC₅₀ value for chronotropic inhibition is 1×10^-5 M, and the IC₅₀ value for inotropic inhibition is 5×10^-6 M^[2].
Dexnafenodone exerts a concentration-dependent inhibitory effect on isolated guinea pig myocardium, producing negative chronotropic and negative inotropic effects with corresponding IC₅₀ values of 1×10^‑5 M and 5×10^‑6 M, respectively, and shifts the calcium concentration-response curve to the right^[1].
Dexnafenodone ((S)-Nafenodone) reduces the action potential amplitude and V_max of atrial and ventricular myocytes, does not alter the resting membrane potential, and increases the ERP/APD₉₀ ratio^[2].
Dexnafenodone inhibits slow calcium-mediated contraction of potassium-depolarized cardiomyocytes, and suppresses isoproterenol-induced slow action potentials at high concentrations^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.