Amiodarone (NSC 85442) HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.
Storage Temp
Store at -80°C
Shipped In
Ice chest + Ice pads
This product requires cold chain shipping. Ground and other economy services are not available.
Action Type
BLOCKER
Mechanism of action
HERG blocker
Product Description
Information
Amiodarone (NSC 85442) HCl Amiodarone (NSC 85442) HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias. In vitro
Amiodarone possesses an inhibitory effect on the fast sodium channel as well as on the slow calcium channel. Amiodarone also has non-competitive antisympathetic effects, and modulates thyroid function and phospholipid metabolism. Amiodarone penetrates deeply into the lipid matrix of the membrane, and is released from cardiac tissues very slowly when washed out. Amiodarone (44–88 μM) depresses Vmax of guinea pig papillary muscle without affecting the resting membrane potential, and that this Vmax inhibition is enhanced in a frequency- or use-dependent manner like Class I antiarrhythmic drugs. Amiodarone (50–88 μM) is also found to suppress the depolarization-induced spontaneous action potentials (abnormal automaticity) in ventricular muscles and in Purkinje fibers.
In vivo
Amiodarone (1.25–25 mg/kg) results in a decrease in sinus rate, a prolongation of effective and functional refractory periods of the atrioventricular node, and a frequency-dependent conduction delay in the atrioventricular node and in the ventricle of anesthetized dogs. Amiodarone (50 mg/kg/day, i.p. for 3–4 weeks) results in significant decreases in the current density of\xa0iK\xa0and\xa0ito\xa0in ventricular cells without affecting\xa0iCa\xa0and\xa0iK1 densities in rabbit. Amiodarone (AM) inhibits intracellular conversion from thyroxine (T4) to triiodothyronine (T3) via 5′-deiodination (5′DI) without affecting intracellular conversion from T4\xa0to reverse T3\xa0(rT3).\xa0 Cell Data
