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Amiodarone HCl Potassium Channel inhibitor

Cat.No.S1979

Amiodarone HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.
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Quality Control

Batch: Purity: 99.98%
99.98

Solubility

In vitro
Batch:

DMSO : 100 mg/mL (146.67 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 20 mg/mL

Water : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 681.77 Formula

C25H29I2NO3.HCl

Storage (From the date of receipt)
CAS No. 19774-82-4 Download SDF Storage of Stock Solutions

Synonyms NSC 85442 SMILES CCCCC1=C(C2=CC=CC=C2O1)C(=O)C3=CC(=C(C(=C3)I)OCCN(CC)CC)I.Cl

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Mechanism of Action

Targets/IC50/Ki
Potassium channel
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 iK and ito in ventricular cells without affecting iCa and iK1 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 to reverse T3 (rT3). 

References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-02-17)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03868150 RECRUITING
Postoperative Atrial Fibrillation
Stanford University
2017-03-01 PHASE4
NCT05841056 RECRUITING
Atrial Fibrillation New Onset
Population Health Research Institute
2024-06-13 PHASE3
NCT06322017 RECRUITING
Atrial Fibrillation
Nantes University Hospital
2024-04-09
NCT07519161 NOT_YET_RECRUITING
Atrial Fibrillation
Shanghai East Hospital
2026-04-07
NCT07405671 NOT_YET_RECRUITING
Atrial Fibrillation (AF); Coronary Artery Disease
Universitaire Ziekenhuizen KU Leuven
2026-09 PHASE4
NCT04748991 NOT_YET_RECRUITING
Atrial Fibrillation; Post-cardiac Surgery
University of Calgary
2026-09 PHASE3

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