Amiodarone 

Amiodarone, a benzofuran-based Class III antiarrhythmic agent, inhibits WT outward ionic current (IhERG) tails with an IC₅₀ of ∼45 nM^[1]. Amiodarone induces cell proliferation and myofibroblast differentiation via ERK1/2 and p38 MAPK signaling in fibroblasts^[2]. Amiodarone can be used in the research of both supraventricular and ventricular arrhythmias^[1].

Amiodarone blocks inward IhERG tails in a high K⁺ external solution ([K⁺]e) of 94 mM with an IC₅₀ of 117.8 nM^[1].
Amiodarone (1 μM) blocks inward IhERG by 68.8%, with concentration response data yielding IC₅₀ and h values of 765.5 nM and 0.9 for T623A hERG^[1].
Amiodarone (1 μM) blocks inward IhERG with an IC₅₀ and h values of 979.2 nM and 1.1 for S624A hERG^[1].
Amiodarone (1-6 μg/mL) induces human embryonic lung fibroblasts (HELFs) cell proliferation and PD98059 or SB203580 suppresses this effect^[2].
Amiodarone (1-6 μg/mL) does not induces HELFs cell apoptosis. Amiodarone (over 15 μg/mL) induces cell apoptosis^[2].
Amiodarone (1, 3 and 6 μg/mL;24 hours) induces α-SMA and vimentin mRNA and protein expression accompanied by increased phosphorylation of ERK1/2 and p38 MAPK^[2].

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

Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Amiodarone can be used in animal modeling to create pulmonary toxicity and liver injury models. After a single oral dose of Amiodarone in rats, the pharmacokinetic characteristics detectable include an absorption half-life of approximately 1.83 hours and a clearance half-life ranging from 15 hours (at a 100 mg/kg dose) to 105 hours (at a 200 mg/kg dose), with an average oral bioavailability of 39%. Amiodarone is primarily distributed in the lungs, liver, thyroid, and adipose tissue, with drug concentrations in the lungs and adipose tissue being significantly higher than in other tissues. Following long-term oral administration, the accumulation of Amiodarone in adipose tissue is notably increased^[3][4][5].

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

645.31

C₂₅H₂₉I₂NO₃

1951-25-3

<54°C Solid, >55°C Liquid

Off-white to light yellow

CCCCC1=C(C(C2=CC(I)=C(OCCN(CC)CC)C(I)=C2)=O)C3=C(O1)C=CC=C3

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Yihong Zhang,et al. Interactions between amiodarone and the hERG potassium channel pore determined with mutagenesis and in silico docking. Biochem Pharmacol. 2016 Aug 1;113:24-35.  [Content Brief]

  [2]. Jie Weng, et al. Amiodarone induces cell proliferation and myofibroblast differentiation via ERK1/2 and p38 MAPK signaling in fibroblasts. Biomed Pharmacother. 2019 Jul;115:108889.  [Content Brief]

  [3]. Plomp TA, et al. Pharmacokinetics and body distribution of amiodarone and desethylamiodarone in rats after oral administration. In Vivo. 1987 Sep-Oct;1(5):265-79.  [Content Brief]

  [4]. Wilson BD, et al. Amiodarone-induced pulmonary toxicity in the rat. Lung. 1989;167(5):301-11.  [Content Brief]

  [5]. Takai S, et al. Establishment of a mouse model for amiodarone-induced liver injury and analyses of its hepatotoxic mechanism. J Appl Toxicol. 2016 Jan;36(1):35-47.  [Content Brief]