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Amiodarone


CAS No. : 1951-25-3

1951-25-3
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Cat. No. : HY-14187
M.Wt: 645.31
Formula: C25H29I2NO3
Purity: >98 %
Solubility: DMSO : ≥ 175 mg/mL
Introduction of 1951-25-3 :

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]. In Vitro: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]. In Vivo: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].

Induction of pulmonary toxicity[4]
Background
Amiodarone promotes the release of cytokines such as TNF, TGF-β, IL-4, and IL-8 by activating NF-κB, while also enhancing the involvement of natural killer cells in immune regulation. This leads to the release of reactive oxygen species, leukocyte aggregation, and intracellular lipid accumulation, thereby inducing pulmonary damage [4].
Specific Modeling Methods
Rat: Fischer • male • 9 to 10 weeks old
Administration: 175 mg/kg • po • once daily, 5 days a week for 12 weeks
Note
(1) Amiodarone is suspended in a 0.5% methylcellulose solution (HY-125861).
(2) The rats are weighed weekly and the drug dose is adjusted if necessary, higher doses of amiodarone could be fatal.
Modeling Indicators
Histological Changes: The number of macrophages, neutrophils, and lymphocytes in the bronchi and alveoli of rats is significantly increased.
Phenotypic Observations: Lung sections of rats show interstitial thickening with accumulation of mononuclear cells, alveoli filled with numerous foamy macrophages, and mild fibrosis.
Correlated Product(s): Methyl cellulose (HY-125861)

Induction of liver injury[5]
Background
Amiodarone is metabolized in the liver by the cytochrome P450 3A4 enzyme to produce metabolites such as desethylamiodarone (DEA), leading to mitochondrial dysfunction, increased intracellular oxidative stress, and lipid metabolism disorders, which in turn activate macrophages (Kupffer cells) in the liver, thereby inducing liver injury in mice[5].
Specific Modeling Methods
Mice: Balb/cCrSlc • male • 8-week-old
Administration: 1000 mg/kg • po • single dose
Note
1. Amiodarone is dissolved in corn oil.
2. Prior to oral administration of Amiodarone, pre-treatment with Dexamethasone (HY-14648) was conducted to induce cytochrome P450 3A4 enzyme expression. Dexamethasone was dissolved in corn oil and administered at a dose of 60 mg/kg via intraperitoneal injection once daily for 3 days. Amiodarone was administered orally 24 hours after the final dose of Dexamethasone.
Modeling Indicators
Molecular Changes: The levels of alanine aminotransferase (ALT) and triglycerides in the plasma of mice are significantly elevated. The release of cytochrome c into the cytosol of liver cells is increased. The ratio of reduced glutathione to oxidized glutathione disulfide in the liver is significantly decreased, indicating increased oxidative stress and reduced cellular antioxidant capacity in the liver.
Correlated Product(s): Dexamethasone (HY-14648)

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