Amiodarone hydrochlorideAmiodarone hydrochloride
MedChemExpress (MCE)
HY-14188
19774-82-4
99.86%
4°C, sealed storage, away from moisture and light *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture and light)
Room temperature in continental US
may vary elsewhere.
Amiodarone hydrochloride, a benzofuran-based Class III antiarrhythmic agent, inhibits WT outwardIhERG tails with an IC50 of ∼45 nM. Amiodarone hydrochloride induces cell proliferation and myofibroblast differentiation via ERK1/2 and p38 MAPK signaling in fibroblasts. Amiodarone hydrochloride can be used in the research of both supraventricular and ventricular arrhythmias.
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 inwardIhERG by 68.8±6.1%, with concentration response data yielding IC50 and h values of 765.5±287.8 nM and 0.9±0.4 for T623A hERG[1]. Amiodarone (1 μM) blocks inward IhERG with an IC50 and h values of 979.2±84.3 nM and 1.1±0.1 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 ug/mL) does not induces HELFs cell apoptosis. Amiodarone (over 15 ug/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].
Amiodarone can be used to create pulmonary fibrosis models. Amiodarone has a large distribution volume and extensive tissue distribution, resulting in a terminal half-life in human plasma of up to 25 days. The major active metabolite of Amiodarone is deethylamiodarone. After oral administration, Amiodarone has low and variable bioavailability and exhibits high lipophilicity[2]. .f12{ font-size: 12px
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} Induction of lung fibrosis model[1] Background Amiodarone induces pulmonary injury by direct toxicity to lung tissue, hypersensitivity reaction, enhanced oxidative stress, alteration of membrane properties and activation of alveolar macrophages and cytokine release. Amiodarone administration can result in interstitial and/or alveolar inflammation and release of inflammatory mediators. Specific Mmodeling Methods Rat: F344 rats • male • 200-225 gAdministration: 6.25 mg/kg • i.t. instillation • in 0.3 mL of water • on days 0 and 2 Note The solution should brought to room temperature before instillation. Modeling Indicators Marker of lung fibrosis: Increased lung collagen content.Higher levels of total protein in lung lavage fluid.Increased LDH activity in bronchoalveolar lavage, and increased lung MPO activity.Increased total cell counts, alveolar macrophages, neutrophils and eosinophils. Correlated Product(s): / Opposite Product(s): Curcumin (HY-N0005)
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[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]. Sabrina Le Bouter, et al. Long-term amiodarone administration remodels expression of ion channel transcripts in the mouse heart. Circulation. 2004 Nov 9
110(19):3028-35. [Content Brief]
[4]. Punithavathi D, et al. Protective effects of curcumin against amiodarone-induced pulmonary fibrosis in rats. Br J Pharmacol. 2003 Aug
139(7):1342-50. [Content Brief]
[5]. Shayeganpour A, et al. Pharmacokinetics of Amiodarone in hyperlipidemic and simulated high fat-meal rat models. Biopharm Drug Dispos. 2005 Sep
26(6):249-57. [Content Brief]
