Amiodarone
(Synonyms: 胺碘酮) 目录号 : GC35322
Amiodarone (NSC 85442,Amiodar,Amiodarone hydrochloride,Nexterone) HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.
Cas No.:1951-25-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Amiodarone (NSC 85442,Amiodar,Amiodarone hydrochloride,Nexterone) HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.
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. [1]
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). [1]
[1] Kodama I, et al. Cardiovasc Res,?997, 35(1), 13-29.
| Cas No. | 1951-25-3 | SDF | |
| 别名 | 胺碘酮 | ||
| Canonical SMILES | CCCCC1=C(C(C2=CC(I)=C(OCCN(CC)CC)C(I)=C2)=O)C3=C(O1)C=CC=C3 | ||
| 分子式 | C25H29I2NO3 | 分子量 | 645.31 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5496 mL | 7.7482 mL | 15.4964 mL |
| 5 mM | 0.3099 mL | 1.5496 mL | 3.0993 mL |
| 10 mM | 0.155 mL | 0.7748 mL | 1.5496 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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1. 首先保证母液是澄清的；
2.
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Acute Amiodarone Pulmonary Toxicity
J Cardiothorac Vasc Anesth 2021 May;35(5):1485-1494.PMID:33262034DOI:10.1053/j.jvca.2020.10.060.
Amiodarone is an effective antiarrhythmic that frequently is used during the perioperative period. Amiodarone possesses a significant adverse reaction profile. Amiodarone-induced pulmonary toxicity (AIPT) is among the most serious adverse effects and is a leading cause of death associated with its use. Despite significant advances in the understanding of AIPT, its etiology and pathogenesis remain incompletely understood. The diagnosis of AIPT is one of exclusion. The clinical manifestations of AIPT are categorized broadly as acute, subacute, and chronic. Acute AIPT is a rarer and more aggressive form of the disease, most often encountered in cardiothoracic surgery. Acute respiratory distress syndrome (ARDS) is the predominating pattern of Amiodarone's acute pulmonary toxicity. The incidence, risk factors, pathogenesis, and diagnosis of acute AIPT are speculative. Early cardiothoracic literature investigating AIPT often attributed Amiodarone to the development of postoperative ARDS. Subsequent studies have found no association between Amiodarone and acute AIPT and ARDS development. As a drug that is frequently prescribed to a patient population deemed most at risk for this fatal disease, the conflicting evidence on acute AIPT needs further investigation and clarification.
Amiodarone: A Comprehensive Guide for Clinicians
Am J Cardiovasc Drugs 2020 Dec;20(6):549-558.PMID:32166725DOI:10.1007/s40256-020-00401-5.
Amiodarone is an effective antiarrhythmic medication frequently used in practice for both ventricular and atrial arrhythmias. Though classified as a class III antiarrhythmic, it affects all phases of the cardiac action potential. However, the drug has several side effects, including thyroid abnormalities, pulmonary fibrosis, and transaminitis, for which routine monitoring is recommended. It also interacts with several medications, such as warfarin, simvastatin, and atorvastatin, and many HIV antiretroviral medications. Given the common use of this medication in medical practice, it is vital that clinicians understand the indications, contraindications, dosing, side effects, and interactions of this medication. A thorough understanding of these topics is essential for clinicians to ensure safe and effective use of Amiodarone.
Pharmacology and pharmacokinetics of Amiodarone
J Clin Pharmacol 1991 Nov;31(11):1061-9.PMID:1753010DOI:10.1002/j.1552-4604.1991.tb03673.x.
Amiodarone is a unique antiarrhythmic agent originally developed as a vasodilator. Classified electrophysiologically as a Type III antiarrhythmic, it also has both nonspecific antisympathetic and direct, fast channel-membrane effects. Hemodynamic effects of orally administered Amiodarone (a negative inotropic agent) are usually negligible, and are usually compensated for by induced vasodilation. Effects on thyroid and hepatic function may help to explain some of the unique pharmacologic as well as toxicologic effects of the drug. Amiodarone is poorly bioavailable (20-80%) and undergoes extensive enterohepatic circulation before entry into a central compartment. The principal metabolite, mono-n-desethyl Amiodarone is also an antiarrhythmic. From this central compartment, it undergoes extensive tissue distribution (exceptionally high tissue/plasma partition coefficients). The distribution half-life of Amiodarone out of the central compartment to peripheral and deep tissue compartments (t1/2 alpha) may be as short as 4 hours. The terminal half-life (t1/2 beta) is both long and variable (9-77 days) secondary to the slow mobilization of the lipophilic medication out of (primarily) adipocytes. A pharmacokinetically based loading scheme is described, and data suggesting a role for routine Amiodarone plasma levels are presented.
Amiodarone
J La State Med Soc 1989 May;141(5):35-8.PMID:2659709doi
Amiodarone is an antiarrhythmic agent with unique electrophysiological and pharmacokinetic properties and a wide spectrum of antiarrhythmic activity. Its clinical efficacy is not confined to ventricular arrhythmias but extends to supraventricular arrhythmias including those associated with Wolff-Parkinson-White Syndrome. Though a highly effective drug, Amiodarone causes significant side effects. In this article, the electrophysiologic and pharmacokinetic properties, the clinical efficacy, and the adverse effects of Amiodarone are reviewed.
Amiodarone and thyroid
Best Pract Res Clin Endocrinol Metab 2009 Dec;23(6):735-51.PMID:19942150DOI:10.1016/j.beem.2009.07.001.
Assessment of TSH and TPO-Ab before starting Amiodarone (AM) treatment is recommended. The usefulness of periodic TSH measurement every 6 months during AM treatment is limited by the often sudden explosive onset of AIT, and the spontaneous return of a suppressed TSH to normal values in half of the cases. AM-induced hypothyroidism develops rather early after starting treatment, preferentially in iodine-sufficient areas and in females with TPO-Ab; it is due to failure to escape from the Wolff-Chaikoff effect, resulting in preserved radioiodine uptake. AM-induced thyrotoxicosis (AIT) occurs at any time during treatment, preferentially in iodine-deficient regions and in males. AIT can be classified in type 1 (iodide-induced thyrotoxicosis, best treated by potassium perchlorate in combination with thionamides and discontinuation of AM) and type 2 (destructive thyrotoxicosis, best treated by prednisone; discontinuation of AM may not be necessary). AIT is associated with a higher rate of major adverse cardiovascular events (especially of ventricular arrhythmias). Uncertainty continues to exist with respect to the feasibility of continuation of AM despite AIT, the appropriate methods to distinguish between AIT type 1 and 2 as well as the advantages of AIT classification into subtypes in view of possible mixed cases, and the best policy when AM needs to be restarted.