Amiodarone HCl

Anti-arrhythmic drug CAS# 19774-82-4

Amiodarone HCl

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Chemical structure

Amiodarone HCl

3D structure

Chemical Properties of Amiodarone HCl

Cas No. 19774-82-4 SDF Download SDF
PubChem ID 441325 Appearance Powder
Formula C25H30ClI2NO3 M.Wt 681.77
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : 24.5 mg/mL (35.94 mM; Need ultrasonic and warming)
Chemical Name 2-Butyl-3-benzofuranyl-4-[2-(diethylamino)ethoxy]-3,5-diiodophenyl ketone hydrochloride
SMILES [H+].[Cl-].CCCCc1oc2ccccc2c1C(=O)c3cc(I)c(OCCN(CC)CC)c(I)c3
Standard InChIKey ITPDYQOUSLNIHG-UHFFFAOYSA-N
Standard InChI InChI=1S/C25H29I2NO3.ClH/c1-4-7-11-22-23(18-10-8-9-12-21(18)31-22)24(29)17-15-19(26)25(20(27)16-17)30-14-13-28(5-2)6-3;/h8-10,12,15-16H,4-7,11,13-14H2,1-3H3;1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Amiodarone HCl

DescriptionBroad-spectrum ion channel blocker; blocks late INa, ICa, IKr and IKs and increases QT. Displays class III antiarrhythmic properties. Also exhibits fungicidal activity; elicits Ca2+ influx in Saccharomyces cerevisiae and causes mitochondrial fragmentation and cell death. Thought to stimulate autophagy by targeting upstream mTORC1 control pathways. Selectively toxic to NSCs in hESC-derived cell populations.

Amiodarone HCl Dilution Calculator

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Amiodarone HCl Molarity Calculator

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Preparing Stock Solutions of Amiodarone HCl

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.4668 mL 7.3339 mL 14.6677 mL 29.3354 mL 36.6693 mL
5 mM 0.2934 mL 1.4668 mL 2.9335 mL 5.8671 mL 7.3339 mL
10 mM 0.1467 mL 0.7334 mL 1.4668 mL 2.9335 mL 3.6669 mL
50 mM 0.0293 mL 0.1467 mL 0.2934 mL 0.5867 mL 0.7334 mL
100 mM 0.0147 mL 0.0733 mL 0.1467 mL 0.2934 mL 0.3667 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Amiodarone HCl

Amiodarone HCl is an anti-arrhythmic drug [1].

Amiodarone HCl has shown a non-competitive inhibition of the chronotropic effect of isoproterenol with a pD’ value of ~4.17. In addition, Amiodarone HCl has been reported to inhibit the norepinephrine-induced contractions in a non-competitive type with a pD’ value of about 4.06. Besides, all the results have been suggested that Amiodarone HCl does not compete with the agonists at their respective recognition sites. Amiodarone HCl has been found to be a different antagonizes types of anonists: β1-adrenergic agonists like isoproterenol, α-adrenergic agonists like norepinephrine and glucagon. Apart from these, Amiodarone HCl has exhibited tissular specificity. The adrenergic (glucagon) antagonism has been shown only on the heart and the arteries. Amiodarone HCl has noted no cpinephrine-induced lipolysis of the epididymal fat pad [1].

References:
[1] Polster P, Broekhuysen J. The adrenergic antagonism of amiodarone. Biochem Pharmacol. 1976 Jan 15;25(2):131-4.

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References on Amiodarone HCl

Screen for chemical modulators of autophagy reveals novel therapeutic inhibitors of mTORC1 signaling.[Pubmed:19771169]

PLoS One. 2009 Sep 22;4(9):e7124.

BACKGROUND: Mammalian target of rapamycin complex 1 (mTORC1) is a protein kinase that relays nutrient availability signals to control numerous cellular functions including autophagy, a process of cellular self-eating activated by nutrient depletion. Addressing the therapeutic potential of modulating mTORC1 signaling and autophagy in human disease requires active chemicals with pharmacologically desirable properties. METHODOLOGY/PRINCIPAL FINDINGS: Using an automated cell-based assay, we screened a collection of >3,500 chemicals and identified three approved drugs (perhexiline, niclosamide, amiodarone) and one pharmacological reagent (rottlerin) capable of rapidly increasing autophagosome content. Biochemical assays showed that the four compounds stimulate autophagy and inhibit mTORC1 signaling in cells maintained in nutrient-rich conditions. The compounds did not inhibit mTORC2, which also contains mTOR as a catalytic subunit, suggesting that they do not inhibit mTOR catalytic activity but rather inhibit signaling to mTORC1. mTORC1 inhibition and autophagosome accumulation induced by perhexiline, niclosamide or rottlerin were rapidly reversed upon drug withdrawal whereas amiodarone inhibited mTORC1 essentially irreversibly. TSC2, a negative regulator of mTORC1, was required for inhibition of mTORC1 signaling by rottlerin but not for mTORC1 inhibition by perhexiline, niclosamide and amiodarone. Transient exposure of immortalized mouse embryo fibroblasts to these drugs was not toxic in nutrient-rich conditions but led to rapid cell death by apoptosis in starvation conditions, by a mechanism determined in large part by the tuberous sclerosis complex protein TSC2, an upstream regulator of mTORC1. By contrast, transient exposure to the mTORC1 inhibitor rapamycin caused essentially irreversible mTORC1 inhibition, sustained inhibition of cell growth and no selective cell killing in starvation. CONCLUSION/SIGNIFICANCE: The observation that drugs already approved for human use can reversibly inhibit mTORC1 and stimulate autophagy should greatly facilitate the preclinical and clinical testing of mTORC1 inhibition for indications such as tuberous sclerosis, diabetes, cardiovascular disease and cancer.

Identification by automated screening of a small molecule that selectively eliminates neural stem cells derived from hESCs but not dopamine neurons.[Pubmed:19774075]

PLoS One. 2009 Sep 23;4(9):e7155.

BACKGROUND: We have previously described fundamental differences in the biology of stem cells as compared to other dividing cell populations. We reasoned therefore that a differential screen using US Food and Drug Administration (FDA)-approved compounds may identify either selective survival factors or specific toxins and may be useful for the therapeutically-driven manufacturing of cells in vitro and possibly in vivo. METHODOLOGY/PRINCIPAL FINDINGS: In this study we report on optimized methods for feeder-free culture of hESCs and hESC-derived neural stem cells (NSCs) to facilitate automated screening. We show that we are able to measure ATP as an indicator of metabolic activity in an automated screening assay. With this optimized platform we screened a collection of FDA-approved drugs to identify compounds that have differential toxicity to hESCs and their neural derivatives. Nine compounds were identified to be specifically toxic for NSCs to a greater extent than for hESCs. Six of these initial hits were retested and verified by large-scale cell culture to determine dose-responsive NSC toxicity. One of the compounds retested, Amiodarone HCl, was further tested for possible effects on postmitotic neurons, a likely target for transplant therapy. Amiodarone HCl was found to be selectively toxic to NSCs but not to differentiated neurons or glial cells. Treated and untreated NSCs and neurons were then interrogated with global gene expression analysis to explore the mechanisms of action of Amiodarone HCl. The gene expression analysis suggests that activation of cell-type specific cationic channels may underlie the toxicity of the drug. CONCLUSIONS/SIGNIFICANCE: In conclusion, we have developed a screening strategy that allows us to rapidly identify clinically approved drugs for use in a Chemistry, Manufacture and Control protocol that can be safely used to deplete unwanted contaminating precursor cells from a differentiated cell product. Our results also suggest that such a strategy is rich in the potential of identifying lineage specific reagents and provides additional evidence for the utility of stem cells in screening and discovery paradigms.

Electrophysiological effects of ranolazine, a novel antianginal agent with antiarrhythmic properties.[Pubmed:15302796]

Circulation. 2004 Aug 24;110(8):904-10.

BACKGROUND: Ranolazine is a novel antianginal agent capable of producing antiischemic effects at plasma concentrations of 2 to 6 micromol/L without reducing heart rate or blood pressure. The present study examines its electrophysiological effects in isolated canine ventricular myocytes, tissues, and arterially perfused left ventricular wedge preparations. METHODS AND RESULTS: Transmembrane action potentials (APs) from epicardial and midmyocardial (M) regions and a pseudo-ECG were recorded simultaneously from wedge preparations. APs were also recorded from epicardial and M tissues. Whole-cell currents were recorded from epicardial and M myocytes. Ranolazine inhibited I(Kr) (IC50=11.5 micromol/L), late I(Na), late I(Ca), peak I(Ca), and I(Na-Ca) (IC50=5.9, 50, 296, and 91 micromol/L, respectively) and I(Ks) (17% at 30 micromol/L), but caused little or no inhibition of I(to) or I(K1). In tissues and wedge preparations, ranolazine produced a concentration-dependent prolongation of AP duration of epicardial but abbreviation of that of M cells, leading to reduction or no change in transmural dispersion of repolarization (TDR). At [K+]o=4 mmol/L, 10 micromol/L ranolazine prolonged QT interval by 20 ms but did not increase TDR. Extrasystolic activity and spontaneous torsade de pointes (TdP) were never observed, and stimulation-induced TdP could not be induced at any concentration of ranolazine, either in normal or low [K+]o. Ranolazine (5 to 20 micromol/L) suppressed early afterdepolarizations (EADs) and reduced the increase in TDR induced by the selective I(Kr) blocker d-sotalol. CONCLUSIONS: Ranolazine produces ion channel effects similar to those observed after chronic amiodarone (reduced I(Kr), I(Ks), late I(Na), and I(Ca)). The actions of ranolazine to suppress EADs and reduce TDR suggest that, in addition to its antianginal actions, the drug may possess antiarrhythmic activity.

Amiodarone induces cytochrome c release and apoptosis through an iodine-independent mechanism.[Pubmed:11095475]

J Clin Endocrinol Metab. 2000 Nov;85(11):4323-30.

Amiodarone (AMD) is one of the most effective antiarrhythmic drugs available. However, its use is often limited by side-effects, mainly hypo- or hyperthyroidism. As AMD displays direct toxic effect on different cell types, we investigated the cytotoxic effect of AMD and its main metabolite, desethylamiodarone (DEA), in thyroid (TAD-2) and nonthyroid (HeLa) cell lines. Both AMD and DEA displayed a dose-dependent toxicity in TAD-2 and HeLa cells, although DEA was more effective. Both TAD-2 and HeLa cells underwent apoptosis, as evidenced by plasma membrane phosphatidylserine exposure and DNA fragmentation. Inhibition of protein synthesis with cycloheximide and inhibition of endogenous peroxidase activity with propylthiouracil did not affect this AMD- and DEA-induced apoptosis in TAD-2 cells. Western blot analysis did not display variations in the expression of p53, Bcl-2, Bcl-XL, and Bax proteins during the treatment with AMD and DEA. Generation of reactive oxygen species, investigated by flow cytometry with dichlorofluorescein diacetate, did not show the production of free radicals during drug treatment. Furthermore, Western blot analysis of cytosolic and mitochondrial fractions prepared from AMD-treated cells demonstrated that AMD induces the release of cytochrome c into the cytosol from the mitochondria. These data indicate that AMD induces cytochrome c release from mitochondria, triggering apoptosis through an iodine-independent mechanism, and that this process is not mediated by modulation of p53, Bcl-2, Bcl-XL, or Bax protein expression and does not involve the generation of free radicals.

Description

Amiodarone hydrochloride is an antiarrhythmic drug for inhibition of ATP-sensitive potassium channel with IC50 of 19.1 μM.

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