DigoxinCAS# 20830-75-5 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 20830-75-5 | SDF | Download SDF |
| PubChem ID | 2724385 | Appearance | Powder |
| Formula | C41H64O14 | M.Wt | 780.94 |
| Type of Compound | Steroids | Storage | Desiccate at -20°C |
| Synonyms | 12β-Hydroxydigitoxin | ||
| Solubility | DMSO : ≥ 28 mg/mL (35.85 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 3-[(3S,5R,8R,9S,10S,12R,13S,14S,17R)-3-[(2R,4S,5S,6R)-5-[(2S,4S,5S,6R)-5-[(2S,4S,5S,6R)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyloxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-2H-furan-5-one | ||
| SMILES | CC1C(C(CC(O1)OC2C(OC(CC2O)OC3C(OC(CC3O)OC4CCC5(C(C4)CCC6C5CC(C7(C6(CCC7C8=CC(=O)OC8)O)C)O)C)C)C)O)O | ||
| Standard InChIKey | LTMHDMANZUZIPE-PUGKRICDSA-N | ||
| Standard InChI | InChI=1S/C41H64O14/c1-19-36(47)28(42)15-34(50-19)54-38-21(3)52-35(17-30(38)44)55-37-20(2)51-33(16-29(37)43)53-24-8-10-39(4)23(13-24)6-7-26-27(39)14-31(45)40(5)25(9-11-41(26,40)48)22-12-32(46)49-18-22/h12,19-21,23-31,33-38,42-45,47-48H,6-11,13-18H2,1-5H3/t19-,20-,21-,23-,24+,25-,26-,27+,28+,29+,30+,31-,33+,34+,35+,36-,37-,38-,39+,40+,41+/m1/s1 | ||
| 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. |
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| 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. |
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| 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. | ||
| Description | Digoxin is a classical Na,K-ATPase inhibitor, with selectivity for the α2β3 isoform over the common α1β1 isoform, used in the treatment of atrial fibrillation and heart failure. Digoxin and other cardiac glycosides can inhibit hypoxia-inducible factor 1 (HIF-1)α synthesis and block tumor growth. |
| Targets | HIF | Sodium Channel | ATPase | Potassium Channel |
| In vivo | Digoxin use in patients with atrial fibrillation and adverse cardiovascular outcomes: a retrospective analysis of the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in[Pubmed: 25749644]Lancet. 2015 Jun 13;385(9985):2363-70.Digoxin is a widely used drug for ventricular rate control in patients with atrial fibrillation (AF), despite a scarcity of randomised trial data.
Digoxin and risk of death in adults with atrial fibrillation: the ATRIA-CVRN study.[Pubmed: 25414270]Circ Arrhythm Electrophysiol. 2015 Feb;8(1):49-58.Digoxin remains commonly used for rate control in atrial fibrillation, but limited data exist supporting this practice and some studies have shown an association with adverse outcomes. We examined the independent association between Digoxin and risks of death and hospitalization in adults with incident atrial fibrillation and no heart failure.
|
| Kinase Assay | Digoxin and other cardiac glycosides inhibit HIF-1alpha synthesis and block tumor growth.[Pubmed: 19020076 ]Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19579-86.A library of drugs that are in clinical trials or use was screened for inhibitors of hypoxia-inducible factor 1 (HIF-1).
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Digoxin Dilution Calculator
Digoxin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.2805 mL | 6.4025 mL | 12.8051 mL | 25.6102 mL | 32.0127 mL |
| 5 mM | 0.2561 mL | 1.2805 mL | 2.561 mL | 5.122 mL | 6.4025 mL |
| 10 mM | 0.1281 mL | 0.6403 mL | 1.2805 mL | 2.561 mL | 3.2013 mL |
| 50 mM | 0.0256 mL | 0.1281 mL | 0.2561 mL | 0.5122 mL | 0.6403 mL |
| 100 mM | 0.0128 mL | 0.064 mL | 0.1281 mL | 0.2561 mL | 0.3201 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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Digoxin is a cardiac glycoside that blocks the sodium-potassium ATPase, as a potent inhibitor of chikungunya virus (CHIKV) infection.
In Vitro:Digoxin, a sodium-potassium ATPase inhibitor, has a negative Z score of −26.67, suggesting a function for the sodium-potassium ATPase in CHIKV infection. Relative to DMSO-treated cells, treatment of U-2 OS cells with Digoxin results in a dose-dependent decrease in CHIKV infection with a half-maximal effective concentration (EC50) of 48.8 nM. Digoxin treatment similarly decreases CHIKV infection of primary human synovial fibroblasts (HSFs) and Vero African green monkey kidney cells with EC50s of 43.9 nM and 67.3 nM, respectively. Digoxin treatment significantly diminishes CHIKV infection in these cell types, with EC50s of 16.2 µM in ST2 cells and 23.2 µM in C2C12 cells, values 330 and 475 times the EC50 of Digoxin in U-2 OS cells. Cell viability is only modestly impaired at 24 h posttreatment with 1 µM Digoxin, a dose 20 times the Digoxin EC50 for CHIKV antiviral activity in these cells[1].
References:
[1]. Ashbrook AW, et al. Antagonism of the Sodium-Potassium ATPase Impairs Chikungunya Virus Infection. MBio. 2016 May 24;7(3). pii: e00693-16.
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Digoxin and other cardiac glycosides inhibit HIF-1alpha synthesis and block tumor growth.[Pubmed:19020076]
Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19579-86.
A library of drugs that are in clinical trials or use was screened for inhibitors of hypoxia-inducible factor 1 (HIF-1). Twenty drugs inhibited HIF-1-dependent gene transcription by >88% at a concentration of 0.4 microM. Eleven of these drugs were cardiac glycosides, including Digoxin, ouabain, and proscillaridin A, which inhibited HIF-1alpha protein synthesis and expression of HIF-1 target genes in cancer cells. Digoxin administration increased latency and decreased growth of tumor xenografts, whereas treatment of established tumors resulted in growth arrest within one week. Enforced expression of HIF-1alpha by transfection was not inhibited by Digoxin, and xenografts derived from these cells were resistant to the anti-tumor effects of Digoxin, demonstrating that HIF-1 is a critical target of Digoxin for cancer therapy.
Meta-analysis of digoxin use and risk of mortality in patients with atrial fibrillation.[Pubmed:25660972]
Am J Cardiol. 2015 Apr 1;115(7):901-6.
There is an ongoing debate on the safety of Digoxin use in patients with atrial fibrillation (AF). To address this issue, the investigators assembled a synthesis of the available evidence on the relation between Digoxin and all-cause mortality in patients with AF. PubMed and the Embase database were systematically searched to identify all eligible studies examining the association between Digoxin use and the mortality risk in AF. Overall hazard ratios and 95% confidence intervals were calculated using the random-effects model. Eleven observational studies were identified that met the inclusion criteria, 5 of which additionally used propensity score matching for statistical adjustment. In total, 318,191 patients were followed up for a mean of 2.8 years. Overall, Digoxin use was associated with a 21% increased risk for mortality (hazard ratio 1.21, 95% confidence interval 1.12 to 1.30). Sensitivity analyses found the results to be robust. In the propensity score-matched AF patients, Digoxin use was associated with a 17% greater risk for mortality (hazard ratio 1.17, 95% confidence interval 1.13 to 1.22). When the AF cohort was grouped into patients with and without heart failure, the use of Digoxin was associated with an increase in mortality in patients with and those without heart failure, and no significant heterogeneity was seen between the groups (p >0.10). In conclusion, the results suggest that Digoxin use was associated with a greater risk for mortality in patients with AF, regardless of concomitant heart failure. A well-powered randomized trial is necessary to reveal the true effect of Digoxin.
Digoxin and risk of death in adults with atrial fibrillation: the ATRIA-CVRN study.[Pubmed:25414270]
Circ Arrhythm Electrophysiol. 2015 Feb;8(1):49-58.
BACKGROUND: Digoxin remains commonly used for rate control in atrial fibrillation, but limited data exist supporting this practice and some studies have shown an association with adverse outcomes. We examined the independent association between Digoxin and risks of death and hospitalization in adults with incident atrial fibrillation and no heart failure. METHODS AND RESULTS: We performed a retrospective cohort study of 14,787 age, sex, and high-dimensional propensity score-matched adults with incident atrial fibrillation and no previous heart failure or Digoxin use in the AnTicoagulation and Risk factors In Atrial fibrillation-Cardiovascular Research Network (ATRIA-CVRN) study within Kaiser Permanente Northern and Southern California. We examined the independent association between newly initiated Digoxin and the risks of death and hospitalization using extended Cox regression. During a median 1.17 (interquartile range, 0.49-1.97) years of follow-up among matched patients with atrial fibrillation, incident Digoxin use was associated with higher rates of death (8.3 versus 4.9 per 100 person-years; P<0.001) and hospitalization (60.1 versus 37.2 per 100 person-years; P<0.001). Incident Digoxin use was independently associated with a 71% higher risk of death (hazard ratio, 1.71; 95% confidence interval, 1.52-1.93) and a 63% higher risk of hospitalization (hazard ratio, 1.63; 95% confidence interval, 1.56-1.71). Results were consistent in subgroups of age and sex and when using intent-to-treat or on-treatment analytic approaches. CONCLUSIONS: In adults with atrial fibrillation, Digoxin use was independently associated with higher risks of death and hospitalization. Given other available rate control options, Digoxin should be used with caution in the management of atrial fibrillation.
Digoxin use in patients with atrial fibrillation and adverse cardiovascular outcomes: a retrospective analysis of the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF).[Pubmed:25749644]
Lancet. 2015 Jun 13;385(9985):2363-70.
BACKGROUND: Digoxin is a widely used drug for ventricular rate control in patients with atrial fibrillation (AF), despite a scarcity of randomised trial data. We studied the use and outcomes of Digoxin in patients in the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF). METHODS: For this retrospective analysis, we included and classified patients from ROCKET AF on the basis of Digoxin use at baseline and during the study. Patients in ROCKET AF were recruited from 45 countries and had AF and risk factors putting them at moderate-to-high risk of stroke, with or without heart failure. We used Cox proportional hazards regression models adjusted for baseline characteristics and drugs to investigate the association of Digoxin with all-cause mortality, vascular death, and sudden death. ROCKET AF was registered with ClinicalTrials.gov, number NCT00403767. FINDINGS: In 14,171 randomly assigned patients, Digoxin was used at baseline in 5239 (37%). Patients given Digoxin were more likely to be female (42% vs 38%) and have a history of heart failure (73% vs 56%), diabetes (43% vs 38%), and persistent AF (88% vs 77%; p<0.0001 for each comparison). After adjustment, Digoxin was associated with increased all-cause mortality (5.41 vs 4.30 events per 100 patients-years; hazard ratio 1.17; 95% CI 1.04-1.32; p=0.0093), vascular death (3.55 vs 2.69 per 100 patient-years; 1.19; 1.03-1.39, p=0.0201), and sudden death (1.68 vs 1.12 events per 100 patient-years; 1.36; 1.08-1.70, p=0.0076). INTERPRETATION: Digoxin treatment was associated with a significant increase in all-cause mortality, vascular death, and sudden death in patients with AF. This association was independent of other measured prognostic factors, and although residual confounding could account for these results, these data show the possibility of Digoxin having these effects. A randomised trial of Digoxin in treatment of AF patients with and without heart failure is needed. FUNDING: Janssen Research & Development and Bayer HealthCare AG.
