HydroquinidineCAS# 1435-55-8 |
- Dihydroquinine
Catalog No.:BCN9879
CAS No.:522-66-7
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 1435-55-8 | SDF | Download SDF |
PubChem ID | 91503 | Appearance | White powder |
Formula | C20H26N2O2 | M.Wt | 326.44 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Synonyms | Dihydroquinidine; (+)-Hydroquinidine; Hydroconquinine | ||
Solubility | DMSO : ≥ 47 mg/mL (143.98 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | (S)-[(2R,4S,5R)-5-ethyl-1-azabicyclo[2.2.2]octan-2-yl]-(6-methoxyquinolin-4-yl)methanol | ||
SMILES | CCC1CN2CCC1CC2C(C3=C4C=C(C=CC4=NC=C3)OC)O | ||
Standard InChIKey | LJOQGZACKSYWCH-LHHVKLHASA-N | ||
Standard InChI | InChI=1S/C20H26N2O2/c1-3-13-12-22-9-7-14(13)10-19(22)20(23)16-6-8-21-18-5-4-15(24-2)11-17(16)18/h4-6,8,11,13-14,19-20,23H,3,7,9-10,12H2,1-2H3/t13-,14-,19+,20-/m0/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 | 1. Hydroquinidine can prevents life-threatening arrhythmic events in patients with short QT syndrome. |
Hydroquinidine Dilution Calculator
Hydroquinidine Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.0634 mL | 15.3168 mL | 30.6335 mL | 61.267 mL | 76.5838 mL |
5 mM | 0.6127 mL | 3.0634 mL | 6.1267 mL | 12.2534 mL | 15.3168 mL |
10 mM | 0.3063 mL | 1.5317 mL | 3.0634 mL | 6.1267 mL | 7.6584 mL |
50 mM | 0.0613 mL | 0.3063 mL | 0.6127 mL | 1.2253 mL | 1.5317 mL |
100 mM | 0.0306 mL | 0.1532 mL | 0.3063 mL | 0.6127 mL | 0.7658 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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Hydroquinidine is an antiarrhythmic agent.
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Hydroquinidine Prevents Life-Threatening Arrhythmic Events in Patients With Short QT Syndrome.[Pubmed:29241489]
J Am Coll Cardiol. 2017 Dec 19;70(24):3010-3015.
BACKGROUND: Short QT syndrome (SQTS) is a rare and life-threatening arrhythmogenic syndrome characterized by abbreviated repolarization. Hydroquinidine (HQ) prolongs the QT interval in SQTS patients, although whether it reduces cardiac events is currently unknown. OBJECTIVES: This study investigated whether long-term treatment with HQ reduces the occurrence of life-threatening arrhythmic events (LAE) (cardiac arrest or sudden cardiac death) in SQTS patients. METHODS: In this cohort study on consecutive SQTS patients, 2 analyses were performed: 1) a matched-period analysis for the occurrence of LAE in 17 SQTS patients who received long-term HQ; and 2) a comparison of the annual incidence of LAE off- and on-HQ in 16 SQTS patients who survived a cardiac arrest. RESULTS: A total of 17 patients (82% male, age 29 +/- 3 years, QTc before treatment 331 +/- 3 ms) received HQ therapy (584 +/- 53 mg/day). Therapy was stopped in 2 cases (12%) due to gastrointestinal intolerance, and 15 patients continued treatment for 6 +/- 1 year. QTc prolongation was observed in all patients (by 60 +/- 6 ms; p < 0.001). We compared the occurrence of LAE during 6 +/- 1 years before and after HQ, observing that patients on HQ experienced a reduction in both the rate of LAE from 40% to 0% (p = 0.03) and the number of LAE per patient from 0.73 +/- 0.3 to 0 (p = 0.026). Furthermore, the annual rate of LAE in the 16 patients with a previous cardiac arrest dropped from 12% before HQ to 0 on therapy (p = 0.028). CONCLUSIONS: We demonstrated for the first time that treatment with HQ was associated with a lower incidence of LAE in SQTS patients. These data point to the importance that quinidine, that in several countries has been removed from the market, remains available worldwide for patients with SQTS. In the present study, therapy with HQ has been proven to be safe, with a relatively low rate of side effects.
Relationships between heart rate variability and antiarrhythmic effects of hydroquinidine.[Pubmed:9310279]
Cardiovasc Drugs Ther. 1997 Jul;11(3):493-8.
Class I antiarrhythmic drugs may increase the incidence of cardiac death, and controlled treatment is required in patients with severe ventricular arrhythmias. Electrophysiologically guided antiarrhythmic therapy remains an important method to manage patients with sustained ventricular tachycardia (VT). The purpose of the study was to evaluate the correlations between baseline heart rate variability in ambulatory electrocardiographic recordings of patients with sustained ventricular tachycardia and the response to Hydroquinidine on VT inducibility, and to look for the changes in heart rate variability during Hydroquinidine treatment. Thirty-five patients with spontaneous and inducible sustained VT were studied. Programmed ventricular stimulation and time and frequency domain analysis of heart rate variability were studied in the control state and 9-12 days after treatment with 300-600 mg of Hydroquinidine. In 11 patients (group I), Hydroquinidine prevented VT induction. In 24 patients (group II), sustained VT remained inducible during treatment with Hydroquinidine. In the control state, heart rate variability was similar in both groups. During treatment with Hydroquinidine, heart rate variability tended to decrease in groups I and II, but the changes were significant only in group II: the coefficient of variance (CV) decreased from 13 +/- 4% to 10% +/- 3% (p < 0.01) and low frequency/high frequency amplitude ratio decreased from 4.6 +/- 3.3 to 2.87 +/- 2.42 (p < 0.05). In conclusion, baseline heart rate variability does not differentiate the responders and nonresponders to Hydroquinidine. Hydroquinidine decreases heart rate variability in all patients, but principally in those with still inducible VT.