Hydroquinidine (Dihydroquinidine)
(Synonyms: 氢化奎宁定; Dihydroquinidine; (+)-Hydroquinidine; Hydroconquinine) 目录号 : GC33706
An alkaloid and antiarrhythmic agent
Cas No.:1435-55-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Hydroquinidine is an alkaloid and derivative of the antiarrhythmic agent quinidine that decreases heart rate variability.1,2,3 It increases the length of the sinus cycle and prolongs QRS duration and ventricular repolarization in anesthetized dogs.2 It has also been imprinted on microspheres as a pseudo-template molecule for recognition of cinchona alkaloids.3 Formulations containing hydroquinidine have been studied for use in treatment of Brugada syndrome, which is a genetic disorder characterized by ventricular fibrillation and a risk of sudden death.4
1.Chimienti, M., Regazzi, M.B., La Rovere, M.T., et al.Comparison of the effectiveness of dihydroquinidine and quinidine on ventricular ectopy after acute and chronic administrationCardiovasc. Drugs Ther.2(5)679-686(1988) 2.Chézalviel, F., Weissenburger, J., Ertzbischoff, O., et al.Comparison of the cardiac electrophysiological effects of flecainide and hydroquinidine in anesthetized dog: Concentration-response relationshipJ. Cardiovasc. Pharmacol.15(1)50-56(1990) 3.Zhou, Q., He, J., Tang, Y., et al.A novel hydroquinidine imprinted microsphere using a chirality-matching N-acryloyl-L-phenylalanine monomer for recognition of cinchona alkaloidsJ. Chromatogr. A.123860-67(2012) 4.Hermida, J.S., Denjoy, I., Clerc, J., et al.Hydroquinidine therapy in Brugada syndromeJ. Am. Coll. Cardiol.43(10)1853-1860(2004)
| Cas No. | 1435-55-8 | SDF | |
| 别名 | 氢化奎宁定; Dihydroquinidine; (+)-Hydroquinidine; Hydroconquinine | ||
| Canonical SMILES | O[C@H]([C@]1([H])[N@@](CC2)C[C@H](CC)[C@@H]2C1)C3=CC=NC4=CC=C(OC)C=C34 | ||
| 分子式 | C20H26N2O2 | 分子量 | 326.43 |
| 溶解度 | DMSO : ≥ 47 mg/mL (143.98 mM) | 储存条件 | 4°C, protect from light, stored under nitrogen |
| 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.0634 mL | 15.3172 mL | 30.6344 mL |
| 5 mM | 0.6127 mL | 3.0634 mL | 6.1269 mL |
| 10 mM | 0.3063 mL | 1.5317 mL | 3.0634 mL |
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动物平均体重 | g | |
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Comparison of the effectiveness of Dihydroquinidine and quinidine on ventricular ectopy after acute and chronic administration
Cardiovasc Drugs Ther 1988 Dec;2(5):679-86.PMID:2484920DOI:10.1007/BF00054209.
The aim of this study was to compare the pharmacokinetics and antiarrhythmic activity of Dihydroquinidine and quinidine in 14 patients (11 men, 3 women, aged 28 to 67 years) with heart disease and chronic, stable, high-frequency premature ventricular beats (PVB) (greater than 100/hr). A randomized, double-blind, crossover, placebo-controlled protocol was utilized. During Holter monitoring the patients were given either Dihydroquinidine or quinidine as the gluconates in an oral solution (600 mg); blood samples were taken 0.5, 1, 1.5, 2, 4, 6, 8, and 12 hours later. The patients were then assigned to three successive treatment periods of 7 days each: Dihydroquinidine HCl (900 mg/day), quinidine polygalacturonate (1,650 mg/day), or placebo. At the end of each period 24-hour Holter monitoring was carried out and a blood sample was taken for determination of drug concentration. By comparing the area under the curves Dihydroquinidine was 59% as available as quinidine; rates of absorption and elimination were similar. Mean peak blood levels of Dihydroquinidine and quinidine were 1.06 +/- 0.34 and 2.15 +/- 0.96 micrograms/ml, respectively. After Dihydroquinidine, eight patients had a positive response (greater than 50% reduction in PVB frequency), while seven patients responded to quinidine. During maintenance treatment both Dihydroquinidine (233 +/- 330) and quinidine (234 +/- 311) reduced the mean PVB frequency per hour compared to placebo (690 +/- 569). Nine patients (64%) on Dihydroquinidine and eight (57%) on quinidine had greater than 70% decrease in mean PVB frequency per hour. Steady-state peak plasma concentrations of Dihydroquinidine and quinidine were 1.10 +/- 0.41 and 2.24 +/- 1.13 micrograms/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
[Propafenone versus Hydroquinidine in long-term pharmacological prophylaxis of atrial fibrillation]
Cardiologia 1992 Feb;37(2):123-7.PMID:1600529doi
New antiarrhythmic class 1C agents have been proposed in the last few years in an attempt to suppress paroxysmal atrial fibrillation at long-term, as the most commonly used class 1A agents such as quinidine gave highly variable results as regards both side-effects and efficacy. The aim of this randomized prospective study is to evaluate the efficacy and safety of oral propafenone at long term in preventing paroxysmal atrial fibrillation and to compare the results with those obtained using agents such as quinidine. Two hundred patients with recurrent episodes of symptomatic atrial fibrillation were enrolled for this study with entry criteria based upon a history of more than 3 crises in the previous 6 months, with electrocardiographic (standard electrocardiogram or dynamic registration) documentation. According to a randomized selection either propafenone at 300 mg twice daily or Hydroquinidine retard 250 mg twice daily were administered to the patients; clinical check-up was carried out every 3 months or if clinical course worsened. The dosages were increased if proved to be inadequate at check-up (i.e. recurrence of atrial fibrillation) up to 300 mg 3 times daily for propafenone and 500 mg twice daily for Hydroquinidine. The efficacy at the 3rd month was 71% for propafenone and 60% for Hydroquinidine, at the 6th month 60% for propafenone and 56% for Hydroquinidine; this trend lowered progressively as the follow-up continued, to 48% for propafenone and 42% for Hydroquinidine (NS). More than 70% of the responder patients assumed 600 mg twice for propafenone or 250 twice for Hydroquinidine. Propafenone had a percentage of 10% side-effects and Hydroquinidine 24% (p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
[Treatment of recurrent ventricular tachycardia with Hydroquinidine. Evaluation of its efficacy with electrophysiological technics]
Arch Mal Coeur Vaiss 1985 Sep;78(9):1346-52.PMID:3936438doi
Electrophysiological investigations were used to test the efficacy of Dihydroquinidine chlorhydrate (600 or 1 200 mg/day) in a prospective study of 18 patients with recurrent ventricular tachycardia documented by electrocardiography. These patients did not respond to an average of 3.1 +/- antiarrhythmic drugs, including amiodarone in 12 patients. Hydroquinidine was well tolerated in 17 patients but had to be withdrawn in 1 patient because of hypotension. The effect of Hydroquinidine on ventricular tachycardia induced by programmed pacing was evaluated after a 48 to 72 hours treatment, 3 to 5 hours after the last dose. After Hydroquinidine it was not possible to induce ventricular tachycardia in 10 patients (58.8%). In the other 7 patients, it was possible to induce a ventricular tachycardia under treatment. In one case, Hydroquinidine aggravated the arrhythmia as the induced tachycardia had a shorter cycle. In the other patients, Hydroquinidine lengthened the tachycardia cycle by an average of 94 +/- 79 ms. The right ventricular refractory period increased cycle by 44 +/- 23 ms. Long-term Hydroquinidine was prescribed for 7 patients, twice in association with amiodarone. Relapse was observed in 2 patients, 1 and 5 months after the onset of treatment. Five patients were well controlled by the treatment. The results of this study demonstrate the efficacy of Hydroquinidine for the prevention of tachycardia induced by stimulation and underline its value in the treatment of sustained, recurrent ventricular tachycardia. This study illustrates the illustrates the importance of electrophysiological techniques for the identification of patients likely to benefit from a given antiarrhythmic treatment.
Relationships between heart rate variability and antiarrhythmic effects of Hydroquinidine
Cardiovasc Drugs Ther 1997 Jul;11(3):493-8.PMID:9310279DOI:10.1023/a:1007709808576.
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.
Hydroquinidine therapy in Brugada syndrome
J Am Coll Cardiol 2004 May 19;43(10):1853-60.PMID:15145111DOI:10.1016/j.jacc.2003.12.046.
Objectives: We sought to assess Hydroquinidine (HQ) efficacy in selected patients with Brugada syndrome (BrS). Background: Management of asymptomatic patients with BrS and inducible arrhythmias remains a key issue. Effectiveness of class Ia antiarrhythmic drugs, which inhibit the potassium transient outward current of the action potential, has been suggested in BrS. Methods: From a cohort of 106 BrS patients, we studied 35 who received HQ (32 men; mean age 48 +/- 11 years). Patients had asymptomatic BrS and inducible arrhythmia (n = 31) or multiple appropriate shocks from an implantable cardioverter-defibrillator (ICD) (n = 4). Asymptomatic patients with inducible arrhythmia underwent electrophysiologic (EP)-guided therapy. When ventricular tachycardia (VT)/ventricular fibrillation (VF) inducibility was not prevented, or in case of HQ intolerance, an ICD was placed. Results: Hydroquinidine prevented VT/VF inducibility in 76% of asymptomatic patients who underwent EP-guided therapy. Syncope occurred in two of the 21 patients who received long-term (17 +/- 13 months) HQ therapy (1 syncope associated with QT interval prolongation and 1 unexplained syncope associated with probable noncompliance). In asymptomatic patients who received an ICD (n = 10), one appropriate shock occurred during a follow-up period of 13 +/- 8 months. In patients with multiple ICD shocks, HQ prevented VT/VF recurrence in all cases during a mean follow-up of 14 +/- 8 months. Conclusions: Hydroquinidine therapy prevented VT/VF inducibility in 76% of asymptomatic patients with BrS and inducible arrhythmia, as well as VT/VF recurrence in all BrS patients with multiple ICD shocks. These preliminary data suggest that preventive treatment by HQ may be an alternative strategy to ICD placement in asymptomatic patients with BrS and inducible arrhythmia.