Details
| Stereochemistry | ABSOLUTE |
| Molecular Formula | C20H24N2O2.2ClH |
| Molecular Weight | 397.339 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 5 / 5 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
Cl.Cl.[H][C@@]1(C[C@@H]2CC[N@]1C[C@@H]2C=C)[C@@H](O)C3=C4C=C(OC)C=CC4=NC=C3
InChI
InChIKey=NNKXWRRDHYTHFP-KAIFKDDSSA-N
InChI=1S/C20H24N2O2.2ClH/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;;/h3-6,8,11,13-14,19-20,23H,1,7,9-10,12H2,2H3;2*1H/t13-,14-,19+,20-;;/m0../s1
| Molecular Formula | C20H24N2O2 |
| Molecular Weight | 324.4168 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 4 / 4 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
| Molecular Formula | ClH |
| Molecular Weight | 36.461 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
DescriptionCurator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/17506538 | https://www.ncbi.nlm.nih.gov/pubmed/22761000 | https://www.ncbi.nlm.nih.gov/pubmed/22512909 | https://www.ncbi.nlm.nih.gov/pubmed/21832259
Curator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/17506538 | https://www.ncbi.nlm.nih.gov/pubmed/22761000 | https://www.ncbi.nlm.nih.gov/pubmed/22512909 | https://www.ncbi.nlm.nih.gov/pubmed/21832259
Quinidine is a pharmaceutical agent that acts as a class I antiarrhythmic agent (Ia) in the heart. It is a stereoisomer of quinine, originally derived from the bark of the cinchona tree. The drug causes increased action potential duration, as well as a prolonged QT interval. Like all other class I antiarrhythmic agents, quinidine primarily works by blocking the fast inward sodium current (INa). Quinidine's effect on INa is known as a 'use-dependent block'. This means at higher heart rates, the block increases, while at lower heart rates, the block decreases. The effect of blocking the fast inward sodium current causes the phase 0 depolarization of the cardiac action potential to decrease (decreased Vmax). Quinidine also blocks the slowly inactivating, tetrodotoxin-sensitive Na current, the slow inward calcium current (ICA), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito. Quinidine is also an inhibitor of the cytochrome P450 enzyme 2D6 and can lead to increased blood levels of lidocaine, beta blockers, opioids, and some antidepressants. Quinidine also inhibits the transport protein P-glycoprotein and so can cause some peripherally acting drugs such as loperamide to have central nervous system side effects, such as respiratory depression if the two drugs are coadministered. Quinidine can cause thrombocytopenia, granulomatous hepatitis, myasthenia gravis, and torsades de pointes, so is not used much today. Torsades can occur after the first dose. Quinidine-induced thrombocytopenia (low platelet count) is mediated by the immune system and may lead to thrombocytic purpura. A combination of dextromethorphan and quinidine has been shown to alleviate symptoms of easy laughing and crying (pseudobulbar affect) in patients with amyotrophic lateral sclerosis and multiple sclerosis. This drug is marketed as Nuedexta in the United States. Intravenous quinidine is also indicated for the treatment of Plasmodium falciparum malaria. However, quinidine is not considered the first-line therapy for P. falciparum. The recommended treatments for P. falciparum malaria, according to the Toronto Notes 2008, are a combination of either quinine and doxycycline or atovaquone and proguanil (Malarone). The drug is also effective for the treatment of atrial fibrillation in horses.
CNS Activity
Originator
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Target ID: CHEMBL4306 |
7300.0 nM [IC50] | ||
Target ID: CHEMBL1980 |
6900.0 nM [IC50] | ||
Target ID: CHEMBL5885 |
2200.0 nM [IC50] | ||
Target ID: CHEMBL1940 |
19820.0 nM [IC50] | ||
Target ID: CHEMBL1075226 |
|||
Target ID: CHEMBL364 |
18.0 nM [IC50] |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
| Primary | QUINIDINE GLUCONATE Approved UseConversion of atrial fibrillation/flutter In patients with symptomatic atrial fibrillation/flutter whose symptoms are not adequately controlled by measures that reduce the rate of ventricular response, quinidine sulfate is indicated as a means of restoring normal sinus rhythm. If this use of quinidine sulfate does not restore sinus rhythm within a reasonable time (see ), then quinidine sulfate should be discontinued. DOSAGE AND ADMINISTRATION Reduction of frequency of relapse into atrial fibrillation/flutter Chronic therapy with quinidine sulfate is indicated for some patients at high risk of symptomatic atrial fibrillation/flutter, generally patients who have had previous episodes of atrial fibrillation/flutter that were so frequent and poorly tolerated as to outweigh, in the judgment of the physician and the patient, the risks of prophylactic therapy with quinidine sulfate. The increased risk of death should specifically be considered. Quinidine sulfate should be used only after alternative measures ( use of other drugs to control the ventricular rate) have been found to be inadequate. e.g., In patients with histories of frequent symptomatic episodes of atrial fibrillation/flutter, the goal of therapy should be an increase in the average time between episodes. In most patients, the tachyarrhythmia during therapy, and a single recurrence should not be interpreted as therapeutic failure. will recur Suppression of ventricular arrhythmias Quinidine sulfate is also indicated for the suppression of recurrent documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgment of the physician are life-threatening. Because of the proarrhythmic effects of quinidine, its use with ventricular arrhythmias of lesser severity is generally not recommended, and treatment of patients with asymptomatic ventricular premature contractions should be avoided. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise. Antiarrhythmic drugs (including quinidine sulfate) have not been shown to enhance survival in patients with ventricular arrhythmias. Treatment of malaria Quinidine sulfate is also indicated in the treatment of life-threatening malaria. Plasmodium falciparum Launch Date1950 |
|||
| Primary | QUINIDINE GLUCONATE Approved UseConversion of atrial fibrillation/flutter In patients with symptomatic atrial fibrillation/flutter whose symptoms are not adequately controlled by measures that reduce the rate of ventricular response, quinidine sulfate is indicated as a means of restoring normal sinus rhythm. If this use of quinidine sulfate does not restore sinus rhythm within a reasonable time (see ), then quinidine sulfate should be discontinued. DOSAGE AND ADMINISTRATION Reduction of frequency of relapse into atrial fibrillation/flutter Chronic therapy with quinidine sulfate is indicated for some patients at high risk of symptomatic atrial fibrillation/flutter, generally patients who have had previous episodes of atrial fibrillation/flutter that were so frequent and poorly tolerated as to outweigh, in the judgment of the physician and the patient, the risks of prophylactic therapy with quinidine sulfate. The increased risk of death should specifically be considered. Quinidine sulfate should be used only after alternative measures ( use of other drugs to control the ventricular rate) have been found to be inadequate. e.g., In patients with histories of frequent symptomatic episodes of atrial fibrillation/flutter, the goal of therapy should be an increase in the average time between episodes. In most patients, the tachyarrhythmia during therapy, and a single recurrence should not be interpreted as therapeutic failure. will recur Suppression of ventricular arrhythmias Quinidine sulfate is also indicated for the suppression of recurrent documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgment of the physician are life-threatening. Because of the proarrhythmic effects of quinidine, its use with ventricular arrhythmias of lesser severity is generally not recommended, and treatment of patients with asymptomatic ventricular premature contractions should be avoided. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise. Antiarrhythmic drugs (including quinidine sulfate) have not been shown to enhance survival in patients with ventricular arrhythmias. Treatment of malaria Quinidine sulfate is also indicated in the treatment of life-threatening malaria. Plasmodium falciparum Launch Date1950 |
|||
| Primary | QUINIDINE GLUCONATE Approved UseConversion of atrial fibrillation/flutter In patients with symptomatic atrial fibrillation/flutter whose symptoms are not adequately controlled by measures that reduce the rate of ventricular response, quinidine sulfate is indicated as a means of restoring normal sinus rhythm. If this use of quinidine sulfate does not restore sinus rhythm within a reasonable time (see ), then quinidine sulfate should be discontinued. DOSAGE AND ADMINISTRATION Reduction of frequency of relapse into atrial fibrillation/flutter Chronic therapy with quinidine sulfate is indicated for some patients at high risk of symptomatic atrial fibrillation/flutter, generally patients who have had previous episodes of atrial fibrillation/flutter that were so frequent and poorly tolerated as to outweigh, in the judgment of the physician and the patient, the risks of prophylactic therapy with quinidine sulfate. The increased risk of death should specifically be considered. Quinidine sulfate should be used only after alternative measures ( use of other drugs to control the ventricular rate) have been found to be inadequate. e.g., In patients with histories of frequent symptomatic episodes of atrial fibrillation/flutter, the goal of therapy should be an increase in the average time between episodes. In most patients, the tachyarrhythmia during therapy, and a single recurrence should not be interpreted as therapeutic failure. will recur Suppression of ventricular arrhythmias Quinidine sulfate is also indicated for the suppression of recurrent documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgment of the physician are life-threatening. Because of the proarrhythmic effects of quinidine, its use with ventricular arrhythmias of lesser severity is generally not recommended, and treatment of patients with asymptomatic ventricular premature contractions should be avoided. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise. Antiarrhythmic drugs (including quinidine sulfate) have not been shown to enhance survival in patients with ventricular arrhythmias. Treatment of malaria Quinidine sulfate is also indicated in the treatment of life-threatening malaria. Plasmodium falciparum Launch Date1950 |
Cmax
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
3.4 μg/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/512840/ |
3.74 mg/kg single, oral dose: 3.74 mg/kg route of administration: Oral experiment type: SINGLE co-administered: |
QUINIDINE plasma | Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: UNKNOWN |
AUC
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
12.8 μg × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/512840/ |
3.74 mg/kg single, oral dose: 3.74 mg/kg route of administration: Oral experiment type: SINGLE co-administered: |
QUINIDINE plasma | Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: UNKNOWN |
T1/2
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
5.8 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/512840/ |
3.74 mg/kg single, oral dose: 3.74 mg/kg route of administration: Oral experiment type: SINGLE co-administered: |
QUINIDINE plasma | Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: UNKNOWN |
|
8 h |
202 mg single, oral dose: 202 mg route of administration: Oral experiment type: SINGLE co-administered: |
QUINIDINE plasma | Homo sapiens population: HEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
Funbound
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
12% |
202 mg single, oral dose: 202 mg route of administration: Oral experiment type: SINGLE co-administered: |
QUINIDINE plasma | Homo sapiens population: HEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
Doses
| Dose | Population | Adverse events |
|---|---|---|
200 mg 4 times / day multiple, oral Dose: 200 mg, 4 times / day Route: oral Route: multiple Dose: 200 mg, 4 times / day Sources: |
unhealthy, 47 years n = 1 Health Status: unhealthy Age Group: 47 years Sex: M Population Size: 1 Sources: |
Disc. AE: Hepatotoxicity... AEs leading to discontinuation/dose reduction: Hepatotoxicity Sources: |
324 mg 5 times / day multiple, oral Dose: 324 mg, 5 times / day Route: oral Route: multiple Dose: 324 mg, 5 times / day Sources: |
unhealthy, 56 yeras n = 1 Health Status: unhealthy Age Group: 56 yeras Sex: F Population Size: 1 Sources: |
Disc. AE: Myalgia... AEs leading to discontinuation/dose reduction: Myalgia (severe, 1 patient) Sources: |
4 g single, oral Overdose |
healthy, 57 years n = 1 Health Status: healthy Age Group: 57 years Sex: F Population Size: 1 Sources: |
Other AEs: Grand mal convulsion, Cardiotoxicity... Other AEs: Grand mal convulsion (1 patient) Sources: Cardiotoxicity (1 patient) |
324 mg 3 times / day multiple, oral Dose: 324 mg, 3 times / day Route: oral Route: multiple Dose: 324 mg, 3 times / day Co-administed with:: digoxin Sources: levothyroxine sodium crystalline warfarin sodium |
unhealthy, 79 years n = 1 Health Status: unhealthy Age Group: 79 years Sex: F Population Size: 1 Sources: |
Disc. AE: Drug-induced lupus erythematosus... AEs leading to discontinuation/dose reduction: Drug-induced lupus erythematosus (1 patient) Sources: |
370 mg 6 times / day multiple, oral Highest studied dose Dose: 370 mg, 6 times / day Route: oral Route: multiple Dose: 370 mg, 6 times / day Sources: |
healthy, > 23 years n = 1 Health Status: healthy Age Group: > 23 years Sex: M Population Size: 1 Sources: |
|
1650 mg single, intravenous Dose: 1650 mg Route: intravenous Route: single Dose: 1650 mg Sources: |
healthy, > 23 years n = 1 Health Status: healthy Age Group: > 23 years Sex: M Population Size: 1 Sources: |
AEs
| AE | Significance | Dose | Population |
|---|---|---|---|
| Hepatotoxicity | Disc. AE | 200 mg 4 times / day multiple, oral Dose: 200 mg, 4 times / day Route: oral Route: multiple Dose: 200 mg, 4 times / day Sources: |
unhealthy, 47 years n = 1 Health Status: unhealthy Age Group: 47 years Sex: M Population Size: 1 Sources: |
| Myalgia | severe, 1 patient Disc. AE |
324 mg 5 times / day multiple, oral Dose: 324 mg, 5 times / day Route: oral Route: multiple Dose: 324 mg, 5 times / day Sources: |
unhealthy, 56 yeras n = 1 Health Status: unhealthy Age Group: 56 yeras Sex: F Population Size: 1 Sources: |
| Cardiotoxicity | 1 patient | 4 g single, oral Overdose |
healthy, 57 years n = 1 Health Status: healthy Age Group: 57 years Sex: F Population Size: 1 Sources: |
| Grand mal convulsion | 1 patient | 4 g single, oral Overdose |
healthy, 57 years n = 1 Health Status: healthy Age Group: 57 years Sex: F Population Size: 1 Sources: |
| Drug-induced lupus erythematosus | 1 patient Disc. AE |
324 mg 3 times / day multiple, oral Dose: 324 mg, 3 times / day Route: oral Route: multiple Dose: 324 mg, 3 times / day Co-administed with:: digoxin Sources: levothyroxine sodium crystalline warfarin sodium |
unhealthy, 79 years n = 1 Health Status: unhealthy Age Group: 79 years Sex: F Population Size: 1 Sources: |
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
Drug as perpetrator
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| yes [IC50 0.051 uM] | likely (co-administration study) Comment: Caution must be exercixed whenever quinidine is prescribed together with drugs metabolized by CYP2C6. Page: 5.0 |
|||
| yes [IC50 18.3 uM] | ||||
| yes [IC50 5.7 uM] | ||||
| yes [IC50 8.7 uM] | ||||
| yes [IC50 9.52 uM] | ||||
| yes [Ki 23.1 uM] | ||||
| yes [Ki 29.2 uM] |
Drug as victim
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
| minor | ||||
| no | ||||
| no | ||||
| yes | ||||
| yes | ||||
Page: 4.0 |
yes | |||
| yes | likely (co-administration study) Comment: coadministration of quinidine causes variable slowing of the metabolism of nifedipine. Interactions with other dihydropyridine calcium channel blockers have not been reported, but these agents (including felodipine, nicardipine, and nimodipine) are all dependent upon P450IIIA4 for metabolism, so similar interactions with quinidine should be anticipated Page: 2.0 |
Tox targets
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
PubMed
| Title | Date | PubMed |
|---|---|---|
| [Congenital myasthenic syndrome (CMS) caused by postsynaptic defects]. | 2001 |
|
| Is it Crohn's disease? A severe systemic granulomatous reaction to sulfasalazine in patient with rheumatoid arthritis. | 2001 |
|
| Cytochrome P450 enzymes involved in the metabolic pathway of the histamine 2 (H2)-receptor antagonist roxatidine acetate by human liver microsomes. | 2001 |
|
| Drug interaction studies with esomeprazole, the (S)-isomer of omeprazole. | 2001 |
|
| Alteration of drug kinetics in rats following exposure to trichloroethylene. | 2001 |
|
| Pharmacokinetic interactions of antimalarial agents. | 2001 |
|
| Evaluation of drug-induced QT interval prolongation: implications for drug approval and labelling. | 2001 |
|
| Importance of QT interval determination and renal function assessment during antiarrhythmic drug therapy. | 2001 Apr |
|
| CIBIS, MERIT-HF, and COPERNICUS trial outcomes: do they complete the chapter on beta-adrenergic blockers as antiarrhythmic and antifibrillatory drugs? | 2001 Apr |
|
| Binding constant determination of drugs toward subdomain IIIA of human serum albumin by near-infrared dye-displacement capillary electrophoresis. | 2001 Aug |
|
| [Pharmacokinetics and drug interactions of antidepressive agents]. | 2001 Aug |
|
| Study of tea polyphenol as a reversal agent for carcinoma cell lines' multidrug resistance (study of TP as a MDR reversal agent). | 2001 Aug |
|
| Independent organic cation transport activity of Na(+)-L-carnitine cotransport system in LLC-PK(1) cells. | 2001 Aug |
|
| Identification of cytochrome P-450 isoforms responsible for cis-tramadol metabolism in human liver microsomes. | 2001 Aug |
|
| Escitalopram (S-citalopram) and its metabolites in vitro: cytochromes mediating biotransformation, inhibitory effects, and comparison to R-citalopram. | 2001 Aug |
|
| Interactions of 1-methyl-4-phenylpyridinium and other compounds with P-glycoprotein: relevance to toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. | 2001 Aug 10 |
|
| Role of transport proteins in drug absorption, distribution and excretion. | 2001 Aug-Sep |
|
| A functional assay for quantitation of the apparent affinities of ligands of P-glycoprotein in Caco-2 cells. | 2001 Feb |
|
| Effect of mdr1a P-glycoprotein gene disruption, gender, and substrate concentration on brain uptake of selected compounds. | 2001 Jul |
|
| Comparison of "type I" and "type II" organic cation transport by organic cation transporters and organic anion-transporting polypeptides. | 2001 Jul |
|
| Cytochrome P450-catalyzed metabolism of ezlopitant alkene (CJ-12,458), a pharmacologically active metabolite of ezlopitant: enzyme kinetics and mechanism of an alkene hydration reaction. | 2001 Jul |
|
| A direct injection capillary electrophoretic technique for miniaturized high-throughput metabolic screening of the CYP 3A4 enzyme using quinidine as a probe. | 2001 Jul |
|
| Novel target genes of the yeast regulator Pdr1p: a contribution of the TPO1 gene in resistance to quinidine and other drugs. | 2001 Jul 11 |
|
| In vitro evaluation of quinidine sensitivity in Brazilian Plasmodium falciparum isolates: comparative analysis to quinine and chloroquine. | 2001 Jul-Aug |
|
| Heterotropic cooperativity of cytochrome P450 3A4 and potential drug-drug interactions. | 2001 Jun |
|
| Synchronized neural activity in the Drosophila memory centers and its modulation by amnesiac. | 2001 Jun |
|
| Establishment of the transformants expressing human cytochrome P450 subtypes in HepG2, and their applications on drug metabolism and toxicology. | 2001 Jun |
|
| Calcium-activated potassium current in single Novikoff cell. | 2001 Mar |
|
| Effect of hydrophilic substances on liberation of quinidine from starch - alginate sphere. | 2001 Mar-Apr |
|
| Metabolism of amiodarone (Part III): identification of rabbit cytochrome P450 isoforms involved in the hydroxylation of mono-N-desethylamiodarone. | 2001 May |
|
| Oral quinine pharmacokinetics and dietary salt intake. | 2001 May |
|
| Drug block of I(kr): model systems and relevance to human arrhythmias. | 2001 Nov |
|
| Inhibition of cytochrome P4502D6 activity with paroxetine normalizes the ultrarapid metabolizer phenotype as measured by nortriptyline pharmacokinetics and the debrisoquin test. | 2001 Oct |
|
| GAT2/BGT-1 as a system responsible for the transport of gamma-aminobutyric acid at the mouse blood-brain barrier. | 2001 Oct |
|
| In vitro effect of alkaloids on bloodstream forms of Trypanosoma brucei and T. congolense. | 2001 Oct |
|
| Functional characteristics and steroid hormone-mediated regulation of an organic cation transporter in Madin-Darby canine kidney cells. | 2001 Oct |
|
| Interactions of the antimalarial drug mefloquine with the human cardiac potassium channels KvLQT1/minK and HERG. | 2001 Oct |
|
| Functional expression of P-glycoprotein in rat brain microglia. | 2001 Oct |
|
| In vitro metabolism of tegaserod in human liver and intestine: assessment of drug interactions. | 2001 Oct |
|
| Different enantioselective 9-hydroxylation of risperidone by the two human CYP2D6 and CYP3A4 enzymes. | 2001 Oct |
|
| An amino acid residue whose change by mutation affects drug binding to the HERG channel. | 2001 Oct 12 |
|
| Alkaline phosphatase from rat liver and kidney is differentially modulated. | 2001 Sep |
|
| Development of stereoselective nonaqueous capillary electrophoresis system for the resolution of cationic and amphoteric analytes. | 2001 Sep |
|
| Quinidine induced electrocardiographic normalization in two patients with Brugada syndrome. | 2001 Sep |
|
| Inactivation of rat cytochrome P450 2D enzyme by a further metabolite of 4-hydroxypropranolol, the major and active metabolite of propranolol. | 2001 Sep |
|
| Multidrug resistance-associated protein-1 functional activity in Calu-3 cells. | 2001 Sep |
|
| Metabolism of vanoxerine, 1-[2-[bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine, by human cytochrome P450 enzymes. | 2001 Sep |
|
| Three thiadiazinone derivatives, EMD 60417, EMD 66430, and EMD 66398, with class III antiarrhythmic activity but different electrophysiologic profiles. | 2001 Sep |
|
| Purinoreceptors are involved in the control of acute morphine withdrawal. | 2001 Sep 21 |
|
| Pharmacologic conversion of atrial fibrillation: a systematic review of available evidence. | 2001 Sep-Oct |
Patents
Sample Use Guides
Tablet (sulfate):100 to 600 mg/dose orally every 4 to 6 hours; begin at 200 mg/dose and titrate to desired effect (maximum daily dose: 3 to 4 g).
Extended Release: 324 to 648 mg (gluconate) orally every 8 to 12 hours or 300 to 600 mg (sulfate) orally every 8 to 12 hours.
IV: 800 mg of quinidine gluconate diluted to 50 mL and given at a rate not to exceed 1 mL/min.
Route of Administration:
Other
Rat brain pericytes were plated onto the backside of 12-well Transwell filters (pore size: 0.4 μm; 1.5 × 104 cells/filter). The next day, endothelial cells were plated onto the upper surface of the filters. After reaching confluency, the endothelial monolayer was supplied with 550 nM hydrocortisone, 250 μM CPT-cAMP, and 17.5 μM RO-201724 and placed into dishes containing glial cultures for 24 h. Transwell filters containing endothelial cells and pericytes were removed from the plates containing the glial culture. Filters were washed with Ringer-HEPES solution (pH 7.4). Quinidine or digoxin was applied at final concentrations of 0.1 μM and 10 μM, respectively. Radiolabeled quinidine and digoxin as tracers were also added to the radioactive concentration of 1 μCi/mL. The inhibitors were added together with the test compound at final concentrations of 1 μM (LY- 335979 and PSC-833) or 100 μM (quinidine). Samples were taken from the basolateral or apical side, respectively, at 15, 30, and 60 min, and radioactivity was measured using a liquid scintillation counter
| Substance Class |
Chemical
Created
by
admin
on
Edited
Sat Dec 16 09:06:24 GMT 2023
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Sat Dec 16 09:06:24 GMT 2023
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| Record UNII |
HZ5B96234K
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| Record Status |
Validated (UNII)
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| Record Version |
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SUB125749
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23623021
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SUB15079MIG
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DTXSID301005551
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100000146238
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85135-88-2
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285-709-5
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PARENT -> SALT/SOLVATE |
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ACTIVE MOIETY |