Details
| Stereochemistry | ABSOLUTE |
| Molecular Formula | 2C20H24N2O2.2H2O.H2O4S |
| Molecular Weight | 782.943 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 10 / 10 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
O.O.OS(O)(=O)=O.COC1=CC=C2N=CC=C([C@H](O)[C@H]3C[C@@H]4CC[N@]3C[C@@H]4C=C)C2=C1.COC5=CC=C6N=CC=C([C@H](O)[C@H]7C[C@@H]8CC[N@]7C[C@@H]8C=C)C6=C5
InChI
InChIKey=ZHNFLHYOFXQIOW-AHSOWCEXSA-N
InChI=1S/2C20H24N2O2.H2O4S.2H2O/c2*1-3-13-12-22-9-7-14(13)10-19(22)20(23)16-6-8-21-18-5-4-15(24-2)11-17(16)18;1-5(2,3)4;;/h2*3-6,8,11,13-14,19-20,23H,1,7,9-10,12H2,2H3;(H2,1,2,3,4);2*1H2/t2*13-,14-,19+,20-;;;/m00.../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 | H2O4S |
| Molecular Weight | 98.078 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
| Molecular Formula | H2O |
| Molecular Weight | 18.0153 |
| 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 |
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| 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 |
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 |
Disc. AE: Myalgia... AEs leading to discontinuation/dose reduction: Myalgia (severe, 1 patient) Sources: |
4 g single, oral Overdose |
healthy, 57 years |
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 Sources: |
unhealthy, 79 years |
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 |
|
1650 mg single, intravenous Dose: 1650 mg Route: intravenous Route: single Dose: 1650 mg Sources: |
healthy, > 23 years |
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 |
| 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 |
| Cardiotoxicity | 1 patient | 4 g single, oral Overdose |
healthy, 57 years |
| Grand mal convulsion | 1 patient | 4 g single, oral Overdose |
healthy, 57 years |
| 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 Sources: |
unhealthy, 79 years |
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
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 |
|---|---|---|
| Quinidine-induced lupus nephritis. | 1976 May 3 |
|
| Metabolism of 3-methylindole by porcine liver microsomes: responsible cytochrome P450 enzymes. | 2000 Jun |
|
| TASK-3, a new member of the tandem pore K(+) channel family. | 2000 Mar 31 |
|
| [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 |
|
| Pharmacokinetic interactions of antimalarial agents. | 2001 |
|
| Simultaneous measurement of plasma ropivacaine and bupivacaine concentrations by HPLC with UV detection. | 2001 Apr |
|
| Angiotensin II type I receptor modulates intracellular free Mg2+ in renally derived cells via Na+-dependent Ca2+-independent mechanisms. | 2001 Apr 27 |
|
| Binding constant determination of drugs toward subdomain IIIA of human serum albumin by near-infrared dye-displacement capillary electrophoresis. | 2001 Aug |
|
| Escitalopram (S-citalopram) and its metabolites in vitro: cytochromes mediating biotransformation, inhibitory effects, and comparison to R-citalopram. | 2001 Aug |
|
| A functional assay for quantitation of the apparent affinities of ligands of P-glycoprotein in Caco-2 cells. | 2001 Feb |
|
| Single oral loading dose of propafenone for pharmacological cardioversion of recent-onset atrial fibrillation. | 2001 Feb |
|
| Effect of coadministered drugs and ethanol on the binding of therapeutic drugs to human serum in vitro. | 2001 Feb |
|
| Modulation of P450 CYP3A4-dependent metabolism by P-glycoprotein: implications for P450 phenotyping. | 2001 Feb |
|
| From the Centers for Disease Control and Prevention. Availability and use of parenteral quinidine gluconate for severe or complicated malaria. | 2001 Feb 14 |
|
| A method for the simultaneous evaluation of the activities of seven major human drug-metabolizing cytochrome P450s using an in vitro cocktail of probe substrates and fast gradient liquid chromatography tandem mass spectrometry. | 2001 Jan |
|
| A high-performance liquid chromatographic assay for the determination of desbutylhalofantrine enantiomers in rat plasma. | 2001 Jan-Apr |
|
| 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 |
|
| Novel target genes of the yeast regulator Pdr1p: a contribution of the TPO1 gene in resistance to quinidine and other drugs. | 2001 Jul 11 |
|
| Establishment of the transformants expressing human cytochrome P450 subtypes in HepG2, and their applications on drug metabolism and toxicology. | 2001 Jun |
|
| Mechanism-based inactivation of CYP2D6 by 5-fluoro-2-[4-[(2-phenyl-1H-imidazol-5-yl)methyl]-1-piperazinyl]pyrimidine. | 2001 Jun |
|
| Calcium-activated potassium current in single Novikoff cell. | 2001 Mar |
|
| Identification of the cytochrome P450 enzymes involved in the N-demethylation of sildenafil. | 2001 Mar |
|
| Characterization of (+/-)-bufuralol hydroxylation activities in liver microsomes of Japanese and Caucasian subjects genotyped for CYP2D6. | 2001 Mar |
|
| Capillary electrophoretic separation, immunochemical recognition and analysis of the diastereomers quinine and quinidine and two quinidine metabolites in body fluids. | 2001 Mar |
|
| Ascorbic acid-induced modulation of venous tone in humans. | 2001 Mar |
|
| Acute canine model for drug-induced Torsades de Pointes in drug safety evaluation-influences of anesthesia and validation with quinidine and astemizole. | 2001 Mar |
|
| Moxifloxacin: clinical efficacy and safety. | 2001 Mar 1 |
|
| Effect of hydrophilic substances on liberation of quinidine from starch - alginate sphere. | 2001 Mar-Apr |
|
| Metabolism of sulfinpyrazone sulfide and sulfinpyrazone by human liver microsomes and cDNA-expressed cytochrome P450s. | 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 |
|
| 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 |
|
| Purinoreceptors are involved in the control of acute morphine withdrawal. | 2001 Sep 21 |
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
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| Record UNII |
J13S2394HE
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Validated (UNII)
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| Classification Tree | Code System | Code | ||
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NCI_THESAURUS |
C93038
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NCI_THESAURUS |
C271
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EMA ASSESSMENT REPORTS |
NUEDEXTA (AUTHORIZED: NEUROBEHAVIORAL MANIFESTATIONS)
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FDA ORPHAN DRUG |
556716
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| Code System | Code | Type | Description | ||
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1595509
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PRIMARY | |||
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C48014
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6591-63-5
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QUINIDINE SULFATE
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PRIMARY | Description: Colourless, needle-like crystals or a white, crystalline powder; odourless. Solubility: Sparingly soluble in water; soluble in ethanol (~750 g/l) TS; practically insoluble in ether R and acetone R. Category: Antidysrhythmic drug. Storage: Quinidine sulfate should be kept in a well-closed container, protected from light. Additional information: Quinidine sulfate has a very bitter taste. It darkens in colour on exposure to light. Definition: Quinidine sulfate contains not less than 99.0% and not more than 101.0% of total alkaloids, calculated as (C20H24N2O2)2,H2SO4 and with reference to the dried substance. | ||
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656862
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DBSALT000363
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CHEMBL1294
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SUB15083MIG
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DTXSID101017271
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J13S2394HE
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SUB15082MIG
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J13S2394HE
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28593
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9069
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m9446
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PARENT -> SALT/SOLVATE | |||
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
||
|
IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
| Related Record | Type | Details | ||
|---|---|---|---|---|
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ACTIVE MOIETY |