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Details

Stereochemistry ABSOLUTE
Molecular Formula 2C20H24N2O2.2H2O.H2O4S
Molecular Weight 782.9452
Optical Activity UNSPECIFIED
Defined Stereocenters 10 / 10
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of QUINIDINE SULFATE

SMILES

C=C[C@@]1([H])CN2CC[C@@]1([H])C[C@]2([H])[C@]([H])(c3ccnc4ccc(cc34)OC)O.C=C[C@@]1([H])CN2CC[C@@]1([H])C[C@]2([H])[C@]([H])(c3ccnc4ccc(cc34)OC)O.OS(=O)(=O)O.O.O

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

HIDE SMILES / InChI

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

Molecular Formula H2O4S
Molecular Weight 98.0796
Charge 0
Count
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Molecular Formula C20H24N2O2
Molecular Weight 324.4175
Charge 0
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 4 / 4
E/Z Centers 0
Optical Activity UNSPECIFIED

Description
Curator's Comment:: 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.

Approval Year

TargetsConditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
QUINIDINE GLUCONATE

Approved Use

Conversion 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 Date

-614563200000
Primary
QUINIDINE GLUCONATE

Approved Use

Conversion 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 Date

-614563200000
Primary
QUINIDINE GLUCONATE

Approved Use

Conversion 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 Date

-614563200000
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
3.4 μg/mL
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

AUC

ValueDoseCo-administeredAnalytePopulation
12.8 μg × h/mL
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

T1/2

ValueDoseCo-administeredAnalytePopulation
5.8 h
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

Funbound

ValueDoseCo-administeredAnalytePopulation
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

Doses

DosePopulationAdverse 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
Health Status: unhealthy
Age Group: 47 years
Sex: M
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
Health Status: unhealthy
Age Group: 56 yeras
Sex: F
Sources:
Disc. AE: Myalgia...
AEs leading to
discontinuation/dose reduction:
Myalgia (severe, 1 patient)
Sources:
4 g single, oral
Overdose
Dose: 4 g
Route: oral
Route: single
Dose: 4 g
Sources:
healthy, 57 years
Health Status: healthy
Age Group: 57 years
Sex: F
Sources:
Other AEs: Grand mal convulsion, Cardiotoxicity...
Other AEs:
Grand mal convulsion (1 patient)
Cardiotoxicity (1 patient)
Sources:
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
Health Status: unhealthy
Age Group: 79 years
Sex: F
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
Health Status: healthy
Age Group: > 23 years
Sex: M
Sources:
1650 mg single, intravenous
Dose: 1650 mg
Route: intravenous
Route: single
Dose: 1650 mg
Sources:
healthy, > 23 years
Health Status: healthy
Age Group: > 23 years
Sex: M
Sources:
AEs

AEs

AESignificanceDosePopulation
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
Health Status: unhealthy
Age Group: 47 years
Sex: M
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
Health Status: unhealthy
Age Group: 56 yeras
Sex: F
Sources:
Cardiotoxicity 1 patient
4 g single, oral
Overdose
Dose: 4 g
Route: oral
Route: single
Dose: 4 g
Sources:
healthy, 57 years
Health Status: healthy
Age Group: 57 years
Sex: F
Sources:
Grand mal convulsion 1 patient
4 g single, oral
Overdose
Dose: 4 g
Route: oral
Route: single
Dose: 4 g
Sources:
healthy, 57 years
Health Status: healthy
Age Group: 57 years
Sex: F
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
Sources:
unhealthy, 79 years
Health Status: unhealthy
Age Group: 79 years
Sex: F
Sources:
OverviewDrug as perpetrator​

Drug as perpetrator​

TargetModalityActivityMetaboliteClinical 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
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

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
minor
no
no
yes
yes
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
Tox targets
Sourcing

Sourcing

Vendor/AggregatorIDURL
PubMed

PubMed

TitleDatePubMed
Fluorometric screening for metabolism-based drug--drug interactions.
2000 Jul-Aug
[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
Drug interaction studies with esomeprazole, the (S)-isomer of omeprazole.
2001
Evaluation of drug-induced QT interval prolongation: implications for drug approval and labelling.
2001
CIBIS, MERIT-HF, and COPERNICUS trial outcomes: do they complete the chapter on beta-adrenergic blockers as antiarrhythmic and antifibrillatory drugs?
2001 Apr
HPTLC method for the estimation of alkaloids of Cinchona officinalis stem bark and its marketed formulations.
2001 Apr
Cardiovascular effects of verapamil and quinidine at normal and elevated ambient pressure.
2001 Apr
Simultaneous measurement of plasma ropivacaine and bupivacaine concentrations by HPLC with UV detection.
2001 Apr
Simultaneous determination of quinine and four metabolites in plasma and urine by high-performance liquid chromatography.
2001 Apr 15
Influence of phenylalanine-481 substitutions on the catalytic activity of cytochrome P450 2D6.
2001 Apr 15
Quinidine and malaria.
2001 Apr 23
Angiotensin II type I receptor modulates intracellular free Mg2+ in renally derived cells via Na+-dependent Ca2+-independent mechanisms.
2001 Apr 27
High-throughput cytochrome P450 (CYP) inhibition screening via cassette probe-dosing strategy. II. Validation of a direct injection/on-line guard cartridge extraction-tandem mass spectrometry method for CYP2D6 inhibition assessment.
2001 Apr 5
[Pharmacokinetics and drug interactions of antidepressive agents].
2001 Aug
Independent organic cation transport activity of Na(+)-L-carnitine cotransport system in LLC-PK(1) cells.
2001 Aug
Escitalopram (S-citalopram) and its metabolites in vitro: cytochromes mediating biotransformation, inhibitory effects, and comparison to R-citalopram.
2001 Aug
Role of transport proteins in drug absorption, distribution and excretion.
2001 Aug-Sep
A human lymphocyte based ex vivo assay to study the effect of drugs on P-glycoprotein (P-gp) function.
2001 Jan
A high-performance liquid chromatographic assay for the determination of desbutylhalofantrine enantiomers in rat plasma.
2001 Jan-Apr
Comparison of "type I" and "type II" organic cation transport by organic cation transporters and organic anion-transporting polypeptides.
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
Synchronized neural activity in the Drosophila memory centers and its modulation by amnesiac.
2001 Jun
Effect of capillary efflux transport inhibition on the determination of probe recovery during in vivo microdialysis in the brain.
2001 Jun
In vitro stimulation of warfarin metabolism by quinidine: increases in the formation of 4'- and 10-hydroxywarfarin.
2001 Jun
Mechanism-based inactivation of CYP2D6 by 5-fluoro-2-[4-[(2-phenyl-1H-imidazol-5-yl)methyl]-1-piperazinyl]pyrimidine.
2001 Jun
Persistence of Plasmodium falciparum in the placenta after apparently effective quinidine/clindamycin therapy.
2001 Mar
Identification of the cytochrome P450 enzymes involved in the N-demethylation of sildenafil.
2001 Mar
Effect of hydroxyzine on the transport of etoposide in rat small intestine.
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
Moxifloxacin: clinical efficacy and safety.
2001 Mar 1
Genomic and functional characteristics of novel human pancreatic 2P domain K(+) channels.
2001 Mar 23
Metabolism of amiodarone (Part III): identification of rabbit cytochrome P450 isoforms involved in the hydroxylation of mono-N-desethylamiodarone.
2001 May
Quinidine as an antiarrhythmic.
2001 May
Interactions between antiarrhythmic drugs and cardiac memory.
2001 May
Mechanical effects of liriodenine on the left ventricular-arterial coupling in Wistar rats: pressure-stroke volume analysis.
2001 May
Metabolism of sulfinpyrazone sulfide and sulfinpyrazone by human liver microsomes and cDNA-expressed cytochrome P450s.
2001 May
Coumarin substrates for cytochrome P450 2D6 fluorescence assays.
2001 May 15
Evaluation of the contribution to enantioselectivity of quinine and quinidine scaffolds in chemically and physically mixed chiral selectors.
2001 May 5
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
Interactions of the antimalarial drug mefloquine with the human cardiac potassium channels KvLQT1/minK and HERG.
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
Purinoreceptors are involved in the control of acute morphine withdrawal.
2001 Sep 21
Patents

Sample Use Guides

In Vivo Use Guide
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).
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 Fri Jun 25 21:15:17 UTC 2021
Edited
by admin
on Fri Jun 25 21:15:17 UTC 2021
Record UNII
J13S2394HE
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
QUINIDINE SULFATE
EP   MART.   ORANGE BOOK   USP   USP-RS   VANDF   WHO-IP  
Common Name English
QUINICARDINE
Brand Name English
QUINIDINE SULFATE COMPONENT OF NUEDEXTA
Common Name English
QUINIDINE SULFATE HYDRATE
JAN  
Common Name English
QUINIDINE SULFATE [USP]
Common Name English
QUINIDINE SULFATE COMPONENT OF AVP-786
Code English
AVP-786 COMPONENT QUINIDINE SULFATE
Code English
CINCHONAN-9-OL, 6'-METHOXY-, (9S)-, SULFATE, HYDRATE (2:1:2)
Common Name English
QUINIDINI SULFAS [WHO-IP LATIN]
Common Name English
QUINIDINE SULFATE DIHYDRATE
MI   WHO-DD  
Common Name English
QUINIDINE SULFATE [USP-RS]
Common Name English
QUINIDINE SULFATE DIHYDRATE [WHO-DD]
Common Name English
NUEDEXTA COMPONENT QUINIDINE SULFATE
Common Name English
QUINIDINE SULFATE [ORANGE BOOK]
Common Name English
QUINIDINE SULFATE [VANDF]
Common Name English
CIN-QUIN
Brand Name English
QUINIDINE SULFATE [WHO-IP]
Common Name English
QUINIDEX EXTENTABS
Brand Name English
QUINIDINE SULFATE DIHYDRATE [MI]
Common Name English
CINCHONAN-9-OL, 6'-METHOXY-, (9S)-, SULPHATE (2:1) (SALT), DIHYDRATE
Common Name English
QUINIDINE SULFATE [EP MONOGRAPH]
Common Name English
QUINIDINE SULFATE (2:1) (SALT), DIHYDRATE [WHO-IP]
Common Name English
QUINIDINE SULPHATE DIHYDRATE
Common Name English
QUINIDINE SULPHATE
Common Name English
QUINIDEX
Brand Name English
QUINIDINE SULFATE HYDRATE [JAN]
Common Name English
QUINIDINE, SULFATE, HYDRATE (2:1:2)
Common Name English
QUINIDINE SULFATE [MART.]
Common Name English
CINCHONAN-9-OL, 6'-METHOXY-, (9S)-, SULFATE (2:1) (SALT), DIHYDRATE
Common Name English
QUINORA
Brand Name English
Classification Tree Code System Code
NCI_THESAURUS C93038
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
NCI_THESAURUS C271
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
EMA ASSESSMENT REPORTS NUEDEXTA (AUTHORIZED: NEUROBEHAVIORAL MANIFESTATIONS)
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
FDA ORPHAN DRUG 556716
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
Code System Code Type Description
NCI_THESAURUS
C48014
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
CAS
6591-63-5
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
WHO INTERNATIONAL PHARMACOPEIA
QUINIDINE SULFATE
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
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.
PUBCHEM
656862
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
DRUG BANK
DBSALT000363
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
ChEMBL
CHEMBL1294
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
EVMPD
SUB15083MIG
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
FDA UNII
J13S2394HE
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
EVMPD
SUB15082MIG
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY
RXCUI
9069
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY RxNorm
USP_CATALOG
1595509
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY USP-RS
MERCK INDEX
M9446
Created by admin on Fri Jun 25 21:15:17 UTC 2021 , Edited by admin on Fri Jun 25 21:15:17 UTC 2021
PRIMARY Merck Index
Related Record Type Details
PARENT -> SALT/SOLVATE
Related Record Type Details
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
IMPURITY -> PARENT
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