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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
Structure of QUINIDINE DIHYDROCHLORIDE

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

HIDE SMILES / InChI

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

Description
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.

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

1950
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

1950
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

1950
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
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
Dose: 4 g
Route: oral
Route: single
Dose: 4 g
Sources:
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)
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
Co-administed with::
digoxin
levothyroxine sodium
crystalline warfarin sodium
Sources:
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

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
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
Dose: 4 g
Route: oral
Route: single
Dose: 4 g
Sources:
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
Dose: 4 g
Route: oral
Route: single
Dose: 4 g
Sources:
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
levothyroxine sodium
crystalline warfarin sodium
Sources:
unhealthy, 79 years
n = 1
Health Status: unhealthy
Age Group: 79 years
Sex: F
Population Size: 1
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: 5.0
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

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: 2.0
Tox targets
Sourcing

Sourcing

Vendor/AggregatorIDURL
PubMed

PubMed

TitleDatePubMed
[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
CIBIS, MERIT-HF, and COPERNICUS trial outcomes: do they complete the chapter on beta-adrenergic blockers as antiarrhythmic and antifibrillatory drugs?
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
Quinidine and malaria.
2001 Apr 23
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
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 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
Establishment of the transformants expressing human cytochrome P450 subtypes in HepG2, and their applications on drug metabolism and toxicology.
2001 Jun
Effect of capillary efflux transport inhibition on the determination of probe recovery during in vivo microdialysis in the brain.
2001 Jun
Calcium-activated potassium current in single Novikoff cell.
2001 Mar
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 hydrophilic substances on liberation of quinidine from starch - alginate sphere.
2001 Mar-Apr
Oral quinine pharmacokinetics and dietary salt intake.
2001 May
Bufuralol metabolism by guinea pig adrenal and hepatic microsomes.
2001 May
Interactions between antiarrhythmic drugs and cardiac memory.
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
Effect of P-glycoprotein on flavopiridol sensitivity.
2001 May 18
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
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

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). 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 Sat Dec 16 09:06:24 GMT 2023
Edited
by admin
on Sat Dec 16 09:06:24 GMT 2023
Record UNII
HZ5B96234K
Record Status Validated (UNII)
Record Version
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Name Type Language
QUINIDINE DIHYDROCHLORIDE
WHO-DD  
Common Name English
Quinidine dihydrochloride [WHO-DD]
Common Name English
(S)-((2R,5R)-5-ETHENYL-1-AZABICYCLO(2.2.2)OCTAN-2-YL)-(6-METHOXYQUINOLIN-4-YL)METHANOL, DIHYDROCHLORIDE
Systematic Name English
QUINIDINE HCL
Common Name English
(9S)-6'-METHOXYCINCHONAN-9-OL DIHYDROCHLORIDE
Systematic Name English
J311.864I
Code English
CINCHONAN-9-OL, 6'-METHOXY-, DIHYDROCHLORIDE, (9S)-
Systematic Name English
(S)-(6-METHOXY-4-QUINOLYL)-((1S,2R,4S,5R)-5-VINYLQUINUCLIDIN-2-YL)METHANOL DIHYDROCHLORIDE
Systematic Name English
Code System Code Type Description
EVMPD
SUB125749
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
PUBCHEM
23623021
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
EVMPD
SUB15079MIG
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
EPA CompTox
DTXSID301005551
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
SMS_ID
100000146238
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
CAS
85135-88-2
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
FDA UNII
HZ5B96234K
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
ECHA (EC/EINECS)
285-709-5
Created by admin on Sat Dec 16 09:06:24 GMT 2023 , Edited by admin on Sat Dec 16 09:06:24 GMT 2023
PRIMARY
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