Details
Stereochemistry | ABSOLUTE |
Molecular Formula | C20H24N2O2.H2O4S |
Molecular Weight | 422.495 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 5 / 5 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
OS(O)(=O)=O.[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=AKYHKWQPZHDOBW-VJAUXQICSA-N
InChI=1S/C20H24N2O2.H2O4S/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;1-5(2,3)4/h3-6,8,11,13-14,19-20,23H,1,7,9-10,12H2,2H3;(H2,1,2,3,4)/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 | H2O4S |
Molecular Weight | 98.078 |
Charge | 0 |
Count |
|
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
DescriptionSources: https://www.drugs.com/pro/quinidine.htmlCurator'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
Sources: https://www.drugs.com/pro/quinidine.html
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 Sources: https://www.ncbi.nlm.nih.gov/pubmed/17506538 |
7300.0 nM [IC50] | ||
Target ID: CHEMBL1980 Sources: https://www.ncbi.nlm.nih.gov/pubmed/17506538 |
6900.0 nM [IC50] | ||
Target ID: CHEMBL5885 Sources: https://www.ncbi.nlm.nih.gov/pubmed/17506538 |
2200.0 nM [IC50] | ||
Target ID: CHEMBL1940 Sources: https://www.ncbi.nlm.nih.gov/pubmed/22761000 |
19820.0 nM [IC50] | ||
Target ID: CHEMBL1075226 Sources: https://www.ncbi.nlm.nih.gov/pubmed/17506538 |
|||
Target ID: CHEMBL364 Sources: https://www.ncbi.nlm.nih.gov/pubmed/22512909 |
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 |
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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 |
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 |
---|---|---|---|---|
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
no | |||
Page: 14.0 |
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 | ||||
Page: 2.0 |
no | |||
no | ||||
yes | ||||
yes | ||||
Sources: https://pubmed.ncbi.nlm.nih.gov/10628900/ Page: 4.0 |
yes | |||
Page: 2.0 |
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 |
---|---|---|
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 |
|
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 |
|
Cardiovascular effects of verapamil and quinidine at normal and elevated ambient pressure. | 2001 Apr |
|
Factors influencing the prediction of steady state concentrations of digoxin. | 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 |
|
Quinidine and malaria. | 2001 Apr 23 |
|
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 |
|
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 |
|
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 |
|
A functional assay for quantitation of the apparent affinities of ligands of P-glycoprotein in Caco-2 cells. | 2001 Feb |
|
Effect of coadministered drugs and ethanol on the binding of therapeutic drugs to human serum in vitro. | 2001 Feb |
|
Species plays an important role in drug-induced prolongation of action potential duration and early afterdepolarizations in isolated Purkinje fibers. | 2001 Jan |
|
How do I prolong QT? Let me count the ways. | 2001 Jan |
|
Transport of [3H]MPP+ in an immortalized rat brain microvessel endothelial cell line (RBE 4). | 2001 Jan |
|
Evaluation of a vincristine resistant Caco-2 cell line for use in a calcein AM extrusion screening assay for P-glycoprotein interaction. | 2001 Jan |
|
A high-performance liquid chromatographic assay for the determination of desbutylhalofantrine enantiomers in rat plasma. | 2001 Jan-Apr |
|
Effect of mdr1a P-glycoprotein gene disruption, gender, and substrate concentration on brain uptake of selected compounds. | 2001 Jul |
|
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 |
|
Ascorbic acid-induced modulation of venous tone in humans. | 2001 Mar |
|
Genomic and functional characteristics of novel human pancreatic 2P domain K(+) channels. | 2001 Mar 23 |
|
Effect of hydrophilic substances on liberation of quinidine from starch - alginate sphere. | 2001 Mar-Apr |
|
Bufuralol metabolism by guinea pig adrenal and hepatic microsomes. | 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 |
|
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 |
|
In vitro metabolism of tegaserod in human liver and intestine: assessment of drug interactions. | 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 |
|
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 |
Patents
Sample Use Guides
In Vivo Use Guide
Sources: https://www.drugs.com/pro/quinidine.html
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
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/21832259
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
Fri Dec 15 15:13:35 GMT 2023
by
admin
on
Fri Dec 15 15:13:35 GMT 2023
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Record UNII |
6K043Q65TR
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Record Status |
Validated (UNII)
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Record Version |
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55377
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DTXSID401020744
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100000085673
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C009764
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747-45-5
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SUB126873
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212-020-9
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22817455
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SUB22060
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6K043Q65TR
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SOLVATE->ANHYDROUS | |||
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PARENT -> SALT/SOLVATE |
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ACTIVE MOIETY |