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Systematic (IUPAC) name
(9S)-6'-methoxycinchonan- 9-ol
Clinical data
Routes of
Pharmacokinetic data
Bioavailability 70-80%
Metabolism 50-90% Hepatic
Biological half-life 6-8h
Excretion Renal
CAS Number 56-54-2
ATC code C01BA01 (WHO)
PubChem CID 5953
DrugBank APRD00136

(2-ethenyl- 4-azabicyclo [2.2.2] oct- 5-yl)- (6-methoxyquinolin- 4-yl)- methanol,
6'-methoxy- α-(5-vinyl- 2-quinuclidinyl)- 4-quinoline methanol,

(S)- (6-methoxyquinolin- 4-yl) ((2R,4S,5R)- 5-vinylquinuclidin- 2-yl) methanol
Chemical data
Formula C20H24N2O2
Molar mass 324.417 g/mol[[Script error: No such module "String".]]
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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.


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 that 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.

At micromolar concentrations, quinidine inhibits Na⁺/K⁺-ATPase by binding to the same receptor sites as the digitalis glycosides such as ouabain.

The effect of quinidine on the ion channels is to prolong the cardiac action potential, thereby prolonging the QT interval on the surface ECG.

Other ECG effects include a wide notched P wave, wide QRS complex, depressed ST segment, and U waves. These are the results of both slowed depolarization and repolarization.


The half life of oral quinidine is 6 to 8 hours, and it is eliminated by the cytochrome P450 system in the liver. About 20% is excreted unchanged via the kidneys.

Side effects

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 anti-depressants.

Quinidine also inhibits the transport protein P-glycoprotein and so can cause some peripherally acting drugs such as loperamide to have CNS side effects such as respiratory depression if the two drugs are co-administered.[1]

Quinidine-induced thrombocytopenia (low platelet count) is mediated by the immune system, and may lead to thrombocytic purpura. Discovered by a Danish Merchant seaman with AF who took quinine for malaria prophylaxis during trips to India.  He noted his pulse was regular while in India but irregular at home. Chichonism describes tinnitus and hearing loss with quinidine excess.

Quinidine can cause thrombocytopenia, granulomatous hepatitis, myasthenia gravis, and torsades de pointes and for that reason is not used much today. Torsades can occur after the first dose.

Quinidine intoxication can lead to a collection of symptoms collectively known as cinchonism with tinnitus (ringing in the ears) being among the most characteristic and common symptoms of this toxicity syndrome.

Other uses

Intravenous quinidine is also indicated for treatment of Plasmodium falciparum malaria.[2] However, quinidine is not considered the first line therapy for P. falciparum. The recommended treatments for plasmodium falciparum according to the Toronto Notes 2008 are quinine (not to be confused with "quinidine") + doxycycline combination or atovaquone/proguanil (Malarone TM).

Quinidine sulfate is used in the treatment of atrial fibrillation in the horse.

Quinidine-based ligands are used in AD-mix-β for Sharpless asymmetric dihydroxylation.


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External links

See also


es:Quinidina fa:کینیدین fr:Quinidine hr:Kinidin it:Chinidina hu:Kinidin nl:Kinidine ja:キニジン pl:Chinidyna pt:Quinidina ru:Хинидин tr:Kinidin

  1. Sadeque AJ, Wandel C, He H, Shah S, Wood AJ (2000). "Increased drug delivery to the brain by P-glycoprotein inhibition". Clin. Pharmacol. Ther. 68 (3): 231–7. doi:10.1067/mcp.2000.109156. PMID 11014404. 
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