Quinidine
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| Clinical data | |
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| Trade names | Quinaglute, Quinidex |
| AHFS/Drugs.com | Monograph |
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| Routes of administration |
Oral, IM, IV |
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| Pharmacokinetic data | |
| Bioavailability | 70–85% |
| Metabolism | 50–90% (by liver) |
| Biological half-life | 6–8 hours |
| Excretion | by the liver (20% as unchanged quinidine via urine) |
| Identifiers | |
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| Synonyms | (2-Ethenyl-4-azabicyclo[2.2.2]oct-5-yl)-(6-methoxyquinolin-4-yl)-methanol |
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| ChEMBL | |
| ECHA InfoCard | 100.000.254 |
| Chemical and physical data | |
| Formula | C20H24N2O2 |
| Molar mass | 324.417 g/mol |
| 3D model (Jmol) | |
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  (what is this?)
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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. 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.
At micromolar concentrations, quinidine inhibits Na+/K+-ATPase by binding to the same receptor sites as the digitalis glycosides such as ouabain.
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Wikipedia