出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2012/02/20 16:16:58」(JST)
Systematic (IUPAC) name | |
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4-amino-N-(2-diethylaminoethyl) benzamide | |
Clinical data | |
AHFS/Drugs.com | monograph |
Pregnancy cat. | C(US) |
Legal status | POM (UK) |
Routes | IV, IM, oral |
Pharmacokinetic data | |
Bioavailability | 85% (oral) |
Protein binding | 15 to 20% |
Metabolism | Hepatic (CYP2D6-mediated) |
Half-life | ~2.5 to 4.5 hours |
Excretion | Renal |
Identifiers | |
CAS number | 51-06-9 Y |
ATC code | C01BA02 |
PubChem | CID 4913 |
DrugBank | APRD00509 |
ChemSpider | 4744 Y |
UNII | L39WTC366D Y |
KEGG | D08421 Y |
ChEBI | CHEBI:8428 Y |
ChEMBL | CHEMBL640 Y |
Chemical data | |
Formula | C13H21N3O |
Mol. mass | 235.325 g/mol |
SMILES | eMolecules & PubChem |
InChI
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N(what is this?) (verify) |
Procainamide INN ( /proʊˈkeɪnəmaɪd/; trade names Pronestyl, Procan, Procanbid) is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias, classified by the Vaughan Williams classification system as class Ia.
Contents
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Procainamide was approved by the US FDA on June 2, 1950, under the brand-name Pronestyl.[1]. It was launched by Squibb in 1951.[2]
It blocks open sodium (Na+) channels and prolongs the cardiac action potential (outward potassium (K+) currents may be blocked).http://en.wikipedia.org/wiki/Talk:Procainamide This results in slowed conduction, and ultimately the decreased rate of rise of the action potential, which may result in widening of QRS on electrocardiogram (ECG).
This drug is used for both supraventricular and ventricular arrhythmias. For example, it can be used to convert new-onset atrial fibrillation, though it is suboptimal for this purpose. It can also be used to treat Wolf-Parkinson-White syndrome by prolonging the refractory period of the accessory pathway. Typically use is secondary to lidocaine in patients who are allergic to lidocaine or dysrhythmias that are refractory to lidocaine.
Procainamide is administered intravenously or orally. When administered intravenously, a loading dose should first be given, though care should be taken not to cause hypotension.
Procainamide's major active metabolite is N-acetylprocainamide (NAPA), which is approximately equipotent with the parent drug as an antiarrhythmic agent.[3] NAPA has an elimination half-life about twice that of procainamide, and it can reach somewhat higher plasma levels during chronic procainamide administration.[4] The loading dose is 100 mg IV bolus given slowly over 5 minutes. The maximium dose is 17 mg/kg. Use is discontinued when dysrhythmia is suppressed, or if hypotension ensues, QRS complex widens by 50% or more, or maximum dose is achieved.
Adverse effects include rash, myalgia, hypersensitivity reactions (fever, agranulocytosis), Drug-Induced Lupus Erythematosus[5] (particularly in slow-acetylators), and proarrhythmic effects (e.g., torsades de pointes). Treatment with procainamide can cause antibody production against cellular components, accounting for the systemic lupus erythematosus-like adverse reactions.
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