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Systematic (IUPAC) name
4-amino-N-(2-diethylaminoethyl) benzamide
Clinical data
AHFS/ monograph
  • US: C
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
51-06-9 YesY
PubChem CID 4913
DrugBank DB01035 YesY
ChemSpider 4744 YesY
KEGG D08421 YesY
Chemical data
Formula C13H21N3O
235.325 g/mol
 YesY (what is this?)  (verify)

Procainamide INN (/prˈknəmd/; 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.


Procainamide was approved by the US FDA on June 2, 1950, under the brand name Pronestyl.[1] It was launched by Bristol-Myers Squibb in 1951.[2]


It is a sodium channel blocker which blocks open sodium channels and prolongs the cardiac action potential (outward potassium (K+) currents may be blocked). 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.[3]

Medical uses[edit]

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.[4] It can also be used to treat Wolff-Parkinson-White syndrome by prolonging the refractory period of the accessory pathway.[5]


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.[6] NAPA has an elimination half-life about twice that of procainamide, and it can reach somewhat higher plasma levels during chronic procainamide administration.[7] The loading dose is 100 mg IV bolus given slowly over five minutes. The maximum dose is 17 mg/kg. Use is discontinued when dysrhythmia is suppressed, or if hypotension ensues, the QRS complex widens by 50% or more, or the maximum dose is achieved.

Side effects[edit]

Adverse effects include rash, myalgia, hypersensitivity reactions (fever, agranulocytosis), drug-induced lupus erythematosus[8] (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. The Systemic Lupus Erythematosus reaction may present months or years after the initiation of the drug. A positive anti-histone antibody blood test may be useful in determining whether an SLE presentation is drug induced.[9]


  1. ^ US Food and Drug Administration. "Drugs at FDA: FDA Approved Drug Products". USA: U.S. Food and Drug Administration (FDA). Retrieved 2012-08-13. 
  2. ^ Hollman A (February 1992). "Procaine and procainamide". Br Heart J 67 (2): 143. doi:10.1136/hrt.67.2.143. PMC 1024743. PMID 18610401. 
  3. ^ Zamponi, G. W.; Sui, X.; Codding, P. W.; French, R. J. (1993). "Dual actions of procainamide on batrachotoxin-activated sodium channels: Open channel block and prevention of inactivation". Biophysical Journal 65 (6): 2324–2334. doi:10.1016/S0006-3495(93)81291-8. PMC 1225974. PMID 8312472.  edit
  4. ^ Fenster, P. E.; Comess, K. A.; Marsh, R.; Katzenberg, C.; Hager, W. D. (1983). "Conversion of atrial fibrillation to sinus rhythm by acute intravenous procainamide infusion". American Heart Journal 106 (3): 501–504. doi:10.1016/0002-8703(83)90692-0. PMID 6881022.  edit
  5. ^ Sellers Jr, T. D.; Campbell, R. W.; Bashore, T. M.; Gallagher, J. J. (1977). "Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome". Circulation 55 (1): 15–22. doi:10.1161/01.cir.55.1.15. PMID 830205.  edit
  6. ^ Dutcher, JS; Strong, JM; Lucas, SV; Lee, WK; Atkinson Jr, AJ (1977). "Procainamide and N-acetylprocainamide kinetics investigated simultaneously with stable isotope methodology". Clinical pharmacology and therapeutics 22 (4): 447–57. PMID 902457. 
  7. ^ Drayer, DE; Reidenberg, MM; Sevy, RW (1974). "N-acetylprocainamide: An active metabolite of procainamide". Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine 146 (2): 358–63. doi:10.3181/00379727-146-38104. PMID 4834444. 
  8. ^ Kameda H, Mimori T, Kaburaki J et al. (November 1998). "Systemic sclerosis complicated by procainamide-induced lupus and antiphospholipid syndrome". Br. J. Rheumatol. 37 (11): 1236–9. doi:10.1093/rheumatology/37.11.1236. PMID 9851277. 
  9. ^ Clinical Medicine for the MRCP Paces. Volume 1: Core Clinical Skills. Mehta and Iqbal. Oxford University Press.2010.

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