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E number{{#property:P628}}
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Molar mass369.520 g/mol
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Prajmaline (Neo-gilurythmal)[1] is a class Ia antiarrhythmic agent[2] which has been available since the 1970s.[3] Class Ia drugs increase the time one action potential lasts in the heart.[4] Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor.[5] It acts to stop arrhythmias of the heart through a frequency-dependent block of cardiac sodium channels.[2]


Prajmaline causes a resting block in the heart.[6] A resting block is the depression of a person's Vmax after a resting period. This effect is seen more in the atrium than the ventricle.[6] The effects of some Class I antiarrhythmics are only seen in a patient who has a normal heart rate (~1 Hz).[7] This is due to the effect of a phenomenon called reverse use dependence.[7] The higher the heart rate, the less effect Prajmaline will have.


The drug Prajmaline has been used to treat a number of cardiac disorders. These include: coronary artery disease,[8][9] angina,[8][9] paroxysmal tachycardia and Wolff–Parkinson–White syndrome.[1] Prajmaline has been indicated in the treatment of certain disorders where other antiarrhythmic drugs were not effective.[1]


Prajmaline can be administered orally,[9] parenterally[8] or intravenously.[8] Three days after the last dose, a limited effect has been observed. Therefore it has been suggested that treatment of arrhythmias with Prajmaline must be continuous to see acceptable results.[1]


The main metabolites of Prajmaline are: 21-carboxyprajmaline and hydroxyprajmaline. Twenty percent of the drug is excreted in the urine unchanged.

Daily therapeutic dose is 40–80 mg. Distribution half-life is 10 minutes. Plasma protein binding is 60%. Oral bioavailability is 80%. Elimination half-life is 6 hours. Volume of distribution is 4-5 L/kg. [3]

Side Effects

There are no significant adverse side-effects of Prajmaline when taken alone and with a proper dosage.[1][8][9] Patients who are taking other treatments for their symptoms (e.g. beta blockers and nifedipine) have developed minor transient conduction defects when given Prajmaline.[8]


An overdose of Prajmaline is possible. The range of symptoms seen during a Prajmaline overdose include: no symptoms, nausea/vomiting, bradycardia, tachycardia, hypotension, and death.[3]

Other Potential Uses

Due to Prajmaline's sodium channel-blocking properties, it has been shown to protect rat white matter from anoxia (82 +/- 15%).[10][11] The concentration used causes little suppression of the preanoxic response.[10][11]


  1. 1.0 1.1 1.2 1.3 1.4 Janicki, K., J. Orski, and J. Kakol. "Antiarrhythmic Effects of Prajmaline (Neo-Gilurythmal) in Stable Angina Pectoris." Przegl Lek 52.10 (1995): 485-91. PubMed. Web. 6 Feb. 2011. <>.
  2. 2.0 2.1 Weirich, J., and H. Antoni. "Differential Analysis of the Frequency-Dependent Effects of Class 1 Antiarrhythmic Drugs According to Periodical Ligand Binding." Journal of Cardiovascular Pharmacology 15.6 (1990): 998-1009. PubMed. Web. 6 Feb. 2011. <>.
  3. 3.0 3.1 3.2 Koppel, Claus, Ursula Oberdisse, and Gerhard Heinemeyer. "Clinical Course and Outcome in Class IC Antiarrhythmic Overdose." Clinical Toxicology 28.4 (1990): 433-44. Web. 6 Feb. 2011. <>.
  4. Milne, J. R., K. J. Hellestrand, R. S. Bexton, P. J. Burnett, N. Debbas, and A. Camm. "Class 1 Antiarrhythmic Drugs — Characteristic Electrocardiographic Differences When Assessed by Atrial and Ventricular Pacing." European Heart Journal 5 (1984): 99-107. Web. 6 Feb. 2011. <>.
  5. Hinse, C., and J. Stöckigt. "The Structure of the Ring-opened N Beta-propyl-ajmaline (Neo-Gilurytmal) at Physiological PH Is Obviously Responsible for Its Better Absorption and Bioavailability When Compared with Ajmaline (Gilurytmal)." Pharmazie 55.7 (2000): 531-32. PubMed. Web. 6 Feb. 2011. <>.
  6. 6.0 6.1 Langenfeld, H., J. Weirich, C. Köhler, and K. Kochsiek. "Comparative Analysis of the Action of Class I Antiarrhythmic Drugs (Lidocaine, Quinidine, and Prajmaline) in Rabbit Atrial and Ventricular Myocardium." Journal of Cardiovascular Pharmacology 15.2 (1990): 338-45. PubMed. Web. 6 Feb. 2011. <>.
  7. 7.0 7.1 Langenfeld, H., C. Köhler, J. Weirich, M. Kirstein, and K. Kochsiek. "Reverse Use Dependence of Antiarrhythmic Class Ia, Ib, and Ic: Effects of Drugs on the Action Potential Duration?" Pacing and Clinical Electrophysiology 2nd ser. 15.11 (1992): 2097-102. Web. 6 Feb. 2011. <>.
  8. 8.0 8.1 8.2 8.3 8.4 8.5 Sowton, E., I. D. Sullivan, and J. C. P. Crick. "Acute Haemodynamic Effects of Ajmaline and Prajmaline in Patients with Coronary Heart Disease." European Journal of Clinical Pharmacology 26.2 (1984): 147-50. PubMed. Web. 6 Feb. 2011. <>.
  9. 9.0 9.1 9.2 9.3 Handler, C. E., A. Kritikos, I. D. Sullivan, A. Charalambakis, and E. Sowton. "Effects of Oral Prajmaline Bitartrate on Exercise Test Responses in Patients with Coronary Artery Disease." European Journal of Clinical Pharmacology 28.4 (1985): 371-74. PubMed. Web. 6 Feb. 2011. <>.
  10. 10.0 10.1 Stys, PK. "Protective Effects of Antiarrhythmic Agents against Anoxic Injury in CNS White Matter." Journal of Cerebral Blood Flow & Metabolism 15.3 (1995): 425-32. PubMed. Web. 6 Feb. 2011. <>.
  11. 11.0 11.1 Malek, S., J. Adorante, and P. Stys. "Differential Effects of Na-K-ATPase Pump Inhibition, Chemical Anoxia, and Glycolytic Blockade on Membrane Potential of Rat Optic Nerve." Brain Research 1037.1-2 (2005): 171-79.

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