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procainamide

procainamide Suppliers list
Company Name: Hubei Jusheng Technology Co.,Ltd.
Tel: 86-18871470254
Email: linda@hubeijusheng.com
Products Intro: Product Name:procainamide
CAS:51-06-9
Purity:99% Package:5KG;1KG Remarks:C13H21N3O
Company Name: Alchem Pharmtech,Inc.
Tel: 8485655694
Email: sales@alchempharmtech.com
Products Intro: Product Name:4-Amino-N-(2-diethylaminoethyl)benzamide
CAS:51-06-9
Purity:97+% Package:1g;10g;100g;;1kg Remarks:Z-17550
Company Name: career henan chemical co
Tel: 0086-371-86658258 13203830695
Email: factory@coreychem.com
Products Intro: Product Name:procainamide
CAS:51-06-9
Purity:98-99.9% Package:1KG;1USD
Company Name: Shaanxi Dideu Medichem Co. Ltd
Tel: +86-29-89586680 18192503167
Email: 1005@dideu.com
Products Intro: Product Name:procainamide USP/EP/BP
CAS:51-06-9
Purity:99.9% Package:25kgs/Drum;200kgs/Drum Remarks:FDA GMP CEP Approved Manufacturer
Company Name: Dideu Industries Group Limited
Tel: 029-88380327; 17691182729
Email: Service@dideu.com
Products Intro: Product Name:procainamide USP/EP/BP
CAS:51-06-9
Purity:99.9% Package:1g;1.1USD Remarks:FDA GMP CEP Approved Manufacturer

procainamide manufacturers

  • procainamide USP/EP/BP
  • $1.10 / g
  • 2021-08-12
  • CAS:51-06-9
  • Min. Order: 1g
  • Purity: 99.9%
  • Supply Ability: 100 Tons min
  • procainamide
  • $1.00 / KG
  • 2020-02-05
  • CAS:51-06-9
  • Min. Order: 1KG
  • Purity: 98-99.9%
  • Supply Ability: 100kg
procainamide Basic information
Product Name:procainamide
Synonyms:PROCAINEAMIDE;Novocainamide;Novocaine amide;Novocamid;Procamide;Procainamide;4-Amino-N-[2-(diethylamino)ethyl]benzamide;C07401
CAS:51-06-9
MF:C13H21N3O
MW:235.33
EINECS:200-078-8
Product Categories:
Mol File:51-06-9.mol
procainamide Structure
procainamide Chemical Properties
Melting point 47°C
Boiling point 377.72°C (rough estimate)
density 1.060
refractive index 1.5700 (estimate)
storage temp. Keep in dark place,Inert atmosphere,Room temperature
pkapKa 9.24±0.10 (Uncertain)
Safety Information
RIDADR 2811
HazardClass 6.1
PackingGroup 
Hazardous Substances Data51-06-9(Hazardous Substances Data)
MSDS Information
procainamide Usage And Synthesis
DescriptionProcainamide and its analogs were employed by Dr Claude Beck in a series of cardiac surgeries during the early 1930s. The compound was used to alleviate arrhythmias that present during the procedures, and was selected for its favorable tissue absorption properties. Procainamide’s central amide provides it protection from inactivating esterase action and allows oral administration of the compound. Procainamide was approved for use in the United States in 1950.
UsesProcainamide is used in the management of atrial and ventricular tachydysrhythmias.
UsesProcainamide is intended for treating paroxysmal atrial tachycardia, atrial fibrillation, premature ventricular contraction, and ventricular tachycardia. For quickly reaching therapeutic concentrations, parenternal introduction of procainamide is preferred over cynidine.
DefinitionChEBI: 4-Aminobenzamide substituted on the amide N by a 2-(diethylamino)ethyl group. It is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias.
Biological FunctionsProcainamide (Pronestyl, Procan SR) is a derivative of the local anesthetic agent procaine. Procainamide has a longer half-life, does not cause CNS toxicity at therapeutic plasma concentrations, and is effective orally. Procainamide is a particularly useful antiarrhythmic drug, effective in the treatment of supraventricular, ventricular, and digitalis-induced arrhythmias.
Synthesis Reference(s)Synthesis, p. 714, 1975 DOI: 10.1055/s-1975-23900
Mechanism of actionThe chemical difference between procainamide and procaine lies in the replacement of the ester group with an amide group. The action of procainamide is qualitatively similar to the action of procaine. Its effect on the heart is identical to that of quinidine. As an antiarrhythmic, procainamide is preferred over procaine because unlike procaine, it is better absorbed when taken orally and it is more difficult for the esterases of the plasma to hydrolyze it, which results in long-lasting action.
Clinical UseProcainamide is an effective antiarrhythmic agent when given in sufficient doses at relatively short (3–4 hours) dosage intervals. Procainamide is useful in the treatment of premature atrial contractions, paroxysmal atrial tachycardia, and atrial fibrillation of recent onset. Procainamide is only moderately effective in converting atrial flutter or chronic atrial fibrillation to sinus rhythm, although it has value in preventing recurrences of these arrhythmias once they have been terminated by direct current (DC) cardioversion.
Procainamide can decrease the occurrence of all types of active ventricular dysrhythmias in patients with acute myocardial infarction who are free from A-V dissociation, serious ventricular failure, and cardiogenic shock. About 90% of patients with ventricular premature contractions and 80% of patients with ventricular tachycardia respond to procainamide administration. Although the spectrum of action and electrophysiological effects of quinidine and procainamide are similar, the relatively short duration of action of procainamide has tended to restrict its use to patients who are intolerant of or unresponsive to quinidine.
Side effectsAcute cardiovascular reactions to procainamide administration include hypotension, A-V block, intraventricular block, ventricular tachyarrhythmias, and complete heart block. The drug dosage must be reduced or even stopped if severe depression of conduction (severe prolongation of the QRS interval) or repolarization (severe prolongation of the QT interval) occurs.
Long-term drug use leads to increased antinuclear antibody titers in more than 80% of patients; more than 30% of patients receiving long-term procainamide therapy develop a clinical lupus erythematosus–like syndrome. The symptoms may disappear within a few days of cessation of procainamide therapy, although the tests for antinuclear factor and lupus erythematosus cells may remain positive for several months.
Procainamide, unlike procaine, has little potential to produce CNS toxicity. Rarely, patients may be confused or have hallucinations.
Chemical SynthesisProcainamide, 4-amino-N-[2-(diethylamino)ethyl]benzamide (18.1.3), is synthesized by reacting 4-nitrobenzoic acid chloride with N,N-diethylethylendiamine and subsequent reduction of the nitro group of the resulting 4-nitro-N-[2-(diethylamino)ethyl]benzamide (18.1.2) into an amino group.

Drug interactionsThe inherent anticholinergic properties of procainamide may interfere with the therapeutic effect of cholinergic agents. Patients receiving cimetidine and procainamide may exhibit signs of procainamide toxicity, as cimetidine inhibits the metabolism of procainamide. Simultaneous use of alcohol will increase the hepatic clearance of procainamide. Procainamide may enhance or prolong the neuromuscular blocking activity of the aminoglycosides with the potential of producing respiratory depression. The simultaneous administration of quinidine or amiodarone may increase the plasma concentration of procainamide.
MetabolismMetabolites of procainamide include p-aminobenzoic acid and N-acetylprocainamide. Interestingly, the acetylated metabolite is also active as an antiarrhythmic. Its formation accounts for up to one-third of the administered dose and is catalyzed by the liver enzyme N-acetyl transferase. Because acetylation is strongly influenced by an individual's genetic background, marked variability in the amounts of this active metabolite may be observed from patient to patient. Renal excretion dominates, with approximately 90% of a dose excreted as unchanged drug and metabolites. The elimination half-life is approximately 3.5 hours. A substantial percentage (60–70%) of patients on procainamide show elevated levels of antinuclear antibodies after a few months. Of these patients, between 20 and 30% develop a drug-induced lupus syndrome if therapy is continued. These adverse effects, which are attributed to the aromatic amino group, are observed more frequently and more rapidly in “slow acetylators.” Usually, the symptoms associated with procainamide-induced lupus syndrome subside fairly rapidly after the drug is discontinued. These problems, however, have discouraged long-term procainamide therapy.
Toxicity evaluationProcainamide is a class 1a antiarrhythmic that has a mechanism that resembles quinidine by binding to the transmembrane Nat channels and decreasing the number available for depolarization. This creates a delay of Nat entry into the cardiac myocyte during phase 0 of depolarization. As a result, the upslope of depolarization is slowed and the QRS complex widens. Procainamide may also affect phase 3 of the action potential, resulting in prolongation of repolarization and manifesting as QTc prolongation on the electrocardiogram (EKG). Unlike quinine, however, procainamide lacks alphablocking activity and quinidine’s vagolytic ability.
Vasodilation associated with procainamide toxicity (>10 mg ml°1) is due to interference with ganglionic transmission of catecholamine neurotransmitters and/or central nervous system (CNS) sympathetic inhibition. A reflex tachycardia may occur in response to this vasodilation. Rapid intravenous dosing of procainamide can be dangerous as its initial Vd is less than its final; thus adverse myocardial effects can often be seen as the initial ‘compartment’ and includes the cardiovascular system. Myocardial complications can initially be more pronounced. Procainamide may also have weak anticholinergic effects that produce tachycardia. Negative inotropic effects may occur in toxicity. The NAPA metabolite of procainamide lacks Nat channel blocking activity but still retains blockade of the Kt rectifier currents. It is therefore pharmacologic, similar to a type III antidysrhythmic.
PrecautionsContraindications to procainamide are similar to those for quinidine. Because of its effects on A-V nodal and His-Purkinje conduction, procainamide should be administered with caution to patients with second-degree A-V block and bundle branch block. Procainamide should not be administered to patients who have shown procaine or procainamide hypersensitivity and should be used with caution in patients with bronchial asthma. Prolonged administration should be accompanied by hematological studies, since agranulocytosis may occur.
procainamide Preparation Products And Raw materials
Tag:procainamide(51-06-9) Related Product Information
4-nitro-N-(2-piperidinoethyl)benzenecarboxamide N-ACETYLPROCAINAMIDE HYDROCHLORIDE METOCLOPRAMIDE HCL CYCLOHEXYL[4-(4-NITROBENZOYL)PIPERAZINO]METHANONE N-propionylprocainamide BROMOPRIDE Procainamide hydrochloride MMP INHIBITOR I N-ACETYLPROCAINAMIDE O-DESMETHYL METOCLOPRAMIDE, HYDROCHLORIDE Metoclopramide hydrochloride YM-09151-2, [N-METHYL-3H]- 7-aminoketanserin BUTTPARK 100\02-39 4-AMINO-N-(2-(DIETHYLAMINO)ETHYL)BENZAMIDE SULFATE procainamide 7-azidoketanserin DIMETCARB