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    procainamide

    procainamide
    procainamide structure
    CAS No.
    51-06-9
    Chemical Name:
    procainamide
    Synonyms
    C07401;Procamide;Novocamid;Procainamide;Novocainamide;PROCAINEAMIDE;Novocaine amide;procainamide USP/EP/BP;procainamide Solution, 100ppm;4-Amino-N-(2-diethylaminoethyl)
    CBNumber:
    CB5932746
    Molecular Formula:
    C13H21N3O
    Formula Weight:
    235.33
    MOL File:
    51-06-9.mol

    procainamide 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
    pka
    pKa 9.24±0.10 (Uncertain)
    FDA UNII
    L39WTC366D
    ATC code
    C01BA02
    SAFETY
    • Risk and Safety Statements
    RIDADR  2811
    HazardClass  6.1
    PackingGroup 

    procainamide price

    Manufacturer Product number Product description CAS number Packaging Price Updated Buy
    Usbiological P9005-08 Procainamide 51-06-9 200ug $425 2021-12-16 Buy
    Matrix Scientific 139481 Procainamide hydrochloride 95%+ 51-06-9 5g $449 2021-12-16 Buy
    Matrix Scientific 139481 Procainamide hydrochloride 95%+ 51-06-9 2.500g $298 2021-12-16 Buy
    AK Scientific 7077AB 4-Amino-N-(2-diethylaminoethyl)benzamide 51-06-9 5g $373 2021-12-16 Buy
    Matrix Scientific 139481 Procainamide hydrochloride 95%+ 51-06-9 1g $139 2021-12-16 Buy

    procainamide Chemical Properties,Uses,Production

    Description

    Procainamide 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.

    Uses

    Procainamide is used in the management of atrial and ventricular tachydysrhythmias.

    Uses

    Procainamide 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.

    Definition

    ChEBI: 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 Functions

    Procainamide (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 action

    The 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 Use

    Procainamide 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 effects

    Acute 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 Synthesis

    Procainamide, 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 interactions

    The 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.

    Metabolism

    Metabolites 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 evaluation

    Procainamide 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.

    Precautions

    Contraindications 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

    Raw materials

    Preparation Products


    procainamide Suppliers

    Global( 57)Suppliers
    Supplier Tel Fax Email Country ProdList Advantage
    Hubei Jusheng Technology Co.,Ltd.
    86-18871470254
    027-59599243 linda@hubeijusheng.com CHINA 28229 58
    Alchem Pharmtech,Inc.
    8485655694
    sales@alchempharmtech.com United States 63726 58
    career henan chemical co
    15093356674 0371-55982848
    0086-371-86658258 factory@coreychem.com CHINA 29863 58
    Shaanxi Dideu Medichem Co. Ltd
    18192503167 +86-29-89586680
    +86-29-88380327 1005@dideu.com CHINA 9938 58
    Dideu Industries Group Limited
    029-88380327
    Service@dideu.com CHINA 30015 58
    Energy Chemical 400-005-6266 021-58432009-
    021-58436166 sales8178@energy-chemical.com China 43431 61
    Beijing HuaMeiHuLiBiological Chemical 010-56205725
    010-65763397 waley188@sohu.com China 12341 58
    SynAsst Chemical. 021-60343070
    021-35122006 sales@synasst.com China 12743 55
    Shanghai Raise Chemical Technology Co.,Ltd 15026594951 +86-0556-5030631
    0556-5030632 rs@raise-chem.com China 2026 55
    Bide Pharmatech Ltd. 400-1647117 021-61629020-8031
    +86-21-61629029 sales@bldpharm.com;product07@bidepharm.com China 44285 60

    View Lastest Price from procainamide manufacturers

    Image Release date Product Price Min. Order Purity Supply Ability Manufacturer
    2021-08-12 procainamide USP/EP/BP
    51-06-9
    US $1.10 / g 1g 99.9% 100 Tons min Dideu Industries Group Limited
    2020-02-05 procainamide
    51-06-9
    US $1.00 / KG 1KG 98-99.9% 100kg Career Henan Chemical Co

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