Acecainide
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| Clinical data | |
|---|---|
| Routes of administration |
Oral or intravenous administration IV |
| Pharmacokinetic data | |
| Bioavailability | Oral administration 85% |
| Protein binding | 10% |
| Metabolism | Hepatic |
| Biological half-life | 4.3–15.1 h |
| Excretion | Renal |
| Identifiers | |
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| Synonyms | 2-acetyloxybenzoic acid acetylsalicylate acetylsalicylic acid O-acetylsalicylic acid |
| CAS Number | |
| PubChem CID | |
| ChemSpider | |
| KEGG | |
| ChEBI | |
| ChEMBL | |
| ECHA InfoCard | 100.151.497 |
| Chemical and physical data | |
| Formula | C15H23N3O2 |
| Molar mass | 277.362 g/mol |
| 3D model (JSmol) | |
| Density | 1.1±0.1 g/cm3 g/cm3 |
| Melting point | 138–140 °C (280–284 °F) |
| Boiling point | 465–535 °C (869–995 °F) |
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Acecainide (N-acetylprocainamide, NAPA) is an antiarrhythmic drug. Chemically, it is the N-acetylated metabolite of procainamide. It is a Class III antiarrhythmic agent, whereas procainamide is a Class Ia antiarrhythmic drug. It is only partially as active as procainamide; when checking levels, both must be included in the final calculation.
In the early 1930s, Claude Beck was undertaking pioneer cardiac surgery at the Lakeside Hospital in Cleveland, Ohio. During and after his surgery he was facing problems with arrhythmias. These problems were investigated by Frederick R. Mautz. In these experiments he used drugs similar to cocaine, because these drugs were readily absorbed from mucous membranes and were also known to have some effect on the myocardium. Mautz tried procaine, but its action was short-lived owing to digestion by esterases. From procaine Mautz synthesized procainamide, which is not a substrate for esterases. Procainamide has the additional advantage of being active by mouth. Procainamide was approved by the US FDA on June 2, 1950 under the brand name Pronestyl. In 1951 Pronestyl was launched by Bristol-Myers Squibb, a pharmaceutical company in the US. Along with the discovery of procainamide came the discovery of its metabolite acecainide.
Procainamide is metabolized in the liver to acecainide by N-acetyltransferase, an enzyme that is genetically determined.N-Acetyltransferase is an enzyme that catalyzes the transfer of acetyl groups from acetyl-CoA to arylamines and aromatic amines such as procainamide.
This reaction is known as an acetylation reaction, that refers to the process of introducing an acetyl group (resulting in an acetoxy group) into a compound, namely the substitution of an acetyl group for an active hydrogen atom.
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