which are excreted via the urine. N-acetyl-4-aminobenzoic acid as well as N-acetyl-3-hydroxyprocainamide, N-acetylprocainamide-N-oxide and N-acetyl-4-aminohippuric acid are also metabolites of procainamide. Chemistry 4-amino-N-2-(diethylamino)ethyl-benzamide (also known as para-amino-N-2-(diethylamino)ethyl-benzamide because the amino substituent is attached to the para-position, Arene substitution patterns of the benzene ring) is a synthetic organic compound with the chemical formula C13-H21-N3-O. Procainamide is structurally similar to procaine, but in place of an ester group, procainamide contains an amide group. This substitution is the reason why procainamide exhibits a longer half-life time than procaine. Procainamide belongs to the aminobenzamides. These are aromatic carboxylic acid derivatives consisting of an amide with a benzamide moiety and a triethylamine attached to the amide nitrogen. In certain lines, the para-amino group might become a target site to attach further paraphernalia, e.g. ref. Ex18 in . History Procainamide was approved by the US FDA on June 2, 1950, under the brand name "Pronestyl". It was launched by Bristol-Myers Squibb in 1951. Due to the loss of Indonesia in World War II, the source for cinchona alkaloids, a precursor of quinidine, was reduced. This led to research for a new antiarrhythmic drug. As a result, procaine was discovered, which has similar cardiac effects as quinidine. In 1936 it was found by Mautz that by applying it directly on the myocardium, the ventricular threshold for electrical stimulation was elevated. This mechanism is responsible for the antiarrhythmic effect. However, due to the short duration of action, caused by rapid enzymatic hydrolysis, its therapeutic applications were limited. In addition, procaine also caused tremors and respiratory depression. All these adverse features stimulated the search for an alternative to procaine. Studies were done on various congeners and metabolites and this ultimately led to the discovery of procainamide by Mark et al. It was found that procainamide was effective for treating ventricular arrhythmias, but it had the same toxicity profile as quinidine, and it could cause systemic lupus erythematosus-like syndrome. These negative characteristics slowed the search for new antiarrhythmics based on the chemical structure of procainamide. In 1970 only five drugs were reported. These were the cardiac glycosides, quinidine, propranolol, lidocaine and diphenylhydantoin. In January 1996, extended release procainamide hydrochloride (Procanbid extended-release tablets) was approved by the FDA. References Anilines Antiarrhythmic agents Benzamides Diethylamino compounds Sodium channel blockers