PAS formed part of the standard treatment for tuberculosis prior to the introduction of rifampicin and pyrazinamide.

[14] Gastrointestinal side-effects (nausea, vomiting, diarrhoea) are common; the delayed-release formulation is meant to help overcome this problem.

Patients with glucose-6-phosphate dehydrogenase deficiency should avoid taking aminosalicylic acid as it causes haemolysis.

[21] Some studies have shown that principal antitubercular action of PAS occurs via poisoning of folate metabolism.

[22] It was initially thought that resistance of 4-aminosalicylic acid came from a mutation affecting dihydrofolate reductase (DHFR).

The mutations of isoleucine 43, arginine 49, serine 150, phenylalanine 152, glutamate 153, and alanine 183 were found to affect the binding pocket of the dihydrofolate synthase enzyme.

This will reduce the ability for hydroxy-H2Pte to bind to dihydrofolate synthase and preventing 4-aminosalicylic acid from poisoning the folate metabolism.

[4] It was rediscovered by the Swedish chemist Jörgen Lehmann upon the report that the tuberculosis bacterium avidly metabolized salicylic acid.

[25] The drug proved better than streptomycin, which had nerve toxicity and to which TB could easily develop resistance.