Aminosalicylic acid: Difference between revisions
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'''| [[Aminosalicylic acid adverse reactions|Adverse Reactions]]''' | '''| [[Aminosalicylic acid adverse reactions|Adverse Reactions]]''' | ||
'''| [[Aminosalicylic acid overdosage|Overdosage]]''' | '''| [[Aminosalicylic acid overdosage|Overdosage]]''' | ||
'''| [[Aminosalicylic acid dosage and administration|Dosage and Administration]]''' | '''| [[Aminosalicylic acid dosage and administration|Dosage and Administration]]''' | ||
'''| [[Aminosalicylic acid how supplied|How Supplied]]''' | '''| [[Aminosalicylic acid how supplied|How Supplied]]''' | ||
Revision as of 02:18, 31 December 2013
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chetan Lokhande, M.B.B.S [2]
Synonyms and keywords: para-aminosalicylic acid, p-aminosalicylic acid or 4-aminosalicylic acid; abbreviated 4-ASA, or PAS
Overview
Aminosalicylic acid is an antibiotic used to treat tuberculosis. It has been use for over forty years in the treatment of inflammatory bowel disease (IBD), where it has shown greater potency in Crohn's disease. It is thought to act via NF-κB (nuclear factor-kappa B) inhibition and free radical scavenging.
Aminosalicylic acid is sold in the United States by Jacobus Pharmaceutical as PASER®.
Mesalazine (5-aminosalicylic acid) is a closely related compound that also has medical uses.
Category
Antimycobacterial
US Brand Names
PASER®
FDA Package Insert
Description | Clinical Pharmacology | Microbiology | Indications and Usage | Contraindications | Warnings and Precautions | Adverse Reactions | Overdosage | Dosage and Administration | How Supplied | Labels and Packages
Mechanism of Action
Aminosalicylic acid is an analogue of para-aminobenzoic acid (PABA) and acts as a competitive inhibitor of dihydropteroate synthase 1 (folP1). Its competitive antagonism with PABA is similar to the action of sulfonamides which disrupts biosynthesis in sensitive organisms. Aminosalicylic acid is bacteriostatic against Mycobacterium tuberculosis. It inhibits the onset of bacterial resistance to streptomycin and isoniazid. Other mechanism of action has been postulated to be inhibition of synthesis of the cell wall component, mycobactin, thus reducing iron uptake by M. tuberculosis.