Comparative Pharmacology
Head-to-head clinical analysis: P A S SODIUM versus SODIUM AMINOSALICYLATE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: P A S SODIUM versus SODIUM AMINOSALICYLATE.
P.A.S. SODIUM vs SODIUM AMINOSALICYLATE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
P.A.S. (p-aminosalicylic acid) sodium is a bacteriostatic agent that competitively inhibits the synthesis of folic acid in Mycobacterium tuberculosis by antagonizing the incorporation of p-aminobenzoic acid (PABA) into dihydrofolate. It is selective for mycobacterial folate synthase.
Sodium aminosalicylate inhibits folic acid synthesis in Mycobacterium tuberculosis by competing with para-aminobenzoic acid (PABA) for the enzyme dihydropteroate synthase, thereby blocking bacterial growth.
Oral: 4 g three times daily (total daily dose 12 g); IV: 12 g daily in 2-4 divided doses.
4 g orally three times daily (total daily dose 12 g) for tuberculosis treatment. Also available as 10 g in 250 mL for intravenous infusion over 5-6 hours, typically once daily.
None Documented
None Documented
1 hour (normal renal function); prolonged to 5-7 hours in anuria or severe renal impairment; clinical context: requires frequent dosing or renal dose adjustment
0.75-1.5 hours (parent drug); prolongs to 4-6 hours in renal impairment or with probenecid coadministration. Rapid acetylation phenotype reduces half-life by ~30%.
Renal (80% as active drug and metabolites, primarily acetylated form); fecal (minor; <10%)
Renal: >80% as metabolites (acetylated and free), with 50-60% as N-acetyl-4-aminosalicylic acid; biliary/fecal: <1%.
Category C
Category C
Antitubercular Agent
Antitubercular Agent