Comparative Pharmacology
Head-to-head clinical analysis: INH versus P A S SODIUM.
Peer-Reviewed Evidence
Head-to-head clinical analysis: INH versus P A S SODIUM.
INH vs P.A.S. SODIUM
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
INH inhibits InhA, an enoyl-acyl carrier protein reductase involved in mycolic acid synthesis, essential for the mycobacterial cell wall. It also disrupts NAD and NADH metabolism via the KatG-activated isonicotinoyl-NAD adduct.
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.
300 mg orally once daily (or 15 mg/kg orally once daily, up to 300 mg total) for active tuberculosis; for latent tuberculosis, 300 mg orally once daily or 900 mg orally twice weekly under directly observed therapy.
Oral: 4 g three times daily (total daily dose 12 g); IV: 12 g daily in 2-4 divided doses.
None Documented
None Documented
Fast acetylators: 0.5-1.5 hours; slow acetylators: 2-4 hours. Clinically, slow acetylators have higher risk of peripheral neuropathy and hepatotoxicity.
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
Renal: 75-95% as unchanged drug and metabolites (including acetylisoniazid, isonicotinic acid). Biliary/fecal: minor (<5%).
Renal (80% as active drug and metabolites, primarily acetylated form); fecal (minor; <10%)
Category C
Category C
Antitubercular Agent
Antitubercular Agent