Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
SODIUM P.A.S. vs P.A.S. SODIUM
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Sodium P. A. S. (para-aminosalicylate) inhibits folic acid synthesis in Mycobacterium tuberculosis by competing with para-aminobenzoic acid, thereby suppressing bacterial growth.
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.
Treatment of tuberculosis as part of a multi-drug regimen (FDA-approved),Off-label: treatment of inflammatory bowel disease (ulcerative colitis, Crohn's disease) and other mycobacterial infections
Treatment of tuberculosis (TB) in combination with other antituberculosis agents, particularly in multidrug-resistant TB (FDA-approved).,Off-label: Used as a second-line agent in atypical mycobacterial infections and in Crohn's disease (though not FDA-approved for these indications).
4 g orally three times daily (total 12 g/day). For intravenous administration, 4 g (10 m L of 40% solution) diluted in 250 m L of 5% dextrose or normal saline infused over 2-3 hours three times daily.
Oral: 4 g three times daily (total daily dose 12 g); IV: 12 g daily in 2-4 divided doses.
0.5–1 hour (normal renal function); prolonged to ≥10 hours in renal impairment (requires dose adjustment).
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
Hepatic acetylation via N-acetyltransferase (NAT2); undergoes conjugation with glycine and glucuronic acid.
Primarily metabolized by hepatic acetylation via N-acetyltransferase (NAT); minor pathways include glycine conjugation and renal excretion of unchanged drug.
Primarily renal (80-90% as unchanged drug) via glomerular filtration and tubular secretion; biliary/fecal ≤10%.
Renal (80% as active drug and metabolites, primarily acetylated form); fecal (minor; <10%)
50–60% bound to serum albumin.
50-60% (primarily to albumin)
0.2–0.4 L/kg (suggests low tissue penetration, primarily extracellular).
0.5-0.6 L/kg (indicates distribution into total body water, with some tissue binding)
Oral: ~80–90%. IV: 100%.
Oral: approximately 90% (well absorbed from GI tract)
GFR 30-50 m L/min: administer every 12 hours. GFR 10-30 m L/min: administer every 24 hours. GFR <10 m L/min: administer every 48 hours or avoid use.
Cr Cl <50 m L/min: reduce dose by 50%; Cr Cl <10 m L/min: avoid use or reduce to 25% of normal dose.
Child-Pugh Class A: no adjustment. Child-Pugh Class B: reduce dose by 50%. Child-Pugh Class C: avoid use due to risk of hepatotoxicity.
Child-Pugh A: no adjustment; Child-Pugh B: reduce dose by 50%; Child-Pugh C: avoid use.
Children: 150-300 mg/kg/day orally in 3-4 divided doses, maximum 12 g/day. Intravenous: 150-300 mg/kg/day in divided doses every 6-8 hours.
Oral: 200-300 mg/kg/day in 3-4 divided doses, maximum 12 g/day.
Start at lower end of dosing range (e.g., 4 g orally twice daily) and titrate based on renal function. Monitor for electrolyte disturbances and hepatotoxicity.
Start at lower end of dosing range; monitor renal function and adjust based on Cr Cl; typical initial dose 4 g twice daily.
No FDA black box warning.
None explicitly stated in current FDA labeling; however, caution is advised in hepatic impairment due to risk of hepatitis.
Hepatotoxicity, including hepatic necrosis and jaundice,Hypersensitivity reactions (drug rash, fever, eosinophilia),Gastrointestinal intolerance (nausea, vomiting, diarrhea),Renal impairment may require dose adjustment,Monitor liver function tests, blood counts, and renal function
May cause severe hypersensitivity reactions (e.g., fever, rash, lymphadenopathy).,Hepatic toxicity: risk of hepatitis, especially with prolonged use; monitor liver function.,Renal impairment: dose adjustment required in severe renal disease.,Gastrointestinal intolerance: nausea, vomiting, diarrhea common.,Development of resistance if used as monotherapy.,May induce hemolytic anemia in G6PD deficiency.
Hypersensitivity to para-aminosalicylate or any component,Severe hepatic impairment,Severe renal impairment (Cr Cl < 30 m L/min)
Hypersensitivity to p-aminosalicylic acid or any component.,Severe hepatic impairment.,Severe renal failure (unless dose-adjusted).,Contraindicated in patients with active peptic ulcer disease.
Take with food to minimize gastrointestinal irritation. Avoid alcohol due to hepatotoxicity risk. No significant food-drug interactions except for potential interference with vitamin B12 absorption; consider monitoring B12 levels with prolonged use.
Take with food, especially acidic foods (e.g., applesauce, yogurt) to improve taste and reduce gastrointestinal irritation. Avoid alkaline foods (e.g., milk, antacids) as they may decrease absorption. Avoid alcohol due to increased risk of hepatotoxicity.
PAS is not associated with major congenital malformations. First trimester: no significant increase in defect risk. Second/third trimester: may increase risk of maternal hemolysis in G6PD deficiency; no direct fetal toxicity reported. Limited human data.
First trimester: No evidence of teratogenicity in human studies; limited animal data show no adverse effects. Second trimester: No specific risks identified. Third trimester: No known adverse fetal effects; use only if clearly needed.
PAS enters breast milk in low concentrations; M/P ratio unknown. Considered compatible with breastfeeding by American Academy of Pediatrics, but monitor infant for gastrointestinal disturbances or allergic reactions.
Excreted into breast milk in low amounts; M/P ratio not determined. Considered compatible with breastfeeding; monitor infant for diarrhea or rash.
Pregnancy may decrease serum concentrations due to increased renal clearance. Monitor therapeutic levels if available; consider increasing dose if subtherapeutic. No standard dose adjustment, but individual titration based on clinical response and serum levels recommended.
No pharmacokinetic changes requiring dose adjustment in pregnancy; use standard dosing but monitor for hepatotoxicity, which may be increased.
Sodium P. A. S. (para-aminosalicylic acid) is a second-line antitubercular agent used in combination therapy for multidrug-resistant tuberculosis (MDR-TB). Administer with food to reduce gastrointestinal irritation. Monitor liver function tests due to hepatotoxicity risk. May cause hypothyroidism; monitor thyroid function. Avoid in patients with severe renal impairment (Cr Cl <30 m L/min).
Sodium aminosalicylate (PAS sodium) is a second-line antituberculosis agent used in multidrug-resistant TB (MDR-TB). It is bacteriostatic against Mycobacterium tuberculosis by inhibiting folate synthesis. Must be administered with other antitubercular drugs to prevent resistance. Monitor for hepatotoxicity, hypersensitivity reactions (fever, rash, eosinophilia), and gastrointestinal intolerance. Can cause hypothyroidism; monitor thyroid function. Drug interactions: may increase phenytoin levels; avoid concurrent probenecid (increases PAS levels). PAS granules should be sprinkled on soft acidic food to reduce GI upset.
Take with food to reduce stomach upset.,Complete full course of therapy as prescribed, even if you feel better.,Report any signs of liver problems: yellowing of skin/eyes, dark urine, severe nausea/vomiting.,May cause hypothyroidism; report fatigue, weight gain, or cold intolerance.,Avoid alcohol due to increased risk of liver damage.
Take this medication exactly as prescribed, usually twice daily with food to reduce stomach upset.,Do not skip doses; complete the full course to prevent drug resistance.,Report any signs of liver problems: yellowing of skin/eyes, dark urine, severe abdominal pain.,Notify your doctor if you develop fever, rash, or unusual tiredness.,You may need regular blood tests to monitor thyroid and liver function.,Avoid alcohol while taking this medication.,Keep all appointments for TB treatment monitoring.
No interactions on record
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about SODIUM P.A.S. vs P.A.S. SODIUM, answered by our medical review team.
SODIUM P.A.S. is a Antitubercular Agent that works by Sodium P. A. S. (para-aminosalicylate) inhibits folic acid synthesis in Mycobacterium tuberculosis by competing with para-aminobenzoic acid, thereby suppressing bacterial growth.. P.A.S. SODIUM is a Antitubercular Agent that works by 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.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between SODIUM P.A.S. and P.A.S. SODIUM depend on the specific clinical indication. These are both Antitubercular Agent agents and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of SODIUM P.A.S. is: 4 g orally three times daily (total 12 g/day). For intravenous administration, 4 g (10 m L of 40% solution) diluted in 250 m L of 5% dextrose or normal saline infused over 2-3 hours three times daily.. The standard adult dose of P.A.S. SODIUM is: Oral: 4 g three times daily (total daily dose 12 g); IV: 12 g daily in 2-4 divided doses.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between SODIUM P.A.S. and P.A.S. SODIUM in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. SODIUM P.A.S. is classified as Category C. PAS is not associated with major congenital malformations. First trimester: no significant increase in defect risk. Second/third trimester: may increase risk of maternal hemolysis . P.A.S. SODIUM is classified as Category C. First trimester: No evidence of teratogenicity in human studies; limited animal data show no adverse effects. Second trimester: No specific risks identified. Third trimester: No kn. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.