Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
CAPREOMYCIN SULFATE 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
Inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of m RNA and inhibiting translation initiation. Also alters membrane permeability.
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 pulmonary tuberculosis as part of combination therapy,Salvage therapy for multidrug-resistant tuberculosis
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).
15 mg/kg (up to 1 g) intramuscularly or intravenously once daily for 60 days, then 15 mg/kg (up to 1 g) 2-3 times weekly for 12-18 months in combination with other antituberculosis agents.
Oral: 4 g three times daily (total daily dose 12 g); IV: 12 g daily in 2-4 divided doses.
Terminal elimination half-life: 24-40 hours (prolonged in renal impairment; anuria may extend to 96-120 hours).
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
Not significantly metabolized; primarily excreted unchanged in urine via glomerular filtration.
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). Biliary/fecal elimination: <1%.
Renal (80% as active drug and metabolites, primarily acetylated form); fecal (minor; <10%)
Approximately 30% bound to serum proteins (albumin).
50-60% (primarily to albumin)
0.4-0.6 L/kg (suggests distribution primarily into extracellular fluid; poor CNS penetration unless meninges inflamed).
0.5-0.6 L/kg (indicates distribution into total body water, with some tissue binding)
IM: 100% (only IM route available; no oral formulation).
Oral: approximately 90% (well absorbed from GI tract)
Cr Cl 50-80 m L/min: 15 mg/kg every 24-36 hours; Cr Cl 30-50 m L/min: 15 mg/kg every 48 hours; Cr Cl 10-30 m L/min: 15 mg/kg every 72 hours; Cr Cl <10 m L/min: 15 mg/kg every 96-120 hours.
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.
No dose adjustment required for hepatic impairment; monitor for hepatotoxicity.
Child-Pugh A: no adjustment; Child-Pugh B: reduce dose by 50%; Child-Pugh C: avoid use.
15-30 mg/kg intramuscularly or intravenously once daily (maximum 1 g) for 60 days, then 15-30 mg/kg 2-3 times weekly (maximum 1 g).
Oral: 200-300 mg/kg/day in 3-4 divided doses, maximum 12 g/day.
Initiate at lower end of dosing range; adjust based on renal function due to age-related decline in glomerular filtration rate.
Start at lower end of dosing range; monitor renal function and adjust based on Cr Cl; typical initial dose 4 g twice daily.
None officially listed by FDA; however, use with caution due to potential nephrotoxicity and ototoxicity.
None explicitly stated in current FDA labeling; however, caution is advised in hepatic impairment due to risk of hepatitis.
Nephrotoxicity: Monitor renal function; risk increases with cumulative dose and concomitant nephrotoxic drugs.,Ototoxicity: Can cause vestibular and cochlear damage, especially in patients with renal impairment.,Neuromuscular blockade: May exacerbate weakness in patients with myasthenia gravis or other neuromuscular disorders.,Electrolyte disturbances: Hypokalemia, hypocalcemia, and hypomagnesemia due to renal tubular effects.
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 capreomycin or any component,Pre-existing severe renal impairment (Cr Cl < 30 m L/min) unless benefit outweighs risk,Pre-existing hearing loss
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.
No specific food interactions. However, maintain adequate hydration and electrolyte-rich diet (bananas, potatoes) to mitigate hypokalemia.
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.
Animal studies suggest embryotoxicity and teratogenicity; human data limited. Avoid in first trimester; use in second and third trimesters only if clearly needed. Risk of ototoxicity and nephrotoxicity to fetus.
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.
Small amounts excreted in breast milk; not expected to cause adverse effects in infants due to poor oral absorption. M/P ratio unknown.
Excreted into breast milk in low amounts; M/P ratio not determined. Considered compatible with breastfeeding; monitor infant for diarrhea or rash.
No dose adjustment recommended for pregnancy alone; however, concurrent use may require monitoring and adjustment. No pharmacokinetic changes reported.
No pharmacokinetic changes requiring dose adjustment in pregnancy; use standard dosing but monitor for hepatotoxicity, which may be increased.
Capreomycin is a second-line injectable agent for multidrug-resistant tuberculosis (MDR-TB). Monitor for nephrotoxicity (creatinine, BUN) and ototoxicity (audiometry, vestibular testing). Electrolyte disturbances (hypokalemia, hypomagnesemia) are common; replace aggressively. Administer deep IM injection; rotate sites. Contraindicated in pregnancy (teratogenic). Synergistic with other antituberculars; never use as monotherapy.
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 exactly as prescribed; do not skip doses to prevent resistance.,Report hearing loss, ringing in ears, or dizziness immediately.,Report decreased urine output, swelling, or unusual fatigue.,You will need regular blood tests (kidney function, electrolyte levels).,Avoid alcohol and excessive salt intake.,Contact your doctor if you develop severe injection site pain or fever.
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.
"Decamethonium, a depolarizing neuromuscular blocker, and capreomycin, an aminoglycoside antibiotic, synergistically prolong neuromuscular blockade. Capreomycin decreases acetylcholine release at the motor endplate, while decamethonium persistently depolarizes the postsynaptic membrane, leading to enhanced and prolonged muscle relaxation. This interaction can result in extended respiratory depression and apnea, particularly during anesthesia or in critically ill patients."
"Streptozocin, a nitrosourea alkylating agent, may potentiate the neuromuscular blocking effects of capreomycin, a cyclic polypeptide antibiotic that inhibits neuromuscular transmission by reducing acetylcholine release at the motor endplate. This interaction can lead to prolonged or enhanced muscle weakness, including respiratory depression, particularly in patients with underlying neuromuscular disorders (e.g., myasthenia gravis) or those receiving other neuromuscular blocking agents. The clinical outcome may range from mild skeletal muscle weakness to severe respiratory compromise requiring mechanical ventilation."
"Paromomycin, an aminoglycoside antibiotic, and capreomycin, a polypeptide antibiotic, both possess neuromuscular blocking properties. Their co-administration can result in additive or synergistic neuromuscular blockade, potentially leading to prolonged or enhanced muscle relaxation, respiratory depression, or apnea. This interaction is particularly dangerous in patients receiving general anesthetics, neuromuscular blocking agents, or those with underlying neuromuscular disorders such as myasthenia gravis."
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about CAPREOMYCIN SULFATE vs P.A.S. SODIUM, answered by our medical review team.
CAPREOMYCIN SULFATE is a Antitubercular Agent that works by Inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of m RNA and inhibiting translation initiation. Also alters membrane permeability.. 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 CAPREOMYCIN SULFATE 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 CAPREOMYCIN SULFATE is: 15 mg/kg (up to 1 g) intramuscularly or intravenously once daily for 60 days, then 15 mg/kg (up to 1 g) 2-3 times weekly for 12-18 months in combination with other antituberculosis agents.. 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 CAPREOMYCIN SULFATE 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. CAPREOMYCIN SULFATE is classified as Category C. Animal studies suggest embryotoxicity and teratogenicity; human data limited. Avoid in first trimester; use in second and third trimesters only if clearly needed. Risk of ototoxici. 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.