Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
CAPREOMYCIN SULFATE vs INH
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.
INH inhibits Inh A, 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 Kat G-activated isonicotinoyl-NAD adduct.
Treatment of pulmonary tuberculosis as part of combination therapy,Salvage therapy for multidrug-resistant tuberculosis
First-line treatment and prophylaxis of tuberculosis (TB) caused by Mycobacterium tuberculosis
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.
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.
Terminal elimination half-life: 24-40 hours (prolonged in renal impairment; anuria may extend to 96-120 hours).
Fast acetylators: 0.5-1.5 hours; slow acetylators: 2-4 hours. Clinically, slow acetylators have higher risk of peripheral neuropathy and hepatotoxicity.
Not significantly metabolized; primarily excreted unchanged in urine via glomerular filtration.
Primarily hepatic via N-acetyltransferase 2 (NAT2); also metabolized by cytochrome P450 (CYP2E1) to hepatotoxic metabolites.
Primarily renal (80-90% as unchanged drug via glomerular filtration). Biliary/fecal elimination: <1%.
Renal: 75-95% as unchanged drug and metabolites (including acetylisoniazid, isonicotinic acid). Biliary/fecal: minor (<5%).
Approximately 30% bound to serum proteins (albumin).
0-10% (low binding; primarily albumin).
0.4-0.6 L/kg (suggests distribution primarily into extracellular fluid; poor CNS penetration unless meninges inflamed).
0.6-0.8 L/kg (distributes into total body water, including cerebrospinal fluid and tuberculous cavities).
IM: 100% (only IM route available; no oral formulation).
Oral: ~90%. Intramuscular: ~100%.
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.
In patients with GFR < 30 m L/min, reduce dose to 200 mg daily or 300 mg three times weekly. For GFR 30-50 m L/min, no adjustment necessary. For GFR < 10 m L/min, consider 150 mg daily or 300 mg twice weekly.
No dose adjustment required for hepatic impairment; monitor for hepatotoxicity.
In Child-Pugh class A, no adjustment. In Child-Pugh class B, reduce dose to 200 mg daily. In Child-Pugh class C, use 150 mg daily or avoid if severe hepatic impairment.
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).
10-15 mg/kg orally once daily (max 300 mg) for active tuberculosis; for latent tuberculosis, 10-15 mg/kg orally once daily (max 300 mg) or 20-40 mg/kg orally twice weekly (max 900 mg per dose).
Initiate at lower end of dosing range; adjust based on renal function due to age-related decline in glomerular filtration rate.
No specific dose adjustment required, but monitor for hepatotoxicity and peripheral neuropathy, especially in patients with comorbidities or polypharmacy.
None officially listed by FDA; however, use with caution due to potential nephrotoxicity and ototoxicity.
Severe and sometimes fatal hepatitis (especially in patients >35 years, daily alcohol users, and those with pre-existing liver disease); monitor hepatic function closely.
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.
Hepatotoxicity (monitor LFTs, discontinue if signs of hepatitis),Peripheral neuropathy (pyridoxine prophylaxis recommended),CNS effects (seizures, psychosis; avoid in active CNS disease),Lupus-like syndrome,Drug interactions (e.g., carbamazepine, phenytoin)
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
Acute liver disease,History of INH-induced hepatotoxicity,Previous severe adverse reaction (e.g., drug fever, arthritis)
No specific food interactions. However, maintain adequate hydration and electrolyte-rich diet (bananas, potatoes) to mitigate hypokalemia.
Foods high in tyramine (e.g., aged cheese, cured meats, soy products) may rarely cause hypertensive crisis in patients also taking MAOIs, though interaction is less significant with INH alone. High-fat meals may delay absorption, so avoid fatty foods near dosing time. No specific dietary restrictions beyond taking on empty stomach.
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.
INH (isoniazid) is not known to be a major teratogen. In first trimester, risk of malformations is not significantly increased. In second and third trimesters, there is a potential for hepatotoxicity and peripheral neuropathy, and possibly increased risk of neonatal hemorrhage due to vitamin K deficiency.
Small amounts excreted in breast milk; not expected to cause adverse effects in infants due to poor oral absorption. M/P ratio unknown.
INH is excreted into breast milk in low concentrations (M/P ratio approximately 1.6). Breastfeeding is generally considered safe, but monitor infant for signs of peripheral neuropathy or liver toxicity. The American Academy of Pediatrics considers INH compatible with breastfeeding.
No dose adjustment recommended for pregnancy alone; however, concurrent use may require monitoring and adjustment. No pharmacokinetic changes reported.
No dose adjustment is routinely required for pregnancy. However, due to increased clearance (30-50% higher), some experts recommend monitoring serum INH levels and adjusting dose to maintain therapeutic levels. Pyridoxine supplementation (25-50 mg/day) is recommended to prevent peripheral neuropathy.
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.
Administer on an empty stomach (1 hour before or 2 hours after meals) to maximize absorption. Monitor liver function tests (ALT, AST) at baseline and monthly during therapy. Pyridoxine (vitamin B6) 25-50 mg/day should be co-administered to prevent peripheral neuropathy. Hepatotoxicity risk increases with age, alcohol use, and concurrent use of other hepatotoxic drugs. Slow acetylators are more prone to toxicity. Patients with liver disease require careful monitoring and dose adjustment.
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 on an empty stomach with a full glass of water.,Do not drink alcohol while taking this medication due to increased risk of liver damage.,Report immediately any signs of liver problems: dark urine, yellowing of skin or eyes, persistent nausea, or abdominal pain.,Take vitamin B6 as prescribed to prevent numbness or tingling in hands and feet.,Complete full course of therapy even if you feel better to prevent resistance.,Avoid antacids within 1 hour of taking this medication as they may reduce absorption.
"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 INH, 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.. INH is a Antitubercular Agent that works by INH inhibits Inh A, 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 Kat G-activated isonicotinoyl-NAD adduct.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between CAPREOMYCIN SULFATE and INH 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 INH is: 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.. 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 INH 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. INH is classified as Category C. INH (isoniazid) is not known to be a major teratogen. In first trimester, risk of malformations is not significantly increased. In second and third trimesters, there is a potential. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.