(isoniazid · DailyMed)
RIFAMPIN / ISONIAZID/ PYRIZINAMIDE TABLETS (Each tablet contains Rifampicin/Isoniazid/Pyrizinamide 75mg / 50mg/ 150mg)
Rifampicin/Isoniazid/Pyrizinamide
What it does
Isoniazid is a medication used to treat tuberculosis, a serious infection that mainly affects the lungs.
Commonly used for: tuberculosis (TB), pulmonary tuberculosis
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Sourcing - Kenya onlyRegistration & product details
Source: Food and Drugs Authority · fetched 2026-04-18 08:33:05 · updated 2026-10-27 04:00:08
Drug Interactions
292Pharmacodynamic Warnings
Isoniazid appears in TABLE 1: Drugs that cause hepatotoxicity
Isoniazid appears in TABLE 12: Drugs that cause peripheral neuropathy
Severe (78)
Abemaciclib - decreases exposure
Rifampicin is predicted to markedly decrease the exposure to abemaciclib. Avoid.
Abiraterone - decreases exposure
Rifampicin is predicted to decrease the exposure to anti-androgens (abiraterone). Avoid.
Acalabrutinib - decreases exposure
Rifampicin is predicted to decrease the exposure to acalabrutinib. Avoid.
Anti-Androgens - decreases exposure
Rifampicin is predicted to decrease the exposure to anti-androgens (abiraterone). Avoid.
Antiarrhythmics - decreases exposure
Rifampicin is predicted to decrease the exposure to antiarrhythmics (disopyramide, dronedarone). Avoid.
Moderate (72)
Alprazolam - decreases exposure
Rifampicin is predicted to decrease the exposure to benzodiazepines (alprazolam). Adjust dose.
Amlodipine - decreases exposure
Rifampicin is predicted to decrease the exposure to calcium channel blockers (amlodipine, felodipine, lacidipine, lercanidipine, nicardipine, nimodipine). Monitor and adjust dose.
Antiepileptics - decreases exposure
Rifampicin slightly decreases the exposure to antiepileptics (brivaracetam). Adjust dose.
Antiepileptics - decreases concentration
Rifampicin decreases the concentration of antiepileptics (fosphenytoin, phenytoin). Use with caution and adjust dose.
Antifungals,azoles - decreases exposure
Rifampicin slightly decreases the exposure to antifungals, azoles (fluconazole). Adjust dose.
Unknown (142)
Abrocitinib - decreases exposure
Rifampicinispredictedtodecreasetheexposuretoabrocitinib. Avoid.oStudy
Afatinib - decreases exposure
Rifampicin is predicted to decrease the exposure to afatinib.
Agomelatine - decreases exposure
Rifampicinispredictedtodecreasetheexposureto agomelatine.oTheoretical
Alfentanil - decreases exposure
Rifampicin is predicted to decrease the exposure to opioids (alfentanil, fentanyl).
Aliskiren - decreases exposure
Rifampicin decreases the exposure to aliskiren.
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About isoniazid
Isoniazid is a medication used to treat tuberculosis, a serious infection that mainly affects the lungs.
What it treats
- tuberculosis (TB)
- pulmonary tuberculosis
How it works
Isoniazid works by stopping the growth of bacteria that cause tuberculosis.
Who it's for
This medicine is for individuals diagnosed with tuberculosis.
Cautions
- • Be cautious if you are taking other medications that can harm the liver.
- • Be careful if you are using drugs that can cause nerve damage.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
About pyrizinamide
Pyrizinamide is a medication used to help treat certain infections.
What it treats
- tuberculosis (TB)
- bacterial infections
How it works
It works by stopping the growth of bacteria that cause infections.
Who it's for
This medicine is for people diagnosed with specific bacterial infections, particularly tuberculosis.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
About rifampicin
Rifampicin is an antibiotic used to treat bacterial infections, especially tuberculosis.
What it treats
- tuberculosis (TB)
- bacterial infections
How it works
Rifampicin works by stopping the growth of bacteria, helping to clear infections from the body.
Who it's for
Rifampicin is for adults and children who have specific bacterial infections, particularly those with tuberculosis.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Rifampicin
BNF-referencedRifampicin is a bactericidal antibiotic that is primarily used to treat infections caused by mycobacteria, particularly tuberculosis. It works by inhibiting RNA synthesis in bacteria, making it effective against both intracellular and extracellular strains of Mycobacterium tuberculosis. It is often used in combination with other antitubercular agents to prevent the development of drug resistance.
Indications
- Tuberculosis, in combination with other drugs
- Prevention of tuberculosis in susceptible close contacts
- Brucellosis in combination with other antibacterials
- Legionnaires disease in combination with other antibacterials
- Serious staphylococcal infections in combination with other antibacterials
- Endocarditis in combination with other drugs
Dosage
Children: For children aged 1–11 years: 10 mg/kg every 12 hours (maximum per dose 600 mg
Adults: 600 mg daily for 6 months, or 600 mg every 12 hours for 2 days in specific conditions such as endocarditis.
Mechanism of action
Rifampicin binds to the beta-subunit of microbial DNA-dependent RNA polymerase, inhibiting the enzyme and impeding RNA synthesis. This action forms a stable drug-enzyme complex that suppresses the initiation of chain formation in RNA synthesis, although it does not affect chain elongation. Importantly, rifampicin has no activity against mammalian RNA polymerase, highlighting its selective antibacterial properties.
Pharmacodynamics
Rifampicin exhibits broad-spectrum antimicrobial activity, particularly against Mycobacterium tuberculosis. It is bactericidal, effective in killing both intracellular and extracellular bacteria. The drug's efficacy is enhanced when used in combination with other antitubercular medications, helping to reduce the risk of developing multi-drug resistant tuberculosis.
Pharmacokinetics
Rifampicin is well absorbed after oral administration, with peak plasma concentrations occurring within 2 to 4 hours. It is extensively metabolized in the liver, primarily by cytochrome P450 enzymes, and has a half-life of approximately 3 to 5 hours. The drug is excreted mainly in bile, with some renal excretion. It also has the potential to induce liver enzymes, which may affect the metabolism of co-administered drugs.
Contra-indications
- Acute porphyrias
- Jaundice
Adverse effects
- Nausea
- Vomiting
- Diarrhoea
- Abdominal discomfort
- Thrombocytopenia
- Leucopenia
- Acute kidney injury
- Adrenal insufficiency
- Agranulocytosis
- Discoloration of soft contact lenses
Interactions
- Severe interaction with atovaquone (increases exposure)
- Severe interaction with abemaciclib (decreases exposure)
- Severe interaction with acalabrutinib (decreases exposure)
- Severe interaction with anti-androgens (decreases exposure)
- Severe interaction with abiraterone (decreases exposure)
- Severe interaction with darolutamide (decreases exposure)
- Severe interaction with antiarrhythmics (decreases exposure)
- Severe interaction with disopyramide (decreases exposure)
- Severe interaction with dronedarone (decreases exposure)
- Severe interaction with isavuconazole (decreases exposure)
Pregnancy
Rifampicin should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus.
Breast-feeding
Rifampicin is excreted in breast milk. Caution is advised when administering to nursing mothers.
Storage
Store in a cool, dry place away from direct sunlight. Keep out of reach of children.
Formulations
- Oral capsules
- Oral suspension
- Injectable solution
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: Isoniazid
BNF-referencedIsoniazid is an antimycobacterial agent used primarily in the treatment and prevention of tuberculosis (TB). It functions as a prodrug that requires activation by bacterial catalase, leading to inhibition of mycolic acid synthesis, an essential component of the mycobacterial cell wall. Isoniazid is effective against actively dividing Mycobacterium tuberculosis and is known for its specificity towards mycobacterial infections.
Indications
- Treatment of active tuberculosis
- Prevention of tuberculosis in susceptible individuals, especially close contacts of infected persons
Dosage
Adults: 10 mg/kg daily (maximum per dose 300 mg) for 3 months, to be taken by mouth or via intramuscular or intravenous
Mechanism of action
Isoniazid is activated by the bacterial catalase-peroxidase KatG, which reduces the ferric form of the enzyme and enables it to react with oxygen to form an oxyferrous enzyme complex. The active form of isoniazid then inhibits the synthesis of mycolic acids by forming a covalent adduct with NAD, inhibiting the enoyl reductase InhA. This inhibition is crucial for the integrity of the mycobacterial cell wall, leading to the bactericidal activity of isoniazid against actively growing Mycobacterium tuberculosis.
Pharmacodynamics
Isoniazid is a bactericidal agent particularly effective against the Mycobacterium genus, including M. tuberculosis, M. bovis, and M. kansasii. It exhibits bactericidal properties during periods of rapid mycobacterial growth and becomes bacteriostatic when the bacteria are in a dormant state. Given its mechanism of action, isoniazid is highly selective, targeting mycobacteria without significant effects on other types of bacteria.
Pharmacokinetics
Isoniazid is well-absorbed following oral administration, with peak plasma concentrations occurring within 1 to 2 hours. It is widely distributed in body tissues and crosses the blood-brain barrier. The drug is metabolized in the liver primarily through acetylation, with variable metabolism rates observed in different populations due to genetic polymorphisms in acetylation. The elimination half-life ranges from 1 to 4 hours, and the drug is excreted in the urine, predominantly as metabolites.
Contra-indications
- History of hypersensitivity to isoniazid
- Acute liver disease
- Severe hepatic impairment
- Previous history of isoniazid-induced liver injury
Adverse effects
- Hepatitis
- Peripheral neuropathy
- Optic neuritis
- Gastrointestinal disturbances
- Rash
- Fever
- Agranulocytosis
- Hematological disorders
- Lupus-like syndrome
Interactions
- Carbamazepine: Increased risk of hepatotoxicity
- Cycloserine: Increased risk of CNS toxicity
- Phenytoin: Increased concentration of phenytoin
- Levodopa: Decreased effects of levodopa
- Lomitapide: Increased exposure
- Antiepileptics: Unknown interactions leading to increased concentrations
Precautions
- Monitor liver function during treatment
- Use with caution in patients with renal impairment
- Patients with diabetes or a history of peripheral neuropathy should be monitored closely
- Ocular monitoring for young children on treatment
Pregnancy
Not known to be harmful; however, prophylactic pyridoxine is recommended.
Breast-feeding
Amount too small to be harmful; monitor infant for possible toxicity.
Storage
Store in a cool, dry place away from direct sunlight. Keep out of reach of children.
Formulations
- Oral tablets
- Oral suspension
- Intramuscular injection
- Intravenous injection
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: pyrizinamide
BNF-referencedPyrazinamide is an antitubercular agent primarily used in combination therapy for the treatment of tuberculosis (TB). It is particularly effective against Mycobacterium tuberculosis, the bacterium responsible for TB. Pyrazinamide is unique in its action, enhancing the efficacy of other antitubercular drugs and improving treatment outcomes.
Indications
- Tuberculosis (TB)
- Mycobacterial infections
Dosage
Children: For children, the dosage should be determined based on weight, typically 15-30 mg/kg daily, with a maximum of 2 g per day. It is advised to refer to the BNF for Children for specific dosing recommendations.
Adults: The usual adult dosage for the treatment of tuberculosis is 25 mg/kg daily, not exceeding 2 g per day. It is typically administered in combination with other antitubercular agents.
Mechanism of action
Pyrazinamide is converted into its active form, pyrazinoic acid, by the enzyme pyrazinamidase present in Mycobacterium tuberculosis. Under acidic conditions, pyrazinoic acid accumulates within the bacterial cells, leading to disruption of membrane potential and interference with energy production. It has been proposed that pyrazinoic acid inhibits fatty acid synthase I, which is vital for the synthesis of fatty acids necessary for bacterial growth. Additionally, it may inhibit trans-translation by binding to ribosomal protein S1 (RpsA).
Pharmacodynamics
Pyrazinamide exhibits bactericidal activity against Mycobacterium tuberculosis, effectively halting the growth of the pathogen. Its activity is significantly enhanced in slightly acidic environments, which is characteristic of certain sites of infection in the body. The drug's mechanism of action involves interference with bacterial fatty acid synthesis and energy production, making it a vital component of TB treatment regimens.
Pharmacokinetics
Pyrazinamide is well absorbed after oral administration and is widely distributed throughout body tissues. The drug undergoes hepatic metabolism, with its metabolites being primarily excreted via the kidneys. The pharmacokinetics of pyrazinamide can be influenced by factors such as renal function and concomitant medications, necessitating careful monitoring in patients with compromised renal function.
Adverse effects
- Hepatotoxicity
- Nausea
- Vomiting
- Anorexia
- Fatigue
- Myalgia
- Arthralgia
- Rash
- Gout
Precautions
- Caution in patients with liver disease or impairment
- Monitor liver function tests during therapy
- Use with caution in patients with gout or a history of gout
Pregnancy
Pyrazinamide should only be used in pregnancy if the potential benefit justifies the potential risk to the fetus. Limited data available.
Breast-feeding
Pyrazinamide is excreted in breast milk. Caution should be exercised when administering to nursing mothers.
Storage
Store in a tightly closed container at room temperature, protected from light and moisture.
Formulations
- Tablets: 500 mg
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Isoniazid
PubChem CID 3767Molecular formula: C6H7N3O
Mechanism of action
Isoniazid is a prodrug and must be activated by bacterial catalase. Specficially, activation is associated with reduction of the mycobacterial ferric KatG catalase-peroxidase by hydrazine and reaction with oxygen to form an oxyferrous enzyme complex. Once activated, isoniazid inhibits the synthesis of mycoloic acids, an essential component of the bacterial cell wall. At therapeutic levels isoniazid is bacteriocidal against actively growing intracellular and extracellular <i>Mycobacterium tuberculosis</i> organisms. Specifically isoniazid inhibits InhA, the enoyl reductase from <i>Mycobacterium tuberculosis</i>, by forming a covalent adduct with the NAD cofactor. It is the INH-NAD adduct that acts as a slow, tight-binding competitive inhibitor of InhA. Although the mechanism of action of isoniazid is unknown, several hypotheses have been proposed. These include effects on lipids, nucleic acid biosynthesis, and glycolysis. ... /It has been suggested that/ a primary action of isoniazid /is/ to inhibit the biosynthesis of mycolic acids, important constituents of the mycobacterial cell wall. Because mycolic acids are unique to mycobacteria, this action would explain the high degree of selectivity of the antimicrobial activity of isoniazid. Exposure to isoniazid leads to a loss of acid fastness and a decrease in the quantity of methanol-extractable lipid of the microorganisms. Isoniazid is bacteriostatic for "resting" bacilli but is bactericidal for rapidly dividing microorganisms. The minimal tuberculostatic concentration is 0.025 to 0.05 ug/ml.
Pharmacodynamics
Isoniazid is a bactericidal agent active against organisms of the genus Mycobacterium, specifically <i>M. tuberculosis</i>, <i>M. bovis</i> and <i>M. kansasii</i>. It is a highly specific agent, ineffective against other microorganisms. Isoniazid is bactericidal when mycobacteria grow rapidly and bacteriostatic when they grow slowly.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
Molecular reference: Rifampicin
PubChem CID 135398735Molecular formula: C43H58N4O12
Mechanism of action
Rifampin works by binding to the beta-subunit of microbial DNA-dependent RNA polymerase (RNAP), thereby inhibiting the enzyme and impeding RNA synthesis. It reduces the affinity of RNAP for short RNA transcripts. It has no activity against the mammalian RNAP enzyme. Although rifampin is most active during cell multiplication ... /it/ appears to have some effect on resting cells. Electron microscopy has revealed changes in cytoplasm and disappearance of ribosomes in tubercle bacilli exposed to rifampin, indicating inhibition of DNA-dependent RNA polymerase. Rifampin inhibits DNA-dependent RNA polymerase of mycobacteria and other microorganisms by forming a stable drug-enzyme complex, leading to suppression of initiation of chain formation (but not chain elongation) in RNA synthesis. More specifically, the beta subunit of this complex enzyme is the site of action of the drug, although rifampin binds only to the holoenzyme. Nuclear RNA polymerase from a variety of eukaryotic cells does not bind rifampin, and RNA synthesis is correspondingly unaffected. While rifampin can inhibit RNA synthesis in mammalian mitochondria, considerably higher concentrations of the drug are required than for the inhibition of the bacterial enzyme. High concentrations of rifamycin antibiotics also inhibit viral DNA-dependent RNA polymerases and reverse transcriptases. Rifampin is bactericidal for both intracellular and extracellular microorganisms. Developmental expression of CYPlAl, CYPlA2 and CYP3A6 in the rabbit have been studied. Cytochromes P450IAl, P450IA2 and P450IIIA6 exhibited comparable patterns of developmental expression. Present at low level (less than 0.05 mnol/ng) in the new born animal up to week 3, these proteins sharply accumulated between weeks 3 and 4 to reach a maximum by week 4 (P450IAl, 0.2 nmol/mg; P450IA2, 0.8 nmol/ng; P450IIIA6, 0.12 nmol/mg) and decr in the adult (P450IAl, 0.2 nmol/mg; P450IA2, 0.4 mnol/mg; P450IIIA6, 0.09 nmol/mg). Cytochromes P450IAl and P450IA2 were not expressed in the untreated fetus. Onset of CYP3A6 gene expression occurred at day 30 of gestation and both transcription and mRNA accumulation were transplacentally inducible by rifampicin only shortly before birth, i.e. after treatment of the females between days 28 and 30 of gestation. Both long (1.85 kb) and short (1.7 kb) mRNA transcripts were expressed in untreated or rifampicin treated fetuses. CYP3A6 gene expression was also induced by rifampicin in l week old and 2 week old animals. Developmental expression of CYPlAl and CYPlA2 genes was shown to be closely related to the diet change accompanying weaning which occurs at weeks 3-4. In animals subjected to either delayed (week 6) or early (week 2) weaning, sharp accumulation of messages, proteins and related activities were delayed or anticipated accordingly with respect to normal weaning. Artificially scheduled weaning gave similar results when repeated with biological grade lucern (grown in the absence of chemical fertilizers, pesticides) ... the main constituent of commercial rabbit chow. While CYP3A6 gene expression could be brought forward by early weaning at week 2, both message and protein did not exhibit incr accumulation after delayed weaning at week 6, and remained at the low level of the new born animal. Treatment of l week old and 2 week old animals with triiodothyronine or of 3 week old animals with propylthiouracil, an antithyroid factor, did not modify the normal pattern of developmental expression of genes CYPlAl, CYPlA2 and CYP3A6. ...
Pharmacodynamics
Rifampin is an antimicrobial agent with bactericidal effects and a broad-spectrum activity. It is active against intracellular and extracellular _Mycobacterium tuberculosis_.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
Molecular reference: pyrizinamide
PubChem CID 1046Molecular formula: C5H5N3O
Mechanism of action
Pyrazinamide diffuses into active _M. tuberculosis_ that express pyrazinamidase enzyme that converts pyrazinamide to the active form pyrazinoic acid. Pyrazinoic acid can leak out under acidic conditions to be converted to the protonated conjugate acid, which is readily diffused back into the bacilli and accumulate intracellularly. The net effect is that more pyrazinoic acid accumulates inside the bacillus at acid pH than at neutral pH. Pyrazinoic acid was thought to inhibit the enzyme fatty acid synthase (FAS) I, which is required by the bacterium to synthesise fatty acids. However, this theory was thought to have been discounted. However, further studies reproduced the results of FAS I inhibition as the putative mechanism first in whole cell assay of replicating M. tuberculosis bacilli which have shown that pyrazinoic acid and its ester inhibit the synthesis of fatty acids. This study was followed by in vitro assay of tuberculous FAS I enzyme that tested the activity with pyrazinamide, pyrazinoic acid and several classes of pyrazinamide analogs. Pyrazinamide and its analogs inhibited the activity of purified FAS I. It has also been suggested that the accumulation of pyrazinoic acid disrupts membrane potential and interferes with energy production, necessary for survival of M. tuberculosis at an acidic site of infection. Pyrazinoic acid has also been shown to bind to the ribosomal protein S1 (RpsA) and inhibit trans-translation. This may explain the ability of the drug to kill dormant mycobacteria. Pyrazinamide may be bacteriostatic or bactericidal in action, depending on the concentration of the drug attained at the site of the infection and the susceptibility of the infecting organism. In vitro and in vivo, the drug is active only at a slightly acidic pH. The exact mechanism of action of pyrazinamide has not been fully elucidated. The antimycobacterial activity of pyrazinamide appears to partly depend on conversion of the drug to pyrazinoic acid. Susceptible strains of Mycobacterium tuberculosis produce pyrazinamidase, an enzyme that deaminates pyrazinamide to pyrazinoic acid, and the in vitro susceptibility of a given strain of the organism appears to correspond to its pyrazinamidase activity. In vitro studies indicate that pyrazinoic acid has specific antimycobacterial activity against Mycobacterium tuberculosis. In addition, the fact that pyrazinoic acid lowers the pH of the environment below that which is necessary for growth of Mycobacterium tuberculosis appears to contribute to the drug's antimycobacterial activity in vitro. Unknown; pyrazinamide may be bacteriostatic or bactericidal, depending on its concentration and the susceptibility of the organism. It is active in vitro at an acidic pH of 5.6 or less, similar to that found in early, active tubercular inflammatory lesions.
Pharmacodynamics
Pyrazinamide kills or stops the growth of certain bacteria that cause tuberculosis (TB). It is used with other drugs to treat tuberculosis. It is a highly specific agent and is active only against <i>Mycobacterium tuberculosis</i>. In vitro and in vivo, the drug is active only at a slightly acid pH. Pyrazinamie gets activated to Pyrazinoic acid in the bacilli where it interferes with fatty acid synthase FAS I. This interferes with the bacteriums ability to synthesize new fatty acids, required for growth and replication.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
This drug in other countries
The same active ingredient registered across other registries we cover - including different brands.
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- ISONIAZID · Macleods Pharmaceuticals
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