Rifapentine is a rifamycin antibiotic that is similar in structure and activity to rifampin and rifabutin and that is used in combination with other agents as therapy of tuberculosis, particularly in once or twice weekly regimens. Rifapentine is associated with transient and asymptomatic elevations in serum aminotransferase and is a likely cause of clinically apparent acute liver injury.


Rifapentine (rif" a pen' teen) is a rifamycin antibiotic and a synthetic derivative of natural products of the bacterium, Amycolatopsis mediterranei. The rifamycins are complex macrocyclic antibiotics that have activity against several bacteria, but most prominently M. tuberculosis and several atypical mycobacterial species, probably as a result of inhibition of the DNA dependent RNA polymerase of mycobacteria. These agents are considered bactericidal and are active against both intracellular and extracellular organisms. Rifapentine has a longer half-life than rifampin and rifabutin, which allows for once or twice weekly dosing, which is its major advantage. Rifapentine was approved for use in treating active as well as latent tuberculosis in 1998. It is available as 150 mg film coated tablets under the trade names of Priftin. The recommended dose for active tuberculosis in adults is 600 mg twice weekly for 2 months, followed by 600 mg (~10 mg/kg) once weekly for 4 months as a part of directly observed therapy and in combination with isoniazid or other antituberculosis agents. The recommended regimen for latent tuberculsosis is a 12 week regimen of 600 mg once weekly in combination with isoniazid as directly observed therapy. Pyridoxine (vitamin B6) is commonly given with rifapentine and isoniazid to prevent neuropathy. Side effects of rifapentine are uncommon, but include rash, fever, flu-like symptoms, gastrointestinal upset and orange discoloration of urine and sweat. Rifapentine is intermediate between rifabutin and rifampin in activity as an inducer of the hepatic microsomal drug metabolizing P450 enzymes (CYP 1A2, 2C9, 2C19 and 3A4), the relative potencies being: rifampin (1.0), rifapentine (0.85) and rifabutin (0.4). For this reason, use of other medications (such as many antiretroviral agents, oral contraceptives, beta-blockers, benzodiazepines, cyclosporine, macrolide antibiotics and oral anticoagulants) with rifapentine should be carefully considered and monitored.


Because of its limited use, the effects of rifapentine on the liver have been less well defined than those of rifampin, but they are likely to be similar. Thus, long term therapy with rifapentine is associated with minor, transient elevations in serum aminotransferase levels in 2% to 7% of patients, abnormalities that usually do not require dose adjustment or discontinuation. Clinically apparent liver injury due to rifapentine has not been reported, but it is likely to be similar to rifampin in its potential for causing acute liver injury. Because rifapentine is usually given in combination with isoniazid and/or pyrazinamide, two other known hepatotoxic agents, the cause of the acute liver injury in patients on rifapentine containing regimens may be difficult to relate to a single agent, and some evidence suggests that these combinations are more likely to cause injury than the individual drugs. Typically, the onset of injury due to rifamycins is within 1 to 6 weeks and the serum enzyme pattern is usually hepatocellular at the onset of injury, but can cholestatic and mixed in contrast to isoniazid and pyrazinamide. Extrahepatic manifestations due to rifamycin hepatotoxicity such as fever, rash, arthralgias, edema and eosinophilia are uncommon as is autoantibody formation. This potential for hepatotoxicity has not been specifically demonstrated for rifapentine.

Likelihood score: E* (unproven but suspected cause of clinically apparent liver injury).

Mechanism of Injury

The mechanism of rifamycin associated hepatotoxicity is not known, but these agents are extensively metabolized by the liver and induce multiple hepatic enzymes. Thus, the cause of injury is likely to be due to idiosyncratic metabolic products that are either directly toxic or induce an immunologic reaction.

Outcome and Management

For rifampin, the severity of hepatic injury ranges from asymptomatic elevations in serum aminotransferase levels, jaundice without apparent hepatic injury, symptomatic self-limited hepatitis to severe fulminant liver failure and death. Complete recovery is expected after stopping the drug and is usually rapid and complete. The rifamycins have not been associated with vanishing bile duct syndrome or chronic hepatitis. There is likely to be some cross sensitivity to liver injury among the rifamycins (rifampin, rifabutin, rifapentine), but not with the other first and second line antituberculosis agents. Routine monitoring for seurm enzyme elevations is not recommended except in high risk individuals. Nevertheless, routine monitoring for symptoms of liver disease is recommended for all regimens, whether for clinically active or latent tuberculosis.

Specific, regularly updated recommendations on therapy of tuberculosis can be found on the U.S. Centers for Disease Control and Prevention website: https://www.cdc.gov/tb/topic/treatment/

[First line medications used in the therapy of tuberculosis in the US include ethambutol, isoniazid, pyrazinamide, rifabutin, rifampin, and rifapentine. Second line medications include streptomycin, capreomycin, cycloserine, ethionamide, fluoroquinolones such as levofloxacin and moxifloxacin, aminoglycosides such as amikacin, and para-aminosalicylic acid (PAS).]

Drug Class: Antituberculosis Agents

Other Drugs in the Class: Bedaquiline, Capreomycin, Cycloserine, Ethambutol, Ethionamide, Isoniazid, Pyrazinamide, Rifabutin, Rifampin, Streptomycin



Rifapentine – Priftin®


Antituberculosis Agents


Product labeling at DailyMed, National Library of Medicine, NIH



References updated: 14 June 2018

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    (Among 531 adults with active tuberculosis treated with isoniazid, pyrazinamide, ethambutol and either rifampin or rifapentine [5 days/week] for the first 8 weeks of intensive therapy, hepatitis was reported in 2.8% of rifampin and 4% of rifapentine treated subjects, the later group including 3 serious adverse events due to hepatitis).
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    (In a population based study of drug induced liver injury from Iceland, 96 cases were identified over a 2 year period, including 1 attributed to isoniazid but none to rifampin or other rifamycins).
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    (Metaanalysis of 53 controlled trials of different regimens for latent tuberculosis concluded that rifamycin-only or isoniazid-rifamycin regimens had lower rates of hepatotoxicity than isoniazid-only regimens of 6, 9, or 12-72 months).
  • de Castilla DL, Rakita RM, Spitters CE, Narita M, Jain R, Limaye AP. Short-course isoniazid plus rifapentine directly observed therapy for latent tuberculosis in solid-organ transplant candidates. Transplantation 2014; 97: 206-11. [PubMed: 24142036]
    (Among 17 solid organ transplant candidates with latent tuberculosis who were treated with a 12 week course of weekly isoniazid and rifapentine, none developed ALT or AST elevations more than twice baseline or clinical hepatotoxicity during treatment and none developed active tuberculosis during follow up).
  • Bliven-Sizemore EE, Sterling TR, Shang N, Benator D, Schwartzman K, Reves R, Drobeniuc J, Bock N, Villarino ME; TB Trials Consortium. Three months of weekly rifapentine plus isoniazid is less hepatotoxic than nine months of daily isoniazid for LTBI. Int J Tuberc Lung Dis 2015; 19: 1039-44, i-v. [PMC free article: PMC5080618] [PubMed: 26260821]
    (Among 6862 patients with latent tuberculosis treated with either 9 months of daily oral isoniazid or 3 months of once weekly rifapentine and isoniazid, liver injury requiring discontinuation was more frequent with the 9 month regimen 1.9% vs 0.4%, as was symptomatic hepatotoxicity [1.3% vs 0.3%], but there were no hospitalizations or deaths from liver injury).
  • Chalasani N, Bonkovsky HL, Fontana R, Lee W, Stolz A, Talwalkar J, Reddy KR, et al.; United States Drug Induced Liver Injury Network. Features and outcomes of 899 patients with drug-induced liver injury: the DILIN prospective study. Gastroenterology 2015; 148: 1340-52.e7. [PMC free article: PMC4446235] [PubMed: 25754159]
    (Among 899 cases of drug induced liver injury enrolled in a US prospective study between 2004 and 2013, 408 were attributed to antimicrobial agents including 54 [6%] to antituberculosis agents, mostly due to isoniazid [n=48], occasionally pyrazinamide [n=2], rifampin [n=2] or ethambutol [n=1], but none to rifapentine).
  • Knoll BM, Nog R, Wu Y, Dhand A. Three months of weekly rifapentine plus isoniazid for latent tuberculosis treatment in solid organ transplant candidates. Infection 2017; 45: 335-9. [PubMed: 28276008]
    (Among 12 solid organ transplant candidates found to have latent tuberculosis infection who received 12 weeks of direclty observed therapy with weekly isoniazid and rifapentine, none developed de novo elevations of serum ALT more than twice baseline or had to discontinue therapy early because of adverse events, and none subsequently developed active tuberculosis).
  • Simkins J, Abbo LM, Camargo JF, Rosa R, Morris MI. Twelve-week rifapentine plus isoniazid versus 9-month isoniazid for the treatment of latent tuberculosis in renal transplant candidates. Transplantation 2017; 101: 1468-72. [PubMed: 27548035]
    (Among 153 renal transplant candidates with latent tuberculosis treated with 9 months of isoniazid daily or 12 weeks of weekly rifapentine and isoniazid, the 12 week regimen had a higher rate of compliance and lower rate of ALT and AST elevations [0% vs 5%]; subsequent activation of tuberculosis did not occur with either regimen).
  • Chalasani N, Reddy KRK, Fontana RJ, Barnhart H, Gu J, Hayashi PH, Ahmad J, et al. Idiosyncratic drug induced liver injury in African-Americans is associated with greater morbidity and mortality compared to caucasians. Am J Gastroenterol 2017; 112: 1382-8. [PMC free article: PMC5667647] [PubMed: 28762375]
    (Among 841 Caucasians and 144 African Americans with drug induced liver injury enrolled in a prospective US registry, the most frequent cause in whites was amoxicillin/clavulanate [13.4% vs 4.1%] and in blacks was trimethoprim-sulfamethoxazole [7.6% vs 3.6%], whereas isoniazid represented 4% of cases in both racial groups).
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