{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T11:56:55Z","timestamp":1790251015670,"version":"4.1.0"},"reference-count":0,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[1989,8,1]],"date-time":"1989-08-01T00:00:00Z","timestamp":617932800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[1989,8]]},"abstract":"<jats:p>We investigated the pharmacokinetics of rifabutin in 15 male patients as part of a phase I trial of the treatment of early symptomatic human immunodeficiency virus infection. Six or more patients were studied at each of four different oral dosage levels: 300, 600, 900, and 1,200 mg\/day. Twelve studies were also conducted with tracer doses of intravenous radiolabeled [14C]rifabutin. Blood and urine samples were collected for at least 72 h after the first (day 1) and last (day 28) doses of rifabutin and analyzed by high-pressure liquid chromatography. The plasma concentration data were best described by a two-compartment open model with a terminal half-life of 36 h. Rifabutin was rapidly absorbed, reaching a peak concentration about 2 to 3 h after an oral dose. Peak and trough concentrations for the 1,200-mg dose were 907 and 194 ng\/ml, respectively. Total body clearance was 10 to 18 liters\/h. Oral bioavailability was 12 to 20%. The drug was moderately bound to plasma proteins with a free fraction of 29 +\/- 2% (mean +\/- standard deviation). About 10% of an administered intravenous dose of rifabutin is excreted into the urine unchanged. Renal clearance was 1.5 +\/- 0.2 liters\/h. The volume of distribution was large (8 to 9 liters\/kg), suggesting extensive distribution into the tissues. The area under the curve for the last dose was smaller than that of the first dose, suggesting possible induction of drug-metabolizing enzymes.<\/jats:p>","DOI":"10.1128\/aac.33.8.1237","type":"journal-article","created":{"date-parts":[[2012,6,28]],"date-time":"2012-06-28T00:04:52Z","timestamp":1340841892000},"page":"1237-1241","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":75,"title":["Pharmacokinetics of rifabutin"],"prefix":"10.1128","volume":"33","author":[{"given":"M H","family":"Skinner","sequence":"first","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Hsieh","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Torseth","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"Pauloin","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G","family":"Bhatia","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Harkonen","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T C","family":"Merigan","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T F","family":"Blaschke","sequence":"additional","affiliation":[{"name":"Division of Clinical Pharmacology, Stanford University Medical Center, California 94305."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","container-title":["Antimicrobial Agents and Chemotherapy"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/AAC.33.8.1237","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.asm.org\/doi\/pdf\/10.1128\/AAC.33.8.1237","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,2,21]],"date-time":"2022-02-21T15:10:57Z","timestamp":1645456257000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.asm.org\/doi\/10.1128\/AAC.33.8.1237"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1989,8]]},"references-count":0,"journal-issue":{"issue":"8","published-print":{"date-parts":[[1989,8]]}},"alternative-id":["10.1128\/AAC.33.8.1237"],"URL":"https:\/\/doi.org\/10.1128\/aac.33.8.1237","relation":{},"ISSN":["0066-4804","1098-6596"],"issn-type":[{"value":"0066-4804","type":"print"},{"value":"1098-6596","type":"electronic"}],"subject":[],"published":{"date-parts":[[1989,8]]},"assertion":[{"value":"1989-08-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}