Rifampin (oral): Difference between revisions
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==Overview== | ==Overview== | ||
===Rifampin=== | |||
Rifampin was introduced in 1967,<ref name="isbn0-06-273090-8">{{cite book |author=Long, James W. |title=Essential Guide to Prescription Drugs 1992 |publisher=HarperCollins Publishers |location=New York |year=1991 |pages=925–929 |isbn=0-06-273090-8 |oclc= |doi= |accessdate=}}</ref> as a major addition to the cocktail-drug treatment of [[tuberculosis]] and inactive [[meningitis]], along with [[pyrazinamide]], [[isoniazid]], [[ethambutol]] and [[streptomycin]] ("PIERS"). It requires a prescription in North America. It must be administered regularly daily for several months without break; otherwise, the risk of drug-resistant tuberculosis is greatly increased.<ref name="isbn0-06-273090-8" /> In fact, this is the primary reason it is used in tandem with the three aforementioned drugs, particularly isoniazid.<ref name="Erlich">Erlich, Henry, W Ford Doolittle, Volker Neuhoff, and et al. . Molecular Biology of Rifomycin. New York, NY: MSS Information Corporation, 1973. pp. 44-45, 66-75, 124-130.</ref> This is also the primary motivation behind directly observed therapy for tuberculosis. | |||
==Category== | ==Category== | ||
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==Mechanisms of Action== | ==Mechanisms of Action== | ||
===Rifampin=== | |||
Rifampin inhibits bacterial DNA-dependent RNA synthesis by inhibiting bacterial DNA-dependent [[RNA polymerase]].<ref name="Calvori">{{cite journal |author=Calvori, C.; Frontali, L.; Leoni, L.; Tecce, G. |journal=Nature |title=Effect of rifamycin on protein synthesis |volume=207 |pages=417–8 |year=1965 |doi=10.1038/207417a0 |pmid=4957347 |issue=995}}</ref> | |||
Crystal structure data and biochemical data indicate that rifampicin binds to RNA polymerase at a site adjacent to the RNA polymerase active center and blocks RNA synthesis by physically preventing extension of RNA products beyond a length of 2-3 nucleotides ("steric-occlusion" mechanism).<ref name="Campbell">{{cite journal|author=Campbell, E.A., Korzheva, N., Mustaev, A., Murakami, K., Nair, S., Goldfarb, A., Darst, S.A.|year=2001|title=Structural mechanism for rifampicin inhibition of bacterial RNA polymerase|journal=Cell|volume=104|issue=6|pages=901–12|pmid=11290327|doi=10.1016/S0092-8674(01)00286-0}}</ref><ref name="Feklistov">{{cite journal|author=Feklistov, A., Mekler, V., Jiang, Q., Westblade, L.F., Irschik, H., Jansen, R., Mustaev, A., Darst, S.A., [[Richard H. Ebright|Ebright, R.H.]]|year=2008|title=Rifamycins do not function by allosteric modulation of binding of Mg2+ to the RNA polymerase active center|journal=Proc Natl Acad Sci USA|volume=105|issue=39|pages=14820–5|pmid=18787125|doi=10.1073/pnas.0802822105|pmc=2567451}}</ref> | |||
Resistance to rifampin arises from mutations that alter residues of the rifampin binding site on RNA polymerase, resulting in decreased affinity for rifampin.<ref name=Feklistov/> Resistant mutations map to the ''[[rpoB]]'' gene, encoding RNA polymerase beta subunit. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 18:27, 5 January 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chetan Lokhande, M.B.B.S [2]
Overview
Rifampin
Rifampin was introduced in 1967,[1] as a major addition to the cocktail-drug treatment of tuberculosis and inactive meningitis, along with pyrazinamide, isoniazid, ethambutol and streptomycin ("PIERS"). It requires a prescription in North America. It must be administered regularly daily for several months without break; otherwise, the risk of drug-resistant tuberculosis is greatly increased.[1] In fact, this is the primary reason it is used in tandem with the three aforementioned drugs, particularly isoniazid.[2] This is also the primary motivation behind directly observed therapy for tuberculosis.
Category
Antimycobacterial
US Brand Names
RIFADIN®
FDA Package Insert
Description | Clinical Pharmacology | Microbiology | Indications and Usage | Contraindications | Warnings and Precautions | Adverse Reactions | Overdosage | Clinical Studies | Dosage and Administration | Compatibility, Reconstitution, and Stability | Directions For Use | How Supplied | Labels and Packages
Mechanisms of Action
Rifampin
Rifampin inhibits bacterial DNA-dependent RNA synthesis by inhibiting bacterial DNA-dependent RNA polymerase.[3]
Crystal structure data and biochemical data indicate that rifampicin binds to RNA polymerase at a site adjacent to the RNA polymerase active center and blocks RNA synthesis by physically preventing extension of RNA products beyond a length of 2-3 nucleotides ("steric-occlusion" mechanism).[4][5]
Resistance to rifampin arises from mutations that alter residues of the rifampin binding site on RNA polymerase, resulting in decreased affinity for rifampin.[5] Resistant mutations map to the rpoB gene, encoding RNA polymerase beta subunit.
References
- ↑ 1.0 1.1 Long, James W. (1991). Essential Guide to Prescription Drugs 1992. New York: HarperCollins Publishers. pp. 925–929. ISBN 0-06-273090-8.
- ↑ Erlich, Henry, W Ford Doolittle, Volker Neuhoff, and et al. . Molecular Biology of Rifomycin. New York, NY: MSS Information Corporation, 1973. pp. 44-45, 66-75, 124-130.
- ↑ Calvori, C.; Frontali, L.; Leoni, L.; Tecce, G. (1965). "Effect of rifamycin on protein synthesis". Nature. 207 (995): 417–8. doi:10.1038/207417a0. PMID 4957347.
- ↑ Campbell, E.A., Korzheva, N., Mustaev, A., Murakami, K., Nair, S., Goldfarb, A., Darst, S.A. (2001). "Structural mechanism for rifampicin inhibition of bacterial RNA polymerase". Cell. 104 (6): 901–12. doi:10.1016/S0092-8674(01)00286-0. PMID 11290327.
- ↑ 5.0 5.1 Feklistov, A., Mekler, V., Jiang, Q., Westblade, L.F., Irschik, H., Jansen, R., Mustaev, A., Darst, S.A., Ebright, R.H. (2008). "Rifamycins do not function by allosteric modulation of binding of Mg2+ to the RNA polymerase active center". Proc Natl Acad Sci USA. 105 (39): 14820–5. doi:10.1073/pnas.0802822105. PMC 2567451. PMID 18787125.