Rifamycins: A group of ANTI-BACTERIAL AGENTS characterized by a chromophoric naphthohydroquinone group spanned by an aliphatic bridge not previously found in other known ANTI-BACTERIAL AGENTS. They have been isolated from fermentation broths of Streptomyces mediterranei.Rifabutin: A broad-spectrum antibiotic that is being used as prophylaxis against disseminated Mycobacterium avium complex infection in HIV-positive patients.Nocardia: A genus of gram-positive, aerobic bacteria whose species are widely distributed and are abundant in soil. Some strains are pathogenic opportunists for humans and animals.Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)Antibiotics, Antitubercular: Substances obtained from various species of microorganisms that are, alone or in combination with other agents, of use in treating various forms of tuberculosis; most of these agents are merely bacteriostatic, induce resistance in the organisms, and may be toxic.DNA-Directed RNA Polymerases: Enzymes that catalyze DNA template-directed extension of the 3'-end of an RNA strand one nucleotide at a time. They can initiate a chain de novo. In eukaryotes, three forms of the enzyme have been distinguished on the basis of sensitivity to alpha-amanitin, and the type of RNA synthesized. (From Enzyme Nomenclature, 1992).Anti-Bacterial Agents: Substances that reduce the growth or reproduction of BACTERIA.

*  Products
... rifamycins such as rifampin, St. John's wort, verapamil, or voriconazole. DO NOT START OR STOP any medicine without doctor or ...
*  Tuberculosis | PanACEA
... high dose rifamycins and pyrazinamide) and repurposing of available antibiotics (e.g. moxifloxacin, linezolid and clofazimine ...
*  Impact of Rifaximin Therapy on Intestinal Byproducts in Chronic Kidney Disease - AdisInsight
This study will determine if Rifaximin decreases serum and urine levels of bacterial by-products and inflammatory markers in patients with chronic kidney
*  Escherichia coli (Migula) Castellani and Chalmers ATCC ® 10536&tra
Assay of chloramphenicol Assay of colistin colimycin Assay of rifamycins rifamycin Assay of spectinomycin actinospectacin Assay ... Assay of rifamycins rifamycin. Assay of spectinomycin actinospectacin. Assay of tetracycline. Quality control strain ...
*  Notice to Readers: Updated Guidelines for the Use of Rifamycins for the Treatment of Tuberculosis Among HIV-Infected...
Notice to Readers: Updated Guidelines for the Use of Rifamycins for the Treatment of Tuberculosis Among HIV-Infected Patients ... infection together with rifamycins for the treatment of tuberculosis have been published previously (1,2). New guidelines ...
*  ChemIDplus - 13929-38-9 - ZGRPZDSOGQCHPK-BZUIVQGESA-N - Rifamycin, 4-O-(2-(4-morpholinylamino)-2-oxoethyl)- - Similar...
Rifamycin, 4-O-(2-(4-morpholinylamino)-2-oxoethyl)- - Similar structures search, synonyms, formulas, resource links, and other ... Substance Name: Rifamycin, 4-O-(2-(4-morpholinylamino)-2-oxoethyl)-. RN: 13929-38-9. InChIKey: ZGRPZDSOGQCHPK-BZUIVQGESA-N. ...
*  Stimulation of NADH-dependent microsomal DNA strand cleavage by rifamycin SV | Biochemical Journal
Interactions between rifamycin SV, iron and NADH generating hydroxyl-radical-like species may play a role in some of the ... Rifamycin SV did not significantly increase the high rates of DNA strand cleavage found with NADPH as the microsomal reductant ... Stimulation of NADH-dependent microsomal DNA strand cleavage by rifamycin SV. E Kukiełka, A I Cederbaum ... Rifamycin SV is an antibiotic anti-bacterial agent used in the treatment of tuberculosis. This drug can autoxidize, especially ...
*  Rifamycin - Wikipedia
The rifamycin group includes the "classic" rifamycin drugs as well as the rifamycin derivatives rifampicin (or rifampin), ... to yield the highly active Rifamycin S. Simple reduction of Rifamycin S yielded the hydroquinone form called Rifamycin SV, ... This is due to the high affinity of rifamycins for the prokaryotic RNA polymerase. The selectivity of the rifamycins depends on ... Lepetit introduced Rifampicin, an orally active rifamycin, around 1966. Rifabutin, a derivative of rifamycin S, was invented ...
*  Rifamycin-B oxidase - Wikipedia
... rifamycin O + H2O2 Thus, the two substrates of this enzyme are rifamycin B and O2, whereas its two products are rifamycin O and ... In enzymology, a rifamycin-B oxidase (EC is an enzyme that catalyzes the chemical reaction rifamycin B + O2 ⇌ {\ ... This enzyme is also called rifamycin B oxidase. Han MH, Seong BL, Son HJ, Mheen TI (1983). "Rifamycin B oxidase from ... The systematic name of this enzyme class is rifamycin-B:oxygen oxidoreductase. ...
*  Rifamycin antibiotics | definition of Rifamycin antibiotics by Medical dictionary
What is Rifamycin antibiotics? Meaning of Rifamycin antibiotics medical term. What does Rifamycin antibiotics mean? ... Looking for online definition of Rifamycin antibiotics in the Medical Dictionary? Rifamycin antibiotics explanation free. ... rifamycin. (redirected from Rifamycin antibiotics). Also found in: Dictionary. rifamycin. [rif″ah-mi´sin] any of a family of ... rifamycin. [rif′ah-mi′sin] any of a family of antibiotics biosynthesized from a strain of Streptomyces mediterranei, effective ...
*  "In Vivo" Depression of Either Endotoxin or Virus-Induced Interferons by Rifampicin and Rifamycin Derivatives |...
Several experiments have been carried out in relation to the influence of rifamycin molecules on the interferon production when ... Several experiments have been carried out in relation to the influence of rifamycin molecules on the interferon production when ... "In Vivo" Depression of Either Endotoxin or Virus-Induced Interferons by Rifampicin and Rifamycin Derivatives. ... Depression of Either Endotoxin or Virus-Induced Interferons by Rifampicin and Rifamycin Derivatives. In: Williams J.D., Geddes ...
*  Diversity of Mycobacterium species from marine sponges and their sensitivity to antagonism by sponge-derived rifamycin...
Determination of rifamycin production by LC-MS/MS. The production of rifamycins by Salinispora isolate AQ1M05 was determined ... arenicola strain was confirmed to produce rifamycin B and an additional probable rifamycin-like compound by LC-MS/MS analysis ( ... Hewavitharana AK, Shaw PN, Kim TK & Fuerst JA (2007) Screening of rifamycin producing marine sponge bacteria by LC-MS-MS. J ... Aristoff PA, Garcia GA, Kirchhoff PD & Showalter HDH (2010) Rifamycins - obstacles and opportunities. Tuberculosis 90: 94-118. ...
*  Preparation and application of rifamycin-capped (3-(2-O-β- cyclodextrin)-2-hydroxypropoxy)-propylsilyl-appended silica...
Zhao, J., Tan, D., Chelvi, S.K.T., Yong, E.L., Lee, H.K., Gong, Y. (2010-11-15). Preparation and application of rifamycin- ... Rifamycin-capped (3-(2-O-β-cyclodextrin)-2-hydroxypropoxy)- propylsilyl-appended silica particles (RCD-HPS), a new type of ... This new CSP has a chiral selector with two recognition sites: rifamycin and β-cyclodextrin (β-CD). The chromatographic ... Preparation and application of rifamycin-capped (3-(2-O-β- cyclodextrin)-2-hydroxypropoxy)-propylsilyl-appended silica ...
*  Rifamycin sodium salt 14897-39-3 H-NMR | C-NMR Spectral Analysis NMR Spectrum
Rifamycin sodium salt H-NMR spectral analysis, Rifamycin sodium salt C-NMR spectral analysis ect. ...
*  ChemIDplus - 59232-87-0 - XTPGUQSTSWYULT-TXXBDZDDSA-N - Rifamycin P - Similar structures search, synonyms, formulas, resource...
Rifamycin P - Similar structures search, synonyms, formulas, resource links, and other chemical information. ... Substance Name: Rifamycin P. RN: 59232-87-0. InChIKey: XTPGUQSTSWYULT-TXXBDZDDSA-N. Classification Codes. *. Drug / Therapeutic ...
*  Rifetem - Drugs.com
Rifamycin. Rifamycin is reported as an ingredient of Rifetem in the following countries:. *Turkey ...
*  antimicrobials II Flashcards by laura gibbons | Brainscape
rifamycins uses TB. delay resistance to dapsone in leprosy meningococcal prophylaxis and H. influenza prophylaxis in exposed ...
*  Pure and Applied Chemistry
Recent progress in the chemistry and biochemistry of rifamycins. Sensi, P. Page 15 ...
*  Complete Guide to Prescription & Nonprescription Drugs 2011 - H. Winter Griffith - Google Books
The revised and updated 2011 edition of the most accessible, comprehensive and affordable guide to prescription and nonprescription drugs. The classic guide to all major prescription and nonprescription drugs, featuring revised, up-to date FDA information and an A-Z list of medical conditions and their commonly used drugs for easy reference. It includes coverage of dosage and length of time before the drug takes effect, side effects, special precautions, interactions with other food and drugs, standards for use by different age groups, and much more. It also features a generic and brand name directory, a comprehensive glossary, and complete index by generic, brand, and class name.
*  ATC code J04 - Wikipedia
J04AB03 Rifamycin. J04AB04 Rifabutin. J04AB05 Rifapentin. J04AB30 Capreomycin. J04AC Hydrazides[edit]. J04AC01 Isoniazid. ...
*  Clinical trials in irritable bowel syndro... & related info | Mendeley
Rifamycins. *Rifamycins: therapeutic use. Get free article suggestions today. Mendeley saves you time finding and organizing ...

(1/356) Issues in the treatment of active tuberculosis in human immunodeficiency virus-infected patients.

Most HIV-infected patients with tuberculosis can be treated satisfactorily with standard regimens with expectations of good results. Treatment of tuberculosis in these patients has been complicated by the introduction of HAART, which relies on drugs that interfere with the most potent class of antituberculous medications. Rifampin-free regimens or regimens that employ rifabutin may be acceptable strategies for patients who are receiving protease inhibitors, although these regimens have not been rigorously evaluated in patients with AIDS. At present, there is good reason to believe that a 6-month course of a rifabutin-containing regimen or a 9-12-month course of a regimen of streptomycin, isoniazid, and pyrazinamide should be adequate therapy for most patients with drug-susceptible disease. As the treatment of HIV infection with antiretroviral agents evolves, the treatment of tuberculosis in patients with AIDS is likely to evolve as well. This will require careful coordination of antituberculosis and antiretroviral therapies.  (+info)

(2/356) Effects of the Chinese traditional medicine mao-bushi-saishin-to on therapeutic efficacy of a new benzoxazinorifamycin, KRM-1648, against Mycobacterium avium infection in mice.

The Chinese traditional medicine mao-bushi-saishin-to (MBST), which has anti-inflammatory effects and has been used to treat the common cold and nasal allergy in Japan, was examined for its effects on the therapeutic activity of a new benzoxazinorifamycin, KRM-1648 (KRM), against Mycobacterium avium complex (MAC) infection in mice. In addition, we examined the effects of MBST on the anti-MAC activity of murine peritoneal macrophages (M phi s). First, MBST significantly increased the anti-MAC therapeutic activity of KRM when given to mice in combination with KRM, although MBST alone did not exhibit such effects. Second, MBST treatment of M phi s significantly enhanced the KRM-mediated killing of MAC bacteria residing in M phi s, although MBST alone did not potentiate the M phi anti-MAC activity. MBST-treated M phi s showed decreased levels of reactive nitrogen intermediate (RNI) release, suggesting that RNIs are not decisive in the expression of the anti-MAC activity of such M phi populations. MBST partially blocked the interleukin-10 (IL-10) production of MAC-infected M phi s without affecting their transforming growth factor beta (TGF-beta)-producing activity. Reverse transcription-PCR analysis of the lung tissues of MAC-infected mice at weeks 4 and 8 after infection revealed a marked increase in the levels of tumor necrosis factor alpha, gamma interferon (IFN-gamma), IL-10, and TGF-beta mRNAs. KRM treatment of infected mice tended to decrease the levels of the test cytokine mRNAs, except that it increased TGF-beta mRNA expression at week 4. MBST treatment did not affect the levels of any cytokine mRNAs at week 8, while it down-regulated cytokine mRNA expression at week 4. At week 8, treatment of mice with a combination of KRM and MBST caused a marked decrease in the levels of the test cytokines mRNAs, especially IL-10 and IFN-gamma mRNAs, although such effects were obscure at week 4. These findings suggest that down-regulation of the expression of IL-10 and TGF-beta is related to the combined therapeutic effects of KRM and MBST against MAC infection.  (+info)

(3/356) Antimicrobial activities of benzoxazinorifamycin (KRM-1648) and clarithromycin against Mycobacterium avium-intracellulare complex within murine peritoneal macrophages, human macrophage-like cells and human alveolar epithelial cells.

Profiles of the in-vitro antimicrobial effects of KRM-1648 and clarithromycin against Mycobacterium avium-intracellulare complex (MAC) within murine peritoneal macrophages, the THP-1 human macrophage cell line and the A-549 type II alveolar epithelial cell line were determined. MAC organisms grew more rapidly in A-549 and THP-1 cells than in murine peritoneal macrophages. Peritoneal macrophages produced significant amounts of reactive nitrogen intermediates in response to MAC infection, but A-549 and THP-1 cells did not. KRM-1648 progressively killed M. intracellulare residing in macrophages, but did not completely eliminate M. intracellulare from A-549 and THP-1 cells. Moreover, in the case of M. intracellulare-infected A-549 and THP-1 cells, bacterial regrowth was observed during the middle to late phase of cultivation. Clarithromycin exhibited moderate levels of microbicidal activity against M. intracellulare residing in peritoneal macrophages, THP-1 cells and A-549 cells. The profiles of clarithromycin-mediated killing or inhibition of the intracellular organisms in A-549 and THP-1 cells were similar to those observed for organisms within peritoneal macrophages.  (+info)

(4/356) In vitro anti-Helicobacter pylori activities of new rifamycin derivatives, KRM-1648 and KRM-1657.

The new rifamycin derivatives KRM-1657 and KRM-1648 were evaluated for their in vitro antimicrobial activities against 44 strains of Helicobacter pylori. Although the drugs were not very active against other gram-negative bacteria, the MICs at which 90% of isolates are inhibited for these drugs were lower (0.002 and 0.008 microgram/ml, respectively) than those of amoxicillin and rifampin for H. pylori. Time-kill studies revealed that the bactericidal activities of these agents were due to cell lysis. The results presented here indicate that these new rifamycin derivatives may be useful for the eradication of H. pylori infections.  (+info)

(5/356) Hepatic uptake of the magnetic resonance imaging contrast agent gadoxetate by the organic anion transporting polypeptide Oatp1.

Gadoxetate is a new hepatobiliary magnetic resonance imaging contrast agent. It is specifically taken up by hepatocytes, and its uptake can be inhibited by the coadministration of bromosulfophthalein, suggesting an involvement of one or several of the cloned organic anion transporting polypeptides Oatp1, Oatp2, and/or OATP. In this study, we demonstrated saturable uptake of gadoxetate by Oatp1 cRNA-injected Xenopus laevis oocytes (Km approximately 3.3 mM). In contrast, gadoxetate was not taken up by Oatp2 or OATP cRNA-injected oocytes. Oatp1-mediated gadoxetate uptake (100 microM) could be inhibited by 10 microM bromosulfophthalein (45%), 200 microM taurocholate (92%), 100 microM rifamycin SV (97%), and 100 microM rifampicin (51%). These results show that gadoxetate is a low-affinity substrate of Oatp1. Oatp1-mediated gadoxetate transport demonstrated a similar apparent Km value and cis-inhibition pattern as previously determined in rats in vivo, indicating that Oatp1 is significantly involved in gadoxetate uptake into rat liver.  (+info)

(6/356) Antibiotic combination therapy in patients with chronic, treatment-resistant pouchitis.

BACKGROUND: Pouchitis is the major long-term complication after ileal pouch-anal anastomosis for ulcerative colitis. About 15% of patients have a chronic, treatment-resistant disease. AIMS: To evaluate the efficacy of an antibiotic combination for chronic active, treatment-resistant pouchitis. PATIENTS AND METHODS: Eighteen patients were treated orally with rifaximin 1 g b.d. + ciprofloxacin 500 mg b.d. for 15 days. Symptoms assessment, endoscopic and histological evaluations were performed at screening and after 15 days using the Pouchitis Disease Activity Index (PDAI). Improvement was defined as a decrease of at least 3 points in PDAI score, and remission as a PDAI score of 0. Systemic absorption of rifaximin was determined by high performance liquid chromatography. Faecal samples were collected before and after antibiotic treatment for stool culture. RESULTS: Sixteen out of 18 patients (88.8%) either improved (n=10) or went into remission (n=6); the median PDAI scores before and after therapy were 11 (range 9-17) and 4 (range 0-16), respectively (P < 0.002). No side-effects were reported. Rifaximin plasma levels and urinary excretion were negligible, confirming its mainly topical activity. A significant decrease in total anaerobes and aerobes, enterococci, lactobacilli, bifidobacteria and bacteroides in faecal samples was observed, while the reduction in number of coliforms and Clostridium perfringens did not reach a statistical significance. CONCLUSIONS: A combination of rifaximin and ciprofloxacin was effective in patients with active chronic, treatment-resistant pouchitis, suggesting the need, in these patients, for treatment using antibiotic agents with wide antibacterial spectrum of activity.  (+info)

(7/356) Direct evidence that the rifamycin polyketide synthase assembles polyketide chains processively.

The assembly of the polyketide backbone of rifamycin B on the type I rifamycin polyketide synthase (PKS), encoded by the rifA-rifE genes, is terminated by the product of the rifF gene, an amide synthase that releases the completed undecaketide as its macrocyclic lactam. Inactivation of rifF gives a rifamycin B nonproducing mutant that still accumulates a series of linear polyketides ranging from the tetra- to a decaketide, also detected in the wild type, demonstrating that the PKS operates in a processive manner. Disruptions of the rifD module 8 and rifE module 9 and module 10 genes also result in accumulation of such linear polyketides as a consequence of premature termination of polyketide assembly. Whereas the tetraketide carries an unmodified aromatic chromophore, the penta- through decaketides have undergone oxidative cyclization to the naphthoquinone, suggesting that this modification occurs during, not after, PKS assembly. The structure of one of the accumulated compounds together with (18)O experiments suggests that this oxidative cyclization produces an 8-hydroxy-7, 8-dihydronaphthoquinone structure that, after the stage of proansamycin X, is dehydrogenated to an 8-hydroxynaphthoquinone.  (+info)

(8/356) Kanglemycin C vs ciclosporin on immunosuppression in mice.

AIM: To study inhibitory effects of kanglemycin C (Kan) on the mouse immune system, and compare with the effects of ciclosporin (Cic). METHODS: Delayed hypersensitivity (DH) and cyclophosphamide-potentiated DH induced by dinitrofluorobenzene (DNFB); heart allograft and skin allograft; hemolysin; the phagocytosis of the peritoneal macrophage. RESULTS: Kan (12.5, 25, 50 mg.kg-1.d-1, ig, 8 d) markedly inhibited DH and cyclophosphamide-potentiated DH induced by DNFB (P < 0.01), prolonged survival times of heart and skin allografts (P < 0.01), and decreased the content of hemolysin (P < 0.01), but had no significant effect on the neutral-red phagocytosis of the peritoneal macrophage (P > 0.05). CONCLUSION: Kan had marked suppressive effects on cell-mediated and humoral-mediated immune responses, but no effect on phagocytosis of macrophage.  (+info)

  • rifabutin
  • Two new macrolide antibiotics, clarithromycin and azithromycin, and rifabutin (a rifamycin derivative) have all demonstrated in vitro and in vivo activity against Mycobacterium avium-intracellulare, a common systemic bacterial infection complicating AIDS. (clinicaltrials.gov)
  • The rifamycin group includes the "classic" rifamycin drugs as well as the rifamycin derivatives rifampicin (or rifampin), rifabutin, rifapentine, rifalazil and rifaximin. (wikipedia.org)
  • tuberculosis
  • Guidelines for managing the pharmacologic interactions that can result when patients receive protease inhibitors (PIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs) for treatment of human immunodeficiency virus (HIV) infection together with rifamycins for the treatment of tuberculosis have been published previously ( 1 , 2 ). (cdc.gov)
  • Rifamycins are particularly effective against mycobacteria, and are therefore used to treat tuberculosis, leprosy, and mycobacterium avium complex (MAC) infections. (wikipedia.org)
  • After an extensive modification program Rifampin was eventually produced, that is orally available and has become a mainstay of Tuberculosis therapy Lepetit filed for patent protection of Rifamycin B in the UK in August 1958, and in the US in March 1959. (wikipedia.org)
  • Rifamycins have been used for the treatment of many diseases, the most important one being HIV-related tuberculosis. (wikipedia.org)
  • species
  • A previous study indicated that rifamycin SV can increase NADH-dependent microsomal production of reactive oxygen species. (biochemj.org)
  • These results indicate that rifamycin SV can, in the presence of an iron catalyst, increase microsomal production of reactive oxygen species which can cause DNA-strand cleavage. (biochemj.org)
  • high
  • Rifamycin SV did not significantly increase the high rates of DNA strand cleavage found with NADPH as the microsomal reductant. (biochemj.org)
  • However, despite their activity against bacteria resistant to other antibiotics, the rifamycins themselves suffer from a rather high frequency of resistance. (wikipedia.org)
  • This is due to the high affinity of rifamycins for the prokaryotic RNA polymerase. (wikipedia.org)