ライフサイエンスコーパス: rifamycin

1 in patients also receiving ethambutol and a rifamycin.

2 of complex lipids, including the antibiotic rifamycin.

3 th the drug interaction liability typical of rifamycins.

4 lled six healthy volunteers unexposed to the rifamycins.

5 on initiation inhibitors myxopyronin and the rifamycins.

6 luding antibiotics, such as erythromycin and rifamycins.

7 in Mg2+ concentration confers resistance to rifamycins.

8 ions confer resistance to some but not other rifamycins.

9 TB was defined as resistance to isoniazid, a rifamycin, a fluoroquinolone, and at least 1 of amikacin

10 However, the clinical utility of rifamycins against Mycobacterium abscessus is seriously

11 t has 71% identity (80% similarity) with the rifamycin AHBA synthase from Amycolatopsis mediterranei,

12 rapAT2) of A. mediterranei S699 produced new rifamycin analogs, 24-desmethylrifamycin B and 24-desmet

13 rates of mutation may reflect the choice of rifamycin analogs.

14 robiologic activity of regimens containing a rifamycin and pyrazinamide.

15 (AHBA), the unique biosynthetic precursor of rifamycin and related ansamycins, a series of target-dir

16 arding drug interactions, chiefly related to rifamycins and antiretroviral drugs; and 5) revised reco

17 linked to other antibacterial agents such as rifamycins and oxazolidinones are designed to overcome b

18 rate proof of principle for this subclass of rifamycins and support further expansion of structure-ac

19 m Amycolatopsis mediterranei, which produces rifamycin, and Actinosynnema pretiosum, which produces a

20 ctam, beta-lactam-beta-lactamase inhibitors, rifamycin, and cephalosporin.

21 ted is a 3-drug regimen including macrolide, rifamycin, and ethambutol that is continued for 12 month

22 KSs harboring modules from the erythromycin, rifamycin, and rapamycin synthases.

23 Ansamycins such as rifamycin, ansamitocin, and geldanamycin are an importan

24 Rifamycin antibacterial agents inhibit bacterial RNA pol

25 Rifamycin antibiotics are a key component of TB therapy

26 Rifamycin antibiotics are a valuable class of antimicrob

27 es, and differences in DDI potential between rifamycin antibiotics are not well established.

28 aliniketals and the ansa chain of the potent rifamycin antibiotics, which co-occur in the fermentatio

29 l resistance to a variety of clinically used rifamycin antibiotics.

30 elapse were higher with shorter durations of rifamycins (aOR 2 vs >/=8 months = 5.0 [1.9, 13.2]; 6 vs

31 ll, our results suggest that doxycycline and rifamycin are general inhibitors of Cu(II)-induced beta2

32 ens incorporating the antimicrobial class of rifamycins are designed to improve adherence and complet

33 While rifamycins are the pillar of tuberculosis treatment, the

34 ajority of patients received isoniazid and a rifamycin as part of multidrug regimen.

35 Mutants of the rifH and -J genes produced rifamycin B at 1% and 10%, respectively, of the yields o

36 Inactivation of rifF gives a rifamycin B nonproducing mutant that still accumulates a

37 The assembly of the polyketide backbone of rifamycin B on the type I rifamycin polyketide synthase

38 Rifamycin B, a product of Amycolatopsis mediterranei S69

39 biosynthesis of ansamycin antibiotics, like rifamycin B, involves formation of 3-amino-5-hydroxybenz

40 Use of shorter rifamycin-based regimens for tuberculosis prevention and

41 In adults, compared to mono-H regimens all rifamycin-based regimens were safer, although 4R had the

42 Prevention relies mostly on treatment with rifamycin-based regimens; current vaccines have limited

43 berculosis (TB) prevention, and short course rifamycin-based therapies are preferred.

44 berculosis (TB) prevention, and short course rifamycin-based therapies are preferred.

45 This rifamycin-based TPT induced dysbiosis was characterized

46 region) to document the immediate effect of rifamycin-based TPT on the gut microbiota composition an

47 Among many semisynthetic rifamycins, benzoxazinorifamycins have great potential f

48 site on RNAP is immediately adjacent to the rifamycin binding site.

49 E binding site on RNAP is different from the rifamycin binding site.

50 n regulatory functions in AHBA formation for rifamycin biosynthesis by A. mediterranei.

51 adieno ic acid (P8/1-OG), an intermediate in rifamycin biosynthesis, in an extensively manipulated st

52 omal peptide synthetases/polyketide synthase rifamycin biosynthetic cluster of Amycolatopsis mediterr

53 RifN, product of one of three genes from the rifamycin biosynthetic gene cluster known to be essentia

54 that the saliniketals are byproducts of the rifamycin biosynthetic pathway diverging at the stage of

55 f three-dimensional structure information of rifamycins bound to RNA polymerase (RNAP) and the human

56 o not exhibit cross-resistance, and GE and a rifamycin can bind simultaneously to RNAP.

57 azid/rifapentine group had monoresistance to rifamycin, compared with none of three in the rifampin g

58 A rifamycin-containing regimen that otherwise met pan-tube

59 ure rate of 93% when receiving standard-dose rifamycin-containing regimens.

60 Management of rifamycin DDIs are complex, particularly in patients wit

61 ng sites of other antibiotics, including two rifamycin derivatives, rifabutin and rifapentine, and st

62 omplete cross-resistance among the different rifamycin derivatives.

63 included incidence of severe ADEs, unplanned rifamycin discontinuation, mean time to unplanned regime

64 Here, we show that rifamycins do not affect the affinity of binding of Mg(2

65 Accordingly, GE and rifamycins do not exhibit cross-resistance, and GE and a

66 We conclude that rifamycins do not function by allosteric modulation of b

67 ith ART demonstrated no associations between rifamycin duration, dosing schedule, and outcomes.

68 rolide plus >=1 other drug targeting MAC-PD (rifamycin, ethambutol, fluoroquinolone, or amikacin) pre

69 es the chemical backbone that members of the rifamycin family of antibiotics have in common.

70 Use of rifamycins for >/=8 months and daily dosing in the inten

71 ens showed that various therapies containing rifamycins for 3 months or more were efficacious at prev

72 egravir, and cabotegravir when used with the rifamycins for both tuberculosis treatment and preventio

73 tuberculosis drugs are driven mainly by the rifamycins (for example, the first-line tuberculosis dru

74 he A. mediterranei genome results in loss of rifamycin formation; production of the antibiotic is res

75 Recently, Artsimovitch et al. proposed that rifamycins function by allosteric modulation of binding

76 Mycobacterium tuberculosis monoresistant to rifamycin had very low concentrations of isoniazid.

77 Since 1967, Rifampin (RMP, a Rifamycin) has been used as a first line antibiotic trea

78 (levofloxacin, ethambutol, azithromycin, and rifamycin) has shown some promise in preliminary studies

79 sed by a novel resistance mechanism, namely, rifamycin inactivation by ADP-ribosylation.

80 Additionally, rifamycins induce cytochrome P450 3A4 (CYP3A4), a major

81 We identified rifamycin induced DMEs, cytochrome P450 (CYP) 2C8/3A4/3A

82 XRalpha as key transcriptional regulators of rifamycin induced DMEs.

83 We propose that a rifamycin-induced signal is transmitted over approximate

84 RNA polymerase at a site distinct from where rifamycins interact.

85 Rifampin, a semisynthetic rifamycin, is the cornerstone of current tuberculosis tr

86 Of the agents tested, rifamycins led to DD Mtb generation, an effect lacking i

87 Regimens containing rifamycins may be effective alternatives to isoniazid mo

88 Patients who relapsed with rifamycin monoresistance were younger (median age 29 vs

89 No rifamycin monoresistant relapse has occurred among 1004

90 Relapse with rifamycin monoresistant tuberculosis occurred among HIV-

91 genes that confer resistance to quinolones, rifamycin, multidrug, aminoglycosides, and tetracycline.

92 Monoresistance to rifamycins necessitates longer and more toxic regimens f

93 No rifamycin pharmacokinetic parameter was consistently and

94 sequence; and RifKR10 from module 10 of the rifamycin PKS, whose specificity is unclear from both th

95 oduct structure; RifKR7 from module 7 of the rifamycin PKS, whose stereospecificity cannot be predict

96 ketide backbone of rifamycin B on the type I rifamycin polyketide synthase (PKS), encoded by the rifA

97 ed the acyltransferase domain of module 6 of rifamycin polyketide synthase with that of module 2 of r

98 inactivation of the rifG gene did not affect rifamycin production significantly.

99 ts of the genomic rifG-N and -J mutations on rifamycin production, indicating that all these genes en

100 Accordingly, covalent linkage of GE to a rifamycin provides a bipartite inhibitor having very hig

101 Decarboxylation of rifamycin provides salinisporamycin, which upon truncati

102 d efficacy of regimens containing pretomanid-rifamycin-pyrazinamide among participants with drug-sens

103 Pretomanid-rifamycin-pyrazinamide combinations are potent in mice b

104 f treatment failure or relapse with acquired rifamycin resistance among patients with low CD4 lymphoc

105 e PCR ribotypes present and the emergence of rifamycin resistance during the infection cycle.

106 malabsorption of anti-TB drugs and acquired rifamycin resistance.

107 nine (89%) cases had isolates with acquired rifamycin resistance.

108 Increased occurrence of Rifamycin-resistant (RIF(R) ) TB, approximately 41% of w

109 antibiotics has resulted in the emergence of rifamycin-resistant strains of Mycobacterium tuberculosi

110 synthase (PKS) genes, rifA-rifE, involved in rifamycin (Rf) biosynthesis in Amycolatopsis mediterrane

111 The mycothiol S-conjugate of rifamycin S was produced under physiologically relevant

112 he C(15)-C(27) fragments of chaxamycins A/D, rifamycin S, and the C(12)-C(24) fragment of salinispora

113 metabolite from a biosynthetic precursor to rifamycin S.

114 nalysis assessing the effects of duration of rifamycins, schedule of dosing, and antiretroviral thera

115 A potent rifamycin-sparing regimen could revolutionize the treatm

116 A proposed mechanism in which rifamycins sterically block the extension of nascent RNA

117 rifamyin W to yield both the saliniketal and rifamycin structural classes.

118 cephalosporin, fluoroquinolone, monobactam, rifamycin, sulfonamides, and miscellaneous; and proporti

119 all-molecule inhibitors rifampicin (Rif) and rifamycin SV (Rif SV).

120 ied small molecule amyloid inhibitors (i.e., rifamycin SV and doxycycline), we demonstrate that coval

121 monomer stage, we found that doxycycline and rifamycin SV exert their effect by binding to oligomeric

122 ted the use of another ansamycin antibiotic, rifamycin SV MMX (AEMCOLO) in the treatment of SIBO.

123 The side effect profile of Rifamycin SV MMX has been described elsewhere in the piv

124 We found that two molecules, doxycycline and rifamycin SV, can inhibit beta2m amyloid formation in vi

125 ed together to pinpoint the binding sites of rifamycin SV, doxycycline, and another molecule, suramin

126 In the presence of the antibiotic rifamycin SV, which inhibits amyloid growth of wild-type

127 erated in situ by DEBS KR1, DEBS KR6, or the rifamycin synthase KR7 (RIFS KR7), respectively.

128 Rifamycin synthetase assembles the chemical backbone tha

129 four-module RifA protein (530 kDa) from the rifamycin synthetase could not be efficiently produced i

130 The rifamycin synthetase is primed with a 3-amino-5-hydroxyb

131 he loading and initial elongation modules of rifamycin synthetase reveal that this bimodular protein

132 substrate tolerance of the loading module of rifamycin synthetase suggests that the module has potent

133 Rifamycins, the clinically important antibiotics, target

134 cture-based approach, we rationally redesign rifamycins through strategic modification of the ansa-ch

135 Concomitant use of rifamycins to treat or prevent tuberculosis can result i

136 of our effort to generate better analogs of rifamycin, we substituted the acyltransferase domain of

137 As single agents, these rifamycins were as effective as a standard-of-care four-

138 Rifapentine is a cyclopentyl-substituted rifamycin whose serum half-life is five times that of ri

139 -based regimen (a macrolide, ethambutol, and rifamycin, with or without amikacin) was prescribed for