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1 s115, the molecular target of the antibiotic fosfomycin.
2 egio- and enantiomerically specific epoxide, fosfomycin.
3 turally occurring, broad-spectrum antibiotic fosfomycin.
4 and by exogenous ligands, such as substrate fosfomycin.
5 ber of bacteria have developed resistance to fosfomycin.
6 mydia rendering these organisms resistant to fosfomycin.
7 nthesis and is the target for the antibiotic fosfomycin.
8 (S)-2-hydroxypropylphosphonic acid (HPP) to fosfomycin.
9 amydial MurA was resistant to high levels of fosfomycin.
10 owth of C. trachomatis was also resistant to fosfomycin.
11 li O157:H7 and given either ciprofloxacin or fosfomycin.
12 d they were both inhibited by the antibiotic fosfomycin.
13 the primary site of action of the antibiotic fosfomycin.
14 e dependent on the presence of the substrate fosfomycin.
15 bserved reversible competitive inhibition by fosfomycin.
16 ly resistant to time-dependent inhibition by fosfomycin.
17 mides, aminoglycosides, chloramphenicol, and fosfomycin.
18 y the clinically used irreversible inhibitor fosfomycin.
19 d for the phosphonate-containing antibiotic, fosfomycin.
20 tall the oxirane "warhead" of the antibiotic fosfomycin.
21 s of host cells, and increased resistance to fosfomycin.
22 sphate (G3P), glucose-6-phosphate (G6P), and fosfomycin.
23 a coli host for responding to the antibiotic fosfomycin.
24 t step in the biosynthesis of the antibiotic fosfomycin.
25 ed synergy between ceftazidime-avibactam and fosfomycin.
26 -2-HPP in the biosynthesis of the antibiotic fosfomycin.
27 alcohol of (S)-2-HPP to the epoxide ring of fosfomycin.
28 ynthesis of the clinically useful antibiotic fosfomycin.
29 )-HPP) in the biosynthesis of the antibiotic fosfomycin.
30 bout inhibition/alkylation by the antibiotic fosfomycin.
31 S-HPP) in the biosynthesis of the antibiotic fosfomycin.
33 zyme conferring resistance to the antibiotic fosfomycin [(1R,2S)-1,2-epoxypropylphosphonic acid] orig
34 opyl-1-phosphonate (S-HPP) to the antibiotic fosfomycin [(1R,2S)-epoxypropylphosphonate] in an unusua
36 nt addition of glutathione to the antibiotic fosfomycin, (1R,2S)-epoxypropylphosphonic acid, renderin
40 hanges due to treatment with the antibiotics fosfomycin (a cell-wall biosynthesis inhibitor) and chlo
44 previously been shown to cause resistance to fosfomycin, a potent antibiotic that specifically target
45 colonization studies, patients treated with fosfomycin acquired a new ceftriaxone-resistant or merop
46 tudies and clinical use, the permeability of fosfomycin across the bacterial outer membrane is largel
48 alone and in combination with meropenem and fosfomycin against A. baumannii strains belonging to clo
49 Our findings corroborate that amikacin and fosfomycin alone efficiently reduced P. aeruginosa in tr
50 eruginosa concentrations versus amikacin and fosfomycin, amikacin, CONTROL, and fosfomycin groups (p
52 r, cells lacking BSH are highly sensitive to fosfomycin, an epoxide-containing antibiotic detoxified
53 urred among 10 patients (14.3%) treated with fosfomycin and 14 patients (19.7%) treated with comparat
54 met in 36 of 48 patients (75.0%) assigned to fosfomycin and 30 of 46 patients (65.2%) assigned to cip
55 men), 48 of 70 patients (68.6%) treated with fosfomycin and 57 of 73 patients (78.1%) treated with co
59 al efficacy and safety of the combination of fosfomycin and imipenem as rescue therapy for MRSA infec
60 is the active site nucleophile alkylated by fosfomycin and implicated this residue in the formation
61 of 74 patients who received daptomycin plus fosfomycin and in 34 of 81 patients who were given dapto
62 sed on available literature, the activity of fosfomycin and nitrofurantoin remain high for most cases
63 e expressed more by plasmids, in contrast to fosfomycin and peptide AMR expression by phages, thereby
64 MLS and sulfonamide) via plasmids or phages (fosfomycin and peptide), whereas others were disseminate
66 as used to methylate the clinical antibiotic fosfomycin and the antimalaria clinical candidate fosmid
67 d to catalyze the epoxidation of ( S)-HPP to fosfomycin and the oxidation of ( R)-HPP to 2-oxopropylp
68 ction of P. aeruginosa isolates (n = 198) to fosfomycin and to compare testing agreement rates across
71 4 patients (17.6%) receiving daptomycin plus fosfomycin, and in 4 of 81 patients (4.9%) receiving dap
72 ound to be associated with susceptibility to fosfomycin, and loss of this system or general inhibitio
73 (+), residues that furnish hydrogen bonds to fosfomycin, and residues located in a putative glutathio
75 e (PDC), and MurA with ceftazidime-avibactam-fosfomycin, antimicrobial susceptibility was restored am
77 ent) will determine the clinical efficacy of fosfomycin as step-down oral therapy to treat complicate
78 ma-imido)-triphosphate (AMPPNP), Mg(II), and fosfomycin, at 1.53 and 2.2 angstroms resolution, respec
80 the enzyme that catalyzes the second step of fosfomycin biosynthesis in Streptomyces wedmorensis.
81 eport the crystal structure of FomA from the fosfomycin biosynthetic gene cluster of Streptomyces wed
83 for substrate-free enzyme to 0.23 cm(-1) for fosfomycin-bound enzyme, 0.28 (1) cm(-1) for FosA with p
84 -lactams, including cefuroxime (CEF), and to fosfomycin but that resistant mutants arise due to gain-
85 (S)-2-hydroxypropylphosphonic acid (HPP) to fosfomycin by HPP epoxidase (HppE), which is a mononucle
86 sfomycin resistance protein FomA inactivates fosfomycin by phosphorylation of the phosphonate group o
87 in the molecular simulations, we found that fosfomycin can rapidly permeate the abundant Escherichia
89 accelerated by bound substrate and produces fosfomycin catalytically with a stoichiometry of unity.
90 age demonstrated that ciprofloxacin, but not fosfomycin, caused enhanced intraintestinal transfer of
94 rised 369 participants, of whom 178 received fosfomycin combination therapy and 191 received monother
95 analysis demonstrated an association between fosfomycin combination therapy and treatment success at
96 randomized controlled trials, which assessed fosfomycin combined with daptomycin or cloxacillin versu
97 We aimed to determine the noninferiority of fosfomycin compared to ciprofloxacin as an oral step-dow
100 ansition zone [TZ] and peripheral zone [PZ]) fosfomycin concentrations using liquid chromatography-ta
101 eus (0.3mg dry weight analyzed) treated with fosfomycin, D-boroAla, D-cycloserine, and vancomycin.
102 lysis when exposed to low concentrations of fosfomycin, d-cycloserine, vancomycin, and nisin, indica
105 ies within the zone of inhibition around the fosfomycin disk is occasionally observed upon susceptibi
106 ere randomized 1 to 1 to receive intravenous fosfomycin disodium at 4 g every 6 hours (70 participant
108 EPR spectrum of oxidized iron-reconstituted fosfomycin epoxidase reveals resonances typical of S = (
109 med using a glucose-6-phosphate-supplemented fosfomycin Etest and Kirby-Bauer disk diffusion (DD) ass
111 n and fosfomycin every 6 hours; amikacin and fosfomycin every 6 hours, with IV meropenem every 8 hour
112 alone every 8 hours; nebulized amikacin and fosfomycin every 6 hours; amikacin and fosfomycin every
113 nebulized amikacin every 6 hours; nebulized fosfomycin every 6 hours; IV meropenem alone every 8 hou
115 Here we assess three well known antibiotics, fosfomycin, flomoxef and amikacin, in combination as pot
120 s (penicillin, cephalosporins, streptomycin, fosfomycin, gramicidin S, rapamycin, indolmycin, microci
121 switch to oral fosfomycin trometamol for the fosfomycin group or an active oral drug or parenteral er
122 kacin and fosfomycin, amikacin, CONTROL, and fosfomycin groups (p < 0.05), without significant differ
126 otherapy, we show that ceftazidime-avibactam-fosfomycin has the potential to offer infected patients
127 Although the addition of the substrate, fosfomycin, has no appreciable effect on the association
128 is showed a 91.8% posterior probability that fosfomycin improves treatment success at 8 weeks (median
129 t success was achieved after commencement of fosfomycin in conjunction with high-dose meropenem.
135 These bacteria therefore seem resistant to fosfomycin in vitro, although they are in fact susceptib
137 ombination of polymyxin B with meropenem and fosfomycin inhibited the polymyxin B-resistant subpopula
139 f daptomycin intravenously daily plus 2 g of fosfomycin intravenously every 6 hours, or 10 mg/kg of d
140 oxide-containing phosphonate natural product fosfomycin is a broad-spectrum antibiotic used in the tr
143 the mechanisms of inactivation are similar, fosfomycin is approximately 50 times more potent than te
144 thoprim-sulfamethoxazole, nitrofurantoin, or fosfomycin is indicated for acute cystitis in adult wome
149 n, amikacin and fosfomycin, and amikacin and fosfomycin + IV meropenem effectively reduced P. aerugin
150 In particular, IV meropenem and amikacin and fosfomycin + IV meropenem groups presented lower P. aeru
152 r that interacts strongly with the substrate fosfomycin (Kd = 17 microM) more weakly with the product
153 the 26 participants, mean plasma and urinary fosfomycin levels were 11.4 +/- 7.6 microg/mL and 571 +/
160 ed to step-down treatment with once-daily 3g fosfomycin or twice-daily 0.5g ciprofloxacin for 10 days
161 ed to cycloserine and bacitracin, but not to fosfomycin or valinomycin; these drugs, like beta-lactam
163 her, this work unravels molecular details of fosfomycin permeation through the outer membrane porin O
164 involved in biosynthesis of the antibiotics fosfomycin, phosphinothricin tripeptide, and dehydrophos
167 in and provide a pharmacokinetic analysis of fosfomycin predose concentrations during treatment.
169 e aimed to determine whether daptomycin plus fosfomycin provides higher treatment success than daptom
170 ics of MurA inactivation by terreic acid and fosfomycin reflect the importance of noncovalent binding
171 of glutathione to carbon-1 of the antibiotic fosfomycin, rendering it ineffective as an antibacterial
173 In addition, we assessed the presence of fosfomycin resistance genes from whole-genome sequencing
176 amily of amino acid kinases that include the fosfomycin resistance protein fomA, which deactivates th
181 te-binding site are conserved in the related fosfomycin resistance proteins FosB and FosX, whereas no
183 or the ability of resulting clones to confer fosfomycin resistance to Escherichia coli were used to i
185 nes: fosA, a locus associated with low level fosfomycin resistance, and tnpB transposase on IncFIB(K)
186 ich encodes a BSH-S-transferase that confers fosfomycin resistance, in several S. aureus strains, inc
189 equally inhibit wild type (WT) MurA and the fosfomycin-resistant MurA C115D mutant, showing an addit
191 ted that 2 is a potent inhibitor of MRSA and fosfomycin-resistant MurA, laying the foundation for the
192 nce to the oxirane or phosphonate oxygens of fosfomycin resulted in variants with very low or no acti
195 Administration of ceftazidime-avibactam and fosfomycin separately significantly increased CFUs, by a
196 s the excision of all, and ciprofloxacin and fosfomycin significantly promote the excision of a subse
197 high bacterial burden, ceftazidime-avibactam-fosfomycin significantly reduced the P. aeruginosa colon
200 improve its performance and robustness, the fosfomycin strip, an antibiotic gradient diffusion strip
201 o tigecycline and had very low resistance to fosfomycin, suggesting a potential for these as empiric
203 carry high biological costs, we suggest that fosfomycin susceptibility of strains that generate inner
204 h microdilution may be a reliable method for fosfomycin susceptibility testing against P. aeruginosa
206 products, including the approved antibiotic fosfomycin, the widely used herbicide phosphinothricin (
207 sistance against the Streptomyces antibiotic fosfomycin, these studies support the notion that sigma(
208 y FosA involves the attack by glutathione on fosfomycin to yield the product 1-(S-glutathionyl)-2-hyd
209 novel ways of using an existing antibiotic, fosfomycin, to treat ESBL-producing Enterobacteriaceae (
210 stals (100 mg twice daily for 5-7 days), and fosfomycin trometamol (3 g in a single dose) are all app
211 ticipants) with the option to switch to oral fosfomycin trometamol for the fosfomycin group or an act
217 ording to EUCAST breakpoints for intravenous fosfomycin use, Enterobacterales and Staphylococcus spp.
218 thway of the clinically important antibiotic fosfomycin uses enzymes that catalyse reactions without
219 event-related discontinuations occurred with fosfomycin vs comparators (6 discontinuations [8.5%] vs
227 c, resistances to colistin, tigecycline, and fosfomycin were also observed as a result of repeated, i
231 target of the naturally occurring antibiotic fosfomycin, which covalently attaches to Cys115 in the a
233 hed antibiotic target since the discovery of fosfomycin, which specifically inhibits MurA by covalent
234 high intrinsic resistance to the antibiotic fosfomycin, which targets UDP-MurNAc de novo biosynthesi
235 tance was high; however, coadministration of fosfomycin with ceftazidime-avibactam yielded a lower fr