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1 It cleaved penicillin and was inhibited by sulbactam.
2 inhibited by beta-lactamase inhibitor, i.e. sulbactam.
3 and 71 patients were treated with Ampicillin-Sulbactam.
4 ctam is superior to both clavulanic acid and sulbactam.
5 as well as on the beta-lactamase inhibitor, sulbactam.
6 ination of CMS, a carbapenem, and ampicillin-sulbactam.
7 he same time resistant to I/R and ampicillin/sulbactam.
8 reports on SBL inhibition by tazobactam and sulbactam.
9 s to ampicillin (100 versus 20%), ampicillin-sulbactam (100 versus 13%), vancomycin (100 versus 57%),
10 cultures [53.1%]; institution B: ampicillin-sulbactam, 9 [69.2%]; and institution C: penicillin, 32
11 -lactamase-inhibiting antibiotics ampicillin-sulbactam (A/S) and amoxicillin-clavulanic acid (A/C) fo
12 amoxicillin-clavulanate (AUG) and ampicillin-sulbactam (A/S) susceptibility testing by three differen
13 ure of the inhibitor preacylation complex of sulbactam, a clinical beta-lactamase inhibitor, bound in
15 azole, cefotetan, ampicillin, and ampicillin-sulbactam all promoted persistent high levels of stool V
17 bited increased susceptibility to ampicillin/sulbactam, an important difference compared to ampicilli
21 The pharmacodynamic activity of ampicillin/sulbactam and ceftazidime/avibactam was evaluated agains
23 structures of the beta-lactamase inhibitors sulbactam and clavulanic acid bound to the deacylation-d
25 mately twice as much enamine intermediate as sulbactam and clavulanic acid, which correlates with its
27 ases in resistance were noted for ampicillin-sulbactam and clindamycin, while significant decreases i
28 relationship associated with the activity of sulbactam and durlobactam established in nonclinical inf
30 tablish the MIC test method, combinations of sulbactam and durlobactam were evaluated using a panel o
35 phenotype, we investigated the activities of sulbactam and two novel penem beta-lactamase inhibitors
36 eta-lactamase and the inhibitors tazobactam, sulbactam, and clavulanic acid are followed in single cr
38 clinically relevant inhibitors, tazobactam, sulbactam, and clavulanic acid, and SHV beta-lactamase (
39 that for small ligands, such as tazobactam, sulbactam, and clavulanic acid, the positioning of the l
41 ve inhibitory activities of clavulanic acid, sulbactam, and tazobactam against clinically important b
42 0G variant that reacts with clavulanic acid, sulbactam, and tazobactam in solution, but lacks the cha
43 by the clinical inhibitors (clavulanic acid, sulbactam, and tazobactam), but the prevalence of inhibi
44 gents used in combination, such as colistin, sulbactam, and the tetracyclines, and offer clinical pea
45 he clinically used inhibitors tazobactam and sulbactam are effective in the inhibition of activity of
46 tients receiving prophylaxis with ampicillin-sulbactam, aztreonam and vancomycin, or tigecycline (P =
47 with Enterobacter cloacae versus ampicillin-sulbactam, aztreonam, ticarcillin, and ticarcillin-clavu
48 n most clinical scenarios, a dose-optimized, sulbactam-based regimen is recommended with the addition
49 on both systems (exceptions were ampicillin-sulbactam, cefoxitin, minocycline, and nitrofurantoin).
50 dies of S130G SHV inhibited with tazobactam, sulbactam, clavulanic acid, and 2'-glutaroxy penem sulfo
51 aximal populations at 10, 22, and 29 min for sulbactam, clavulanic acid, and tazobactam, respectively
52 ation demonstrated that high-dose ampicillin/sulbactam combinations were required to achieve 4-6 log1
53 demonstrated 70 and 88 +/- 3 Da fragments of sulbactam covalently attached to the beta-lactamase.
55 statin, penicillin G, ampicillin, ampicillin/sulbactam, doxycycline, and minocycline; acceptable (90%
56 y to obtaining the preacylation complex with sulbactam due to further decreased reactivity toward sub
58 y CRAB meningitis with the administration of sulbactam-durlobactam and meropenem and highlights the n
69 oped beta-lactam agents like cefiderocol and sulbactam-durlobactam, which have demonstrated contrasti
73 t is demonstrated that with the exception of sulbactam, each compound forms observable trans-enamine
74 transferred ceftazidime resistance or showed sulbactam enhancement of oxyimino-beta-lactam susceptibi
75 One of the most promising combinations is sulbactam-ETX2514, whose potent antibacterial activity,
77 t species, with SHV-1, while clavulanate and sulbactam form a mixture of trans-enamine and two labile
79 running the reactions with the two forms of sulbactam in parallel, provides an element of control an
87 n combined with durlobactam, the activity of sulbactam is restored against this problematic pathogen.
90 ith penicillin G, ampicillin, and ampicillin-sulbactam MICs and inhibition zones on penicillin (2-U)
91 am forms a larger population of enamine than sulbactam or clavulanic acid does and that tazobactam's
97 ss spectrometry analysis of SHV inhibited by sulbactam showed that SHV-1 beta-lactamase was unmodifie
103 It is proposed that for the unsubstituted sulbactam the conversion from imine to enamine, which in
105 s us to conclude that, for the unsubstituted sulbactam, the formation of the cross-linked intermediat
108 od susceptibilities but only with ampicillin-sulbactam, ticarcillin-clavulanate, and/or clindamycin.
109 acillin, piperacillin-tazobactam, ampicillin-sulbactam, ticarcillin-clavulanate, cefotaxime, cefoteta
110 a three-day treatment regimen of Ampicillin-Sulbactam to that of a three-day regimen of Ertapenem in
111 hibitors of class A beta-lactamases, such as sulbactam, undergo a complex series of chemical reaction
112 nvestigated the mechanisms of tazobactam and sulbactam using mass spectrometry under denaturing and n
113 and DD were unacceptably high for ampicillin-sulbactam (VM error, 9.8%; minor [m] error, 16.1%), pipe
114 -S, -Q, and -L) variants revealed the Ki for sulbactam was significantly elevated for the R244 varian
117 Li), i.e., the penam sulfones tazobactam and sulbactam, which are mechanism-based inhibitors working