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1 -2-isopropylamino-5,6-dichlorobenzimidazole (maribavir).
2 irals did not preclude treatment response to maribavir.
3 NA initially cleared then rebounded while on maribavir.
4 ed 26 to 130 (median 56) days after starting maribavir.
5  This response synergized with an antiviral, maribavir.
6 d antiviral activity of the anti-HCMV agent, maribavir.
7 otection was provided by the viral inhibitor maribavir.
8 duction and nuclear egress in the absence of maribavir.
9 ausea, and vomiting, were more frequent with maribavir.
10 ect can be antagonized by the antiviral drug maribavir.
11 cells treated with the UL97 kinase inhibitor maribavir.
12 ding frames that could explain resistance to maribavir.
13 ro) as the one responsible for resistance to maribavir.
14 s or with wild-type virus in the presence of maribavir.
15 ectly involved in the mechanism of action of maribavir.
16 al kinase was shown to be a direct target of maribavir.
17 pe virus and was resistant to both BDCRB and maribavir.
18 in II and inhibited by a new antiviral drug, maribavir.
19 cifically inhibited by a new antiviral drug, maribavir.
20 the efficacy and safety of prophylactic oral maribavir (100 mg twice daily) for prevention of CMV dis
21 e randomized to receive CMV prophylaxis with maribavir (100 mg twice daily, 400 mg once daily, or 400
22 gh week 16.352 patients were randomized (235 maribavir; 117 IAT).
23 tant resistant to the benzimidazole compound maribavir (1263W94), reflecting the anti-UL97 effect of
24 nts discontinued treatment due to TEAEs with maribavir (13.2%) than IAT (31.9%).
25 n patients receiving each respective dose of maribavir (15%, P = .001; 30%, P = .051; 15%, P = .002)
26 recipients with CMV-seropositive donors (147 maribavir; 156 ganciclovir).
27 experienced recurrent CMV infection while on maribavir, 23 had available UL97 genotyping data; 17 had
28 experienced recurrent CMV infection while on maribavir, 23 had available UL97 genotyping data; 17 had
29                  Among patients treated (273 maribavir; 274 valganciclovir), the primary endpoint of
30 ontinuations were mostly due to neutropenia (maribavir, 4.0%; valganciclovir, 17.5%).
31 h R/R cytomegalovirus were randomized 2:1 to maribavir 400 mg twice daily or investigator-assigned th
32 st-HCT were stratified and randomized 1:1 to maribavir 400 mg twice daily or valganciclovir (dose-adj
33 ates of 70%, 63%, and 68%, respectively, for maribavir 400, 800, and 1200 mg twice daily.
34 ndomized (1:1:1) to twice-daily dose-blinded maribavir 400, 800, or 1200 mg for up to 24 weeks.
35  of noninferiority of maribavir was not met (maribavir, 69.6%; valganciclovir, 77.4%; adjusted differ
36  events (TEAEs) were similar between groups (maribavir, 97.4%; IAT, 91.4%).
37              Understanding UL97 function and maribavir action should help elucidate this interesting
38 omized trial includes 234 patients receiving maribavir and 116 receiving investigator-assigned standa
39 hin 3 weeks was 62% among those who received maribavir and 56% among those who received valganciclovi
40 t, or cidofovir in 56% of patients receiving maribavir and 68% receiving IAT, including 9 newly pheno
41                                      We used maribavir and a UL97 null mutant, which is severely defi
42 val, and non-CMV infections were similar for maribavir and ganciclovir patients.
43 op substitution G343A) that conferred strong maribavir and ganciclovir resistance in vitro.
44                               Development of maribavir and ganciclovir resistance was compared after
45                    Antiviral drugs including maribavir and letermovir are in development and prospect
46  residues and was sensitive to inhibition by maribavir and to a mutation that inactivates UL97 cataly
47 eek 16, 52.7% and 48.5% of patients treated (maribavir and valganciclovir, respectively) maintained C
48                             Among them, 63% (maribavir) and 21% (IAT) were treatment responders.
49 ointestinal adverse events was reported with maribavir, and a higher incidence of neutropenia was rep
50 was passaged in increasing concentrations of maribavir, and resistant virus was isolated.
51 lliliter]) were randomly assigned to receive maribavir at a dose of 400, 800, or 1200 mg twice daily
52  CMV infection within 6 weeks after starting maribavir at a dose of 800 mg twice daily; T409M resista
53                                              Maribavir at a dose of at least 400 mg twice daily had e
54                      Novel therapies such as maribavir, brincidofovir, and letermovir should be furth
55                      These results show that maribavir can reduce the incidence of CMV infection and,
56 ent-to-treat analysis, the noninferiority of maribavir compared to oral ganciclovir for prevention of
57 d on the prespecified noninferiority margin, maribavir demonstrated comparable CMV viremia clearance
58 he most common TEAE (78/120; 65%) and led to maribavir discontinuation in 1 patient.
59 response to treatment were similar among the maribavir dose groups.
60                    In a phase 2, open-label, maribavir dose-blinded trial, recipients of hematopoieti
61 ntional therapy (trial 202) and 119 received maribavir for asymptomatic infection (trial 203).
62 ntional therapy (trial 202) and 119 received maribavir for asymptomatic infection (trial 203).
63  number (n = 241) received valganciclovir or maribavir for at least 21 days (median, 55-56 days).
64 parate Phase 2 trials, 120 patients received maribavir for cytomegalovirus (CMV) infection failing co
65 parate phase 2 trials, 120 patients received maribavir for cytomegalovirus (CMV) infection failing co
66                   The safety and efficacy of maribavir for preemptive treatment of CMV infection in t
67 had postbaseline data available - 117 in the maribavir group and 39 in the valganciclovir group.
68      A greater percentage of patients in the maribavir group discontinued the trial medication becaus
69  worsened during treatment was higher in the maribavir group than in the valganciclovir group (52 of
70 r incidence of neutropenia were found in the maribavir group.
71 igenemia was lower in each of the respective maribavir groups (15%, P = .046; 19%, P = .116; 15%, P =
72  CMV DNA was lower in each of the respective maribavir groups (7%, P = .001; 11%, P = .007; 19%, P =
73                                              Maribavir >=400 mg twice daily was active against RR CMV
74                                              Maribavir had fewer treatment discontinuations due to TE
75                                              Maribavir had no adverse effect on neutrophil or platele
76                                              Maribavir has multimodal anti-cytomegalovirus activity t
77                    The investigational agent maribavir has shown promise as preemptive treatment; in
78    The ineffectiveness of the UL97 inhibitor maribavir in clinical trials might be better explained w
79 egalovirus (CMV) activity and safety of oral maribavir in CMV-seropositive allogeneic stem-cell trans
80  detected in 60 (26%) of those randomized to maribavir, including 49 (48%) of 103 nonresponders and 2
81 pylamino-5,6-dichlorobenzimidazole (1263W94; maribavir), inhibits viral DNA synthesis and nuclear egr
82                                              Maribavir is a benzimidazole riboside with activity agai
83                                              Maribavir is active against RR CMV strains.
84                                              Maribavir is an oral benzimidazole riboside with potent
85             At a dose of 100 mg twice daily, maribavir is safe but not adequate for prevention of CMV
86 stant or refractory CMV infection, including maribavir, letermovir, and adoptive T-cell transfer.
87                                              Maribavir (MBV) inhibits Epstein-Barr virus (EBV) replic
88  cytomegalovirus (CMV) UL97 kinase inhibitor maribavir (MBV) is undergoing clinical antiviral trials.
89                               More recently, maribavir (MBV), an l-ribofuranoside benzimidazole, has
90 compounds with new molecular targets such as maribavir (MBV), FV-100, AIC361, and AIC246.
91         When T2294 was serially passed under maribavir (MBV), phenotypic changes and viral UL97 mutat
92 viral activity of the pUL97 kinase inhibitor maribavir (MBV).
93  Testing the recombinants for sensitivity to maribavir narrowed the locus of resistance to genes UL26
94 kinase activity using the antiviral compound maribavir or deletion of the UL97 gene resulted in decre
95 nt of infected cells with the UL97 inhibitor maribavir or infection with a UL97 mutant led to a punct
96      Inhibition of UL97 kinase activity with maribavir or mutation of an essential amino acid in the
97                 Among 547 patients receiving maribavir or valganciclovir for first-episode cytomegalo
98                                              Maribavir partially restored structural features, includ
99  pp65 antigenemia or CMV DNA PCR compared to maribavir patients at both 100 days (20% vs. 60%; p < 0.
100  disease in placebo patients but none in the maribavir patients.
101                                              Maribavir preemptive therapy failed to demonstrate nonin
102                                          One maribavir recipient developed a novel UL97 gene mutation
103 sistance mutations were detected in 24 (10%) maribavir recipients at 35-125 days (median, 56 days) af
104               Addition of the HCMV inhibitor maribavir reduced viral spread but failed to restore act
105 tient 3 developed ganciclovir (PK-L595S) and maribavir resistance (PK-T409M).
106 med in 17 (74%) of 23 patients with emergent maribavir resistance after retreatment with an alternati
107 enotyped mutation C480F conferred high-grade maribavir resistance and low-grade ganciclovir resistanc
108                  After 3-8 weeks of therapy, maribavir resistance emerged earlier and more frequently
109 ral shedding was cleared without evidence of maribavir resistance in an isolate obtained after therap
110 ion and showed slight growth attenuation and maribavir resistance in cell culture.
111 tions T409M, H411Y or C480F emerge to confer maribavir resistance in patients with recurrent CMV infe
112 ions T409M, H411Y, or C480F emerge to confer maribavir resistance in patients with recurrent CMV infe
113                      Posttreatment, emergent maribavir resistance mutations were detected in 60 (26%)
114                            Detected baseline maribavir resistance mutations were UL27 L193F (n = 1) a
115                              The most common maribavir resistance mutations were UL97 T409M (n = 34),
116                The relatively rapid onset of maribavir resistance probably resulted from incomplete v
117 UL97 mutations T409M and H411Y, which confer maribavir resistance.
118 ents confirmed that UL27 mutations conferred maribavir resistance.
119  patients; 13 developed mutations conferring maribavir resistance.
120 bound in plasma cytomegalovirus DNA while on maribavir strongly suggests emerging drug resistance.
121 patients (e.g., ganciclovir, letermovir, and maribavir) target later stages of the HCMV life cycle.
122 ese strains showed lower-grade resistance to maribavir than the UL97 mutant.
123                                        After maribavir therapy (400-1200 mg twice daily), UL97 mutati
124                                        After maribavir therapy (400-1200 mg twice daily), UL97 mutati
125                   Although noninferiority of maribavir to valganciclovir for the primary endpoint was
126 e-resistant structures in mutant-infected or maribavir-treated cells under conditions where the virus
127  rare in the cytoplasm of mutant-infected or maribavir-treated cells; the magnitudes of these decreas
128           Significantly more patients in the maribavir versus IAT group achieved the primary endpoint
129 of CMV disease was not established (12% with maribavir vs. 8% with ganciclovir: event rate difference
130                                         With maribavir (vs valganciclovir), fewer patients experience
131                                              Maribavir was associated with less acute kidney injury v
132                                              Maribavir was discontinued due to adverse events in 41/1
133                                Resistance to maribavir was mapped to UL97, and this viral kinase was
134 nt of refractory or resistant CMV infection, maribavir was more efficacious and better tolerated when
135 ), the primary endpoint of noninferiority of maribavir was not met (maribavir, 69.6%; valganciclovir,
136                                              Maribavir was superior to IAT for cytomegalovirus viremi
137 mental cytomegalovirus UL97 kinase inhibitor maribavir was used to treat 2 cases of infection in whic
138                                              Maribavir was well-tolerated and associated with fewer h
139  on Ser-38 and was specifically sensitive to maribavir, whereas phosphorylation of this peptide by cA
140        A phase 2 study indicated efficacy of maribavir with fewer treatment-limiting toxicities than

 
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