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1 y and demonstrates the antitumor activity of rimantadine.
2 nel that confer resistance to amantadine and rimantadine.
3                  No included study evaluated rimantadine.
4 rgeted by the antiviral drugs amantadine and rimantadine.
5 e drugs amantadine and its methyl derivative rimantadine.
6  to confer resistance to both amantadine and rimantadine.
7 the M2 ion-channel inhibitors amantadine and rimantadine.
8 cifically blocked by the anti-influenza drug rimantadine.
9 nsitivity to the prototypic channel-blocker, rimantadine.
10 54 subjects received placebo and 51 received rimantadine (100 mg orally, twice a day).
11 h the activation of interferons, vaccines or rimantadine against HPV and the inhibition of EGFR, SHP-
12 group to the methyl adduct of the amantadine/rimantadine analogue, 2-methyl-2-aminoadamantane, led to
13              Seventeen subjects (38%) in the rimantadine and 26 (53%) in the placebo group became ill
14 ues 40-45 with a polar hydrogen bond between rimantadine and aspartic acid residue 44 (D44) that appe
15 dues 40-45 and a polar hydrogen bond between rimantadine and aspartic acid residue 44 (D44).
16  synthesis of deuterium-labeled (R)- and (S)-rimantadine and the characterization of their protein-li
17 st a complex set of interactions between (R)-rimantadine and the M2 proton channel, leading to a high
18  which occur more often with amantadine than rimantadine, and potential drug interactions are additio
19                                  Amantadine, rimantadine, and the newly available drugs zanamivir and
20 The M2 ion channel inhibitors amantadine and rimantadine are effective for prophylaxis, and they decr
21                  Adamantanes (amantadine and rimantadine) are one of the two classes of Food and Drug
22 ss peaks, which indicate that amantadine and rimantadine bind to the pore in the same fashion as for
23 these mutations are likely to interfere with rimantadine binding and lead to a drug insensitive chann
24  our functional data suggest that amantadine/rimantadine binding outside of the channel pore is not t
25  functional data suggest that the amantadine/rimantadine binding site identified on the outside of th
26         Models contained a predicted lumenal rimantadine-binding site, as well as a second druggable
27                                              Rimantadine binds at four equivalent sites near the gate
28  pore-forming helices to which amantadine or rimantadine binds, and compound binding specifically to
29                                 Accordingly, rimantadine blocked an early stage of ZIKV cell culture
30 ution NMR structure of M2(18-60) showed four rimantadines bound to the carboxy-terminal lipid-facing
31 ble agents, the M2 inhibitors amantadine and rimantadine, could only be used to treat influenza A inf
32                   The antiviral E5 inhibitor rimantadine demonstrated remarkable single-agent antitum
33 of the tetrameric M2 channel in complex with rimantadine, determined by NMR.
34                                     Finally, rimantadine effectively blocked ZIKV viraemia in preclin
35                                              Rimantadine had no effect on nasal patency, mucociliary
36                      In mice, treatment with rimantadine had no effect on survival.
37                          In complex with M2, rimantadine has always been characterized as a racemic m
38 gainst influenza in families, amantadine and rimantadine have had inconsistent effectiveness, partly
39                In conclusion, amantadine and rimantadine have no direct and specific inhibitory effec
40              The adamantanes, amantadine and rimantadine, have been used as first-choice antiviral dr
41                                              Rimantadine hydrochloride (alpha-methyl-1-adamantane-met
42  of (13)C-labeled M2TM and methyl-deuterated rimantadine in lipid bilayers showed that the polar amin
43 ot spots at the exterior locations that bind rimantadine in the NMR structure, although these sites a
44 than to His37, in contrast to amantadine and rimantadine in the wild-type channel, suggesting that th
45 f M2 using the anti-viral drug amantadine or rimantadine inhibits viral replication.
46 sults indicate that the pore binding site of rimantadine is correlated with previously reported wides
47             In contrast, the NMR data show 4 rimantadine molecules bound on the outside of the helice
48  pore of the channel, the NMR data show four rimantadine molecules bound on the outside of the helice
49 esults do not support a preventive effect of rimantadine on the development of otologic manifestation
50 ffects of amantadine and a related analogue, rimantadine, on viral protease, helicase, ATPase, RNA-de
51 n of influenza A HlNl virus and treated with rimantadine or placebo.
52        This could be explored by repurposing rimantadine, or development of new M-targeted therapies.
53 ations of vaccination and antiviral therapy (rimantadine, oseltamivir, or zanamivir or no treatment)
54 0-fold improvement over prototypes, suppress rimantadine resistance polymorphisms at submicromolar co
55 nders it insensitive to amantadine (AMT) and rimantadine (RMT) block, but it is unknown whether the i
56  aminoadamantyl drugs such as amantadine and rimantadine (Rmt).
57                   The ion selectivity of the rimantadine-sensitive current through M2 was determined.
58  cloistered for 8 days and challenged with a rimantadine-sensitive strain of influenza A H1N1 virus a
59   Adults were intranasally inoculated with a rimantadine-sensitive strain of influenza A HlNl virus a
60 36 of the A/M2 TM domain show 85% amantadine/rimantadine sensitivity and specific activity comparable
61                               Amantadine and rimantadine share features that would make them useful a
62 s are minimal upon addition of the inhibitor rimantadine, suggesting that the drug does not bind to S
63         Anti-influenza drugs, amantadine and rimantadine, targeting the M2 channel from influenza A v
64                        Unlike amantadine and rimantadine that target the M2 protein of influenza A vi
65 vir, laninamivir, baloxavir, amantadine, and rimantadine) that enrolled 19 096 individuals (mean age
66                       Vaccination and use of rimantadine, the most cost-beneficial strategy, was $30.
67                  Both patients are receiving rimantadine therapy and performing well, with functionin
68 e mapping, but has a too narrow pore for the rimantadine to access the internal hot spot, and hence t
69  can be exploited using the HPV E5 inhibitor rimantadine to improve outcomes for head and neck cancer
70 lled into a randomized double-blind study of rimantadine treatment of experimental influenza A infect
71                       Compared with placebo, rimantadine treatment reduced viral shedding, systemic s
72                       A beneficial effect of rimantadine was documented for virus shedding, symptom l
73    Futhermore, the (15)N-labeled ammonium of rimantadine was observed near A30 (13)Cbeta and G34 (13)
74                          The IC50 values for rimantadine were low across all genotypes, ranging from
75 l drug amantadine (and its methyl derivative rimantadine), whereas BM2 channel activity is not affect
76 ity of p7 can be inhibited by amantadine and rimantadine, which are potent blockers of the influenza
77 ne-containing adamantyl drugs amantadine and rimantadine, which have been shown to bind specifically
78 sensitive to antiviral drugs, amantadine and rimantadine, while the S31N mutant viruses, such as the
79 target of the antiviral drugs amantadine and rimantadine, whose effectiveness has been abolished by a
80  for the anti-influenza drugs amantadine and rimantadine, whose effectiveness was diminished by the a
81 target of the antiviral drugs amantadine and rimantadine, whose use has been discontinued due to wide
82 y in vitro and in cell culture compared with rimantadine, with efficacy demonstrably linked to virion
83 ly approved antiviral agents are amantadine, rimantadine, zanamivir [Relenza, Glaxo Wellcome, Inc., R