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1 bitor previously under clinical development (pleconaril).
2 , ribavirin, and the anti-picornaviral agent pleconaril.
3 This density could be displaced by pleconaril.
5 al structures of EV-D68 and its complex with pleconaril, a capsid-binding compound that had been deve
6 nd study assessed the efficacy and safety of pleconaril, a novel antiviral drug with broad-spectrum a
7 studies showing that the antiviral effect of pleconaril against HRV16 is greater on the infectivity o
9 -onset T1D received antiviral treatment with pleconaril and ribavirin (n = 47) or placebo (n = 49) fo
10 the serum C-peptide AUC being higher in the pleconaril and ribavirin treatment group compared to the
12 h small-molecule antiviral compounds such as pleconaril bind and inhibit functions associated with th
13 irus 16 (HRV16) and HRV14 are incubated with pleconaril, drug occupancy in the binding pocket is lowe
14 Other potentially useful treatments, such as pleconaril for enteroviral meningoencephalitis are under
15 hese data support the safety and efficacy of pleconaril in decreasing the signs and symptoms and vira
18 e development of capsid-function inhibitors (pleconaril), inhibitors of 3C protease (AG7088), and rec
21 ncy in the binding pocket is lower than when pleconaril is introduced during assembly prior to crysta
22 s after receiving the initial dose of either pleconaril or placebo, subjects were inoculated intranas
23 he virus developed reduced susceptibility to pleconaril, precluding the in-vivo use of this drug.
24 istant RVs using RV-B5 (1 of the 7 naturally pleconaril-resistant rhinoviruses) and OBR-5-340, a bioa
25 cently developed pyrazolopyrimidines inhibit pleconaril-resistant RVs and EVs, and computational mode
26 We studied the mechanism of inhibition of pleconaril-resistant RVs using RV-B5 (1 of the 7 natural
30 spiratory illness symptom scores (P=.013) in pleconaril-treated as compared with placebo-treated subj
32 om patients enrolled in clinical trials with pleconaril were distinct from those that confer natural