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When screened against HRV serotype-14 the best compound was shown to have very good 3CP inhibition (kobs/[I]=270,000 M−1 s−1) and potent in vitro antiviral activity (EC50=7.0 nM).
The IC50's of the best compounds were superior to their parent compound febrifugine.
The best compounds were [Fe(bpy 3]Tf2 (Tf = CF3SO3−, bpy = 2.2′-bipyridine) and [Co(bpy 3]Tf2 which generated current densities of the order of 30 mA/cm2 in thin layer static cells.
The best compounds were further evaluated in an antiviral plaque reduction assay using engineered WT, V27A and S31N M2 influenza A strains with otherwise identical genetic background.
Four of these compounds were found to be effective in inhibiting HIV-1 infection, with the best compounds being 5f and 5h, which exhibited significant inhibition on HIV-1IIIB infection at micromolar levels with low cytotoxicity.
Ultimately, the best compounds were characterized using in vivo models of cardiac function (rat and dog).
The best compounds were up to 17-fold more potent than F1, with IC50 values in the low micromolar range (F70−F73, Figure 3A).
The best understood compound is nisin, which uses its N-terminal A- and B-rings to bind the membrane-bound peptidoglycan precursor lipid II, the same biological target as the clinical antibiotic vancomycin.
However, determination of concomitant cytotoxicity is also important for selecting the best compound, which was found to be 10-fold more potent than verapamil.
To the author's best knowledge, this compound is reported here for the first time as being present in P. riparius (Table 1 ).
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