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In contrast, although both abacavir and the metabolites of flucloxacillin are able to bind to abacavir-insensitive HLA-B*5703, the binding affinities are lower as indicated by their greater GlideScores (Supplementary Table 4).
These binding affinities are among the tightest known to bind filamin with the exception of the platelet specific protein, GPIbα, which has an affinity of 0.1 μM.
In comparison to those of synaptotagmin I, otoferlin's calcium binding affinities are equivalent or slightly higher, as the C2B domain of synaptotagmin binds calcium with solution Kd values in the range of 300 600 μM.
Experimentally measured binding affinities are available for all protein-ligand complexes provided in the PDBbind database.
Conversely, the drugs with low plasma protein binding affinities are limited in their ability to perfuse tissues and reach the site of action [9].
We can assume that the experimental settings for the measured drug target pairs in each dataset were the same and the binding affinities are comparable.
Similar(11)
Linear correlations between the predicted binding scores and the experimentally measured binding affinities were observed.
The binding affinities were evaluated over a range of 2.5 40 mmol/L concentrations.
The binding affinities were estimated as a Docking score (Glide score + Epik state penalties).
The residual binding affinities were computed as: Delta G^{res} = Delta G^{exp } - Delta G^{pred} (5).
Receptor binding affinities were measured in vitro by the competitive binding analysis.
More suggestions(13)
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