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With the aim to elucidate the structural features governing the differential inhibitory binding behavior of these inhibitors, molecular modeling studies were undertaken to generate atomic models compatible with the experimental data available.
The modeling studies were conducted using a 3D finite element model of the uncoiled cochlea and consisted of simulation of the RW membrane vibration amplitude in the frequency range 0.4 10 kHz in both the pre-stapedotomy and post-stapedotomy states.
Molecular modeling studies were carried out to ascertain the binding of the model compound to the active site of β-tubulin.
Molecular modeling studies were carried out to optimize the pharmacophore.
Molecular modeling studies were done to verify the biological activity.
Molecular modeling studies were performed to explain biological results.
Molecular modeling studies were performed, including both pharmacophore and structure-based approaches.
Furthermore, molecular modeling studies were performed in order to rationalize the obtained biological results.
Molecular modeling studies were performed to predict the binding modes between individual derivatives and hAChE/hBChE.
Molecular modeling studies were carried out on a series of benzimidazole and imidazo[1,2-a]pyridines as Plk1 inhibitors.
Molecular modeling studies were used to assess the fit of these compounds within the active site of human DHFR.
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