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This choice was also supported by results of our earlier, large-scale modeling study, where a linear kernel performed on par with the nonlinear but required dramatically less computational resources [22].

A molecular modeling study where (12d) was docked in the binding site of COX-2 showed that the MeSO2 COX-2 pharmacophore was positioned in the vicinity of the secondary COX-2 binding site near Val523.

A molecular modeling study where 8 was docked in the binding site of COX-2 indicated that the p-MeSO2 COX-2 pharmacophore group on the C-2 phenyl ring is oriented in the vicinity of the COX-2 secondary pocket (Arg513, Phe518 and Val523) and the carboxylic acid substituent can interact with Ser530.

A molecular modeling study where 7b and 7f were docked in the binding site of COX-2 showed that the p-MeSO2NH and N3 substituents on the C-1 phenyl ring are oriented in the vicinity of the COX-2 secondary pocket (His90, Arg513, Phe518, and Val523).

A molecular modeling study where 9e was docked in the binding site of COX-2 showed that the p-MeSO2 substituent on the C-2 phenyl ring is oriented in the vicinity of the COX-2 secondary pocket (Arg513, Phe518 and Val523) and the carboxyl group can interact with Arg120.

A molecular modeling study where 9f was docked in the binding site of COX-2 showed that the para-SO2Me substituent on the C-1 phenyl ring is oriented in the vicinity of the secondary COX-2 binding site near Val523.

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The significant cytotoxicity and tubulin inhibition by SA-2 was streamlined by molecular modeling studies where it was docked at the curcumin binding site of tubulin.

In vivo biological evaluation of these compounds for their effects on the blood pressure of normotensive cats was consistent with the results of molecular modeling studies, where compounds IXa and IXe exhibited hypotensive activity, while compounds IXb, IXc, and IXg resulted in increasing the blood pressure of the experimental animals at different doses.

By carrying out modeling studies, where you can experiment with different inputs and circuit designs, Kispersky et al. examined a range of different cases: correlated noise, and a number of model three-neuron networks with various connection patterns.

This is further corroborated by our molecular modeling studies, where GO was predicted to preferentially bind at the entrance of the catalytic site of AMCase, mimicking interactions with AMCase inhibitors.

Our model differs from this modeling study in several ways.

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