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Drug development protein binding pocket

The mechanism of action proposed is based on a direct binding to the channel and the following partial block of the ATP-binding pocket of CFTR (French et al., 1997), a mechanism similar to that used by genistein to inhibit the activity of other ATP-utilizing enzymes such as protein kinases and topoisomerase II (Polkowski and Mazurek, 2000 and refs therein). The selection of flavonoid compounds or the development of synthetic drugs reasonably selective for CFTR activation might be an area for future clinical trials. [Pg.203]

See other pages where Drug development protein binding pocket is mentioned: [Pg.16]    [Pg.59]    [Pg.100]    [Pg.145]    [Pg.1902]    [Pg.623]    [Pg.34]    [Pg.412]    [Pg.623]    [Pg.156]    [Pg.9]    [Pg.349]    [Pg.45]    [Pg.27]    [Pg.65]    [Pg.172]    [Pg.190]    [Pg.241]    [Pg.3]    [Pg.168]    [Pg.151]    [Pg.202]    [Pg.329]    [Pg.56]    [Pg.158]    [Pg.190]    [Pg.366]    [Pg.194]    [Pg.578]    [Pg.60]    [Pg.84]    [Pg.94]    [Pg.249]    [Pg.601]    [Pg.171]    [Pg.658]    [Pg.64]    [Pg.287]    [Pg.265]    [Pg.1123]    [Pg.279]    [Pg.411]    [Pg.436]    [Pg.50]    [Pg.119]    [Pg.132]    [Pg.194]    [Pg.578]    [Pg.27]    [Pg.29]   
See also in sourсe #XX -- [ Pg.1902 ]



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Binding pocket

Drug binding

POCKET

Protein binding pocket

Protein drugs

Protein pockets

Protein, proteins pockets

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