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Pelz, Nicholas F; Bian, Zhiguo; Zhao, Bin; Shaw, Subrata; Tarr, James C; Belmar, Johannes; Gregg, Claire; Camper, DeMarco V; Goodwin, Craig M; Arnold, Allison L; Sensintaffar, John L; Friberg, Anders; Rossanese, Olivia W; Lee, Taekyu; Olejniczak, Edward T; Fesik, Stephen W
Journal of medicinal chemistry, 03/2016, Letnik: 59, Številka: 5Journal Article
Myeloid cell leukemia-1 (Mcl-1) is a member of the Bcl-2 family of proteins responsible for the regulation of programmed cell death. Amplification of Mcl-1 is a common genetic aberration in human cancer whose overexpression contributes to the evasion of apoptosis and is one of the major resistance mechanisms for many chemotherapies. Mcl-1 mediates its effects primarily through interactions with pro-apoptotic BH3 containing proteins that achieve high affinity for the target by utilizing four hydrophobic pockets in its binding groove. Here we describe the discovery of Mcl-1 inhibitors using fragment-based methods and structure-based design. These novel inhibitors exhibit low nanomolar binding affinities to Mcl-1 and >500-fold selectivity over Bcl-xL. X-ray structures of lead Mcl-1 inhibitors when complexed to Mcl-1 provided detailed information on how these small-molecules bind to the target and were used extensively to guide compound optimization.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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