Androgen receptor degradation by the proteolysis-targeting chimera ARCC-4 outperforms enzalutamide in cellular models of prostate cancer drug resistance.

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作者： Jemilat,Salami ^[1] ; Shanique,Alabi ^[2] ; Ryan R,Willard ^[3] ; Nick J,Vitale ^[3] ; Jing,Wang ^[3] ; Hanqing,Dong ^[3] ; Meizhong,Jin ^[3] ; Donald P,McDonnell ^[4] ; Andrew P,Crew ^[3] ; Taavi K,Neklesa ^[3] ; Craig M,Crews ^[5]

作者单位： Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, 06511, CT, USA. ^[1] Department of Pharmacology, Yale School of Medicine, New Haven, 06510, CT, USA. ^[2] Arvinas, LLC, 5 Science Park, New Haven, 06511, CT, USA. ^[3] Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, 27710, NC, USA. ^[4] Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, 06511, CT, USA. craig.crews@yale.edu. ^[5] Department of Pharmacology, Yale School of Medicine, New Haven, 06510, CT, USA. craig.crews@yale.edu. ^[6] Department of Chemistry, Yale University, New Haven, 06511, CT, USA. craig.crews@yale.edu. ^[7]

DOI 10.1038/s42003-018-0105-8

PMID 30271980

发布时间 2020-11-25

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Communications biology

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Androgen receptor degradation by the proteolysis-targeting chimera ARCC-4 outperforms enzalutamide in cellular models of prostate cancer drug resistance.

Communications biology

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Communications biology

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Androgen receptor degradation by the proteolysis-targeting chimera ARCC-4 outperforms enzalutamide in cellular models of prostate cancer drug resistance.

Communications biology

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Communications biology

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