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• W2893495711 abstract "Recently, proteolysis targeting chimera (PROTAC) technology is highlighted in drug discovery area as a new therapeutic approach. PROTAC as a heterobifunctional molecule is comprised of two ligands, which recruit target protein and E3 ligase, respectively. To degrade the anaplastic lymphoma kinase (ALK) fusion protein, such as NPM-ALK or EML4-ALK, we generated several ALK-PROTAC molecules consisted of ceritinib, one of the ALK inhibitors, and ligand of von Hippel-Lindau (VHL) E3 ligase. Among these molecules, TD-004 effectively induced ALK degradation and inhibited the growth of ALK fusion positive cell lines, SU-DHL-1 and H3122. We also confirmed that TD-004 significantly reduced the tumor growth in H3122 xenograft model." @default.
• W2893495711 created "2018-10-05" @default.
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• W2893495711 date "2018-10-01" @default.
• W2893495711 modified "2023-10-16" @default.
• W2893495711 title "Induced protein degradation of anaplastic lymphoma kinase (ALK) by proteolysis targeting chimera (PROTAC)" @default.
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• W2893495711 doi "https://doi.org/10.1016/j.bbrc.2018.09.169" @default.
• W2893495711 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30274779" @default.
• W2893495711 hasPublicationYear "2018" @default.
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