Proteolysis-targeting chimera (PROTAC) for targeted protein degradation and cancer therapy

Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3)....

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Vydáno v:	Journal of hematology and oncology Ročník 13; číslo 1; s. 50 - 14
Hlavní autoři:	Li, Xin, Song, Yongcheng
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London BioMed Central 13.05.2020 BioMed Central Ltd Springer Nature B.V BMC
Témata:	Animals Antineoplastic agents Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacokinetics Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Breast cancer Cancer Cancer Research Cancer therapies Cancer therapy Cancer treatment Cell growth Clinical trials Degradation Drug Discovery Drug dosages Gene expression Health aspects Hematological malignancies Hematology Humans Leukemia Ligands Ligases Lymphoma Medicine Medicine & Public Health Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - metabolism Nucleic acids Oncology Pharmacodynamics Pharmacokinetics PROTAC Proteasomes Proteins Proteolysis Proteolysis - drug effects Review RNA polymerase Targeted protein degradation Technology application Therapeutic targets Ubiquitin Ubiquitin-protein ligase Ubiquitination Ubiquitination - drug effects PROTAC Targeted protein degradation Cancer therapy Hematological malignancies
ISSN:	1756-8722, 1756-8722
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Abstract	Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3). Upon binding to the POI, the PROTAC can recruit E3 for POI ubiquitination, which is subjected to proteasome-mediated degradation. PROTAC complements nucleic acid-based gene knockdown/out technologies for targeted protein reduction and could mimic pharmacological protein inhibition. To date, PROTACs targeting ~ 50 proteins, many of which are clinically validated drug targets, have been successfully developed with several in clinical trials for cancer therapy. This article reviews PROTAC-mediated degradation of critical oncoproteins in cancer, particularly those in hematological malignancies. Chemical structures, cellular and in vivo activities, pharmacokinetics, and pharmacodynamics of these PROTACs are summarized. In addition, potential advantages, challenges, and perspectives of PROTAC technology in cancer therapy are discussed.
AbstractList	Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3). Upon binding to the POI, the PROTAC can recruit E3 for POI ubiquitination, which is subjected to proteasome-mediated degradation. PROTAC complements nucleic acid-based gene knockdown/out technologies for targeted protein reduction and could mimic pharmacological protein inhibition. To date, PROTACs targeting ~ 50 proteins, many of which are clinically validated drug targets, have been successfully developed with several in clinical trials for cancer therapy. This article reviews PROTAC-mediated degradation of critical oncoproteins in cancer, particularly those in hematological malignancies. Chemical structures, cellular and in vivo activities, pharmacokinetics, and pharmacodynamics of these PROTACs are summarized. In addition, potential advantages, challenges, and perspectives of PROTAC technology in cancer therapy are discussed. Abstract Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3). Upon binding to the POI, the PROTAC can recruit E3 for POI ubiquitination, which is subjected to proteasome-mediated degradation. PROTAC complements nucleic acid-based gene knockdown/out technologies for targeted protein reduction and could mimic pharmacological protein inhibition. To date, PROTACs targeting ~ 50 proteins, many of which are clinically validated drug targets, have been successfully developed with several in clinical trials for cancer therapy. This article reviews PROTAC-mediated degradation of critical oncoproteins in cancer, particularly those in hematological malignancies. Chemical structures, cellular and in vivo activities, pharmacokinetics, and pharmacodynamics of these PROTACs are summarized. In addition, potential advantages, challenges, and perspectives of PROTAC technology in cancer therapy are discussed. Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3). Upon binding to the POI, the PROTAC can recruit E3 for POI ubiquitination, which is subjected to proteasome-mediated degradation. PROTAC complements nucleic acid-based gene knockdown/out technologies for targeted protein reduction and could mimic pharmacological protein inhibition. To date, PROTACs targeting ~ 50 proteins, many of which are clinically validated drug targets, have been successfully developed with several in clinical trials for cancer therapy. This article reviews PROTAC-mediated degradation of critical oncoproteins in cancer, particularly those in hematological malignancies. Chemical structures, cellular and in vivo activities, pharmacokinetics, and pharmacodynamics of these PROTACs are summarized. In addition, potential advantages, challenges, and perspectives of PROTAC technology in cancer therapy are discussed. Keywords: PROTAC, Targeted protein degradation, Cancer therapy, Hematological malignancies Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3). Upon binding to the POI, the PROTAC can recruit E3 for POI ubiquitination, which is subjected to proteasome-mediated degradation. PROTAC complements nucleic acid-based gene knockdown/out technologies for targeted protein reduction and could mimic pharmacological protein inhibition. To date, PROTACs targeting ~ 50 proteins, many of which are clinically validated drug targets, have been successfully developed with several in clinical trials for cancer therapy. This article reviews PROTAC-mediated degradation of critical oncoproteins in cancer, particularly those in hematological malignancies. Chemical structures, cellular and in vivo activities, pharmacokinetics, and pharmacodynamics of these PROTACs are summarized. In addition, potential advantages, challenges, and perspectives of PROTAC technology in cancer therapy are discussed.Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists of a ligand (mostly small-molecule inhibitor) of the protein of interest (POI) and a covalently linked ligand of an E3 ubiquitin ligase (E3). Upon binding to the POI, the PROTAC can recruit E3 for POI ubiquitination, which is subjected to proteasome-mediated degradation. PROTAC complements nucleic acid-based gene knockdown/out technologies for targeted protein reduction and could mimic pharmacological protein inhibition. To date, PROTACs targeting ~ 50 proteins, many of which are clinically validated drug targets, have been successfully developed with several in clinical trials for cancer therapy. This article reviews PROTAC-mediated degradation of critical oncoproteins in cancer, particularly those in hematological malignancies. Chemical structures, cellular and in vivo activities, pharmacokinetics, and pharmacodynamics of these PROTACs are summarized. In addition, potential advantages, challenges, and perspectives of PROTAC technology in cancer therapy are discussed.
ArticleNumber	50
Audience	Academic
Author	Li, Xin Song, Yongcheng
Author_xml	– sequence: 1 givenname: Xin surname: Li fullname: Li, Xin organization: Department of Pharmacology and Chemical Biology, Baylor College of Medicine – sequence: 2 givenname: Yongcheng surname: Song fullname: Song, Yongcheng email: ysong@bcm.edu organization: Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/32404196$$D View this record in MEDLINE/PubMed
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Snippet	Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule consists... Abstract Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. A bifunctional PROTAC molecule...
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SubjectTerms	Animals Antineoplastic agents Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacokinetics Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Breast cancer Cancer Cancer Research Cancer therapies Cancer therapy Cancer treatment Cell growth Clinical trials Degradation Drug Discovery Drug dosages Gene expression Health aspects Hematological malignancies Hematology Humans Leukemia Ligands Ligases Lymphoma Medicine Medicine & Public Health Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - metabolism Nucleic acids Oncology Pharmacodynamics Pharmacokinetics PROTAC Proteasomes Proteins Proteolysis Proteolysis - drug effects Review RNA polymerase Targeted protein degradation Technology application Therapeutic targets Ubiquitin Ubiquitin-protein ligase Ubiquitination Ubiquitination - drug effects
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Title	Proteolysis-targeting chimera (PROTAC) for targeted protein degradation and cancer therapy
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