Cholesteryl ester transfer protein (CETP) as a drug target for cardiovascular disease
Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentratio...
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| Vydané v: | Nature communications Ročník 12; číslo 1; s. 5640 - 10 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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London
Nature Publishing Group UK
24.09.2021
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
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| Abstract | Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer’s disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration.
Despite being studied in clinical trials, CETP inhibitors are not yet an approved treatment for coronary heart disease. Here, by analyzing results from clinical trials and drug target mendelian randomization studies, the authors demonstrate that previous failure of CETP inhibitors are likely compound and not drug target-related. |
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| AbstractList | Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer's disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration.Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer's disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration. Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer’s disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration. Despite being studied in clinical trials, CETP inhibitors are not yet an approved treatment for coronary heart disease. Here, by analyzing results from clinical trials and drug target mendelian randomization studies, the authors demonstrate that previous failure of CETP inhibitors are likely compound and not drug target-related. Despite being studied in clinical trials, CETP inhibitors are not yet an approved treatment for coronary heart disease. Here, by analyzing results from clinical trials and drug target mendelian randomization studies, the authors demonstrate that previous failure of CETP inhibitors are likely compound and not drug target-related. Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer’s disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration.Despite being studied in clinical trials, CETP inhibitors are not yet an approved treatment for coronary heart disease. Here, by analyzing results from clinical trials and drug target mendelian randomization studies, the authors demonstrate that previous failure of CETP inhibitors are likely compound and not drug target-related. Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer's disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration. Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish compound from drug target failure, we compared evidence from clinical trials and drug target Mendelian randomization of CETP protein concentration, comparing this to Mendelian randomization of proprotein convertase subtilisin/kexin type 9 (PCSK9). We show that previous failures of CETP inhibitors are likely compound related, as illustrated by significant degrees of between-compound heterogeneity in effects on lipids, blood pressure, and clinical outcomes observed in trials. On-target CETP inhibition, assessed through Mendelian randomization, is expected to reduce the risk of CHD, heart failure, diabetes, and chronic kidney disease, while increasing the risk of age-related macular degeneration. In contrast, lower PCSK9 concentration is anticipated to decrease the risk of CHD, heart failure, atrial fibrillation, chronic kidney disease, multiple sclerosis, and stroke, while potentially increasing the risk of Alzheimer’s disease and asthma. Due to distinct effects on lipoprotein metabolite profiles, joint inhibition of CETP and PCSK9 may provide added benefit. In conclusion, we provide genetic evidence that CETP is an effective target for CHD prevention but with a potential on-target adverse effect on age-related macular degeneration. Despite being studied in clinical trials, CETP inhibitors are not yet an approved treatment for coronary heart disease. Here, by analyzing results from clinical trials and drug target mendelian randomization studies, the authors demonstrate that previous failure of CETP inhibitors are likely compound and not drug target-related. |
| ArticleNumber | 5640 |
| Author | Chaturvedi, Nishi Price, Jackie F. Zwierzyna, Magdalena Schmidt, Amand F. Charoen, Pimphen Gaunt, Tom R. Drenos, Fotios Sofat, Reecha Lawlor, Deborah A. Giambartolomei, Claudia Bis, Joshua C. Finan, Chris Kivimaki, Mika Hughes, Alun D. Hunt, Nicholas B. Gordillo-Marañón, Maria Wong, Andrew Franceschini, Nora Wannamethee, Goya Hingorani, Aroon D. Mook-Kanamori, Dennis O. O’Donnell, Christopher J. Papacosta, Olia |
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surname: Charoen fullname: Charoen, Pimphen organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, Department of Tropical Hygiene, Faculty of Tropical Medicine, Mahidol University, Integrative Computational BioScience (ICBS) Center, Mahidol University – sequence: 5 givenname: Fotios surname: Drenos fullname: Drenos, Fotios organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, Department of Life Sciences, College of Health, Medicine, and Life Sciences, Brunel University London – sequence: 6 givenname: Mika orcidid: 0000-0002-4699-5627 surname: Kivimaki fullname: Kivimaki, Mika organization: Department of Epidemiology and Public Health, University College London – sequence: 7 givenname: Deborah A. orcidid: 0000-0002-6793-2262 surname: Lawlor fullname: Lawlor, Deborah A. organization: MRC Integrative Epidemiology Unit at the University of Bristol, Population Health, Bristol Medical School, University of Bristol, Bristol NIHR Bristol Biomedical Research Centre, University Hospitals Bristol National Health Service Foundation Trust and University of Bristol – sequence: 8 givenname: Claudia orcidid: 0000-0003-2786-1225 surname: Giambartolomei fullname: Giambartolomei, Claudia organization: Istituto Italiano di Tecnologia, Central RNA Lab – sequence: 9 givenname: Olia surname: Papacosta fullname: Papacosta, Olia organization: Primary Care and Population Health, University College London – sequence: 10 givenname: Nishi orcidid: 0000-0002-6211-2775 surname: Chaturvedi fullname: Chaturvedi, Nishi organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, MRC Unit for Lifelong Health and Ageing at UCL – sequence: 11 givenname: Joshua C. orcidid: 0000-0002-3409-1110 surname: Bis fullname: Bis, Joshua C. organization: Cardiovascular Health Research Unit, Department of Medicine, University of Washington – sequence: 12 givenname: Christopher J. orcidid: 0000-0002-2667-8624 surname: O’Donnell fullname: O’Donnell, Christopher J. organization: Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Department of Medicine, VA Boston Healthcare System – sequence: 13 givenname: Goya surname: Wannamethee fullname: Wannamethee, Goya organization: Primary Care and Population Health, University College London – sequence: 14 givenname: Andrew orcidid: 0000-0003-2079-4779 surname: Wong fullname: Wong, Andrew organization: MRC Unit for Lifelong Health and Ageing at UCL – sequence: 15 givenname: Jackie F. surname: Price fullname: Price, Jackie F. organization: Usher Institute, University of Edinburgh – sequence: 16 givenname: Alun D. orcidid: 0000-0001-5432-5271 surname: Hughes fullname: Hughes, Alun D. organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, UCL British Heart Foundation Research Accelerator, MRC Unit for Lifelong Health and Ageing at UCL – sequence: 17 givenname: Tom R. orcidid: 0000-0003-0924-3247 surname: Gaunt fullname: Gaunt, Tom R. organization: MRC Integrative Epidemiology Unit at the University of Bristol, Population Health, Bristol Medical School, University of Bristol, Bristol NIHR Bristol Biomedical Research Centre, University Hospitals Bristol National Health Service Foundation Trust and University of Bristol – sequence: 18 givenname: Nora surname: Franceschini fullname: Franceschini, Nora organization: Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina – sequence: 19 givenname: Dennis O. surname: Mook-Kanamori fullname: Mook-Kanamori, Dennis O. organization: Department of Clinical Epidemiology, Leiden University Medical Center – sequence: 20 givenname: Magdalena orcidid: 0000-0002-7445-6030 surname: Zwierzyna fullname: Zwierzyna, Magdalena organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, UCL British Heart Foundation Research Accelerator – sequence: 21 givenname: Reecha surname: Sofat fullname: Sofat, Reecha organization: Institute of Health Informatics, University College London – sequence: 22 givenname: Aroon D. orcidid: 0000-0001-8365-0081 surname: Hingorani fullname: Hingorani, Aroon D. organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, UCL British Heart Foundation Research Accelerator, Health Data Research UK – sequence: 23 givenname: Chris orcidid: 0000-0002-3319-1937 surname: Finan fullname: Finan, Chris organization: Institute of Cardiovascular Science, Faculty of Population Health, University College London, UCL British Heart Foundation Research Accelerator, Department of Cardiology, Division Heart and Lungs, University Medical Center Utrecht, Health Data Research UK |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34561430$$D View this record in MEDLINE/PubMed |
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| Snippet | Development of cholesteryl ester transfer protein (CETP) inhibitors for coronary heart disease (CHD) has yet to deliver licensed medicines. To distinguish... Despite being studied in clinical trials, CETP inhibitors are not yet an approved treatment for coronary heart disease. Here, by analyzing results from... |
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| SubjectTerms | 140/131 45/43 631/154/556 692/308/2779 692/699/75 Age Age related diseases Alzheimer's disease Amides - therapeutic use Anticholesteremic Agents - therapeutic use Asthma Benzodiazepines - therapeutic use Blood pressure Cardiovascular disease Cardiovascular diseases Cardiovascular Diseases - metabolism Cardiovascular Diseases - prevention & control Cholesterol Ester Transfer Proteins - antagonists & inhibitors Cholesterol Ester Transfer Proteins - genetics Cholesterol Ester Transfer Proteins - metabolism Cholesteryl ester transfer protein Clinical trials Congestive heart failure Coronary artery disease Coronary Disease - metabolism Coronary Disease - prevention & control Diabetes mellitus Esters - therapeutic use Eye diseases Fibrillation Heart diseases Heart failure Heterogeneity Humanities and Social Sciences Humans Inhibitors Kexin Kidney diseases Kidneys Lipids Macular degeneration Mendelian Randomization Analysis Metabolites multidisciplinary Multiple sclerosis Neurodegenerative diseases Oxazolidinones - therapeutic use Pressure effects Proprotein convertases Proteins Quinolines - therapeutic use Randomization Renal failure Risk Science Science (multidisciplinary) Subtilisin Sulfhydryl Compounds - therapeutic use Therapeutic targets |
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| Title | Cholesteryl ester transfer protein (CETP) as a drug target for cardiovascular disease |
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