Development, synthesis and validation of improved c‐Myc/Max inhibitors
The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse li...
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| Published in | Journal of cellular and molecular medicine Vol. 28; no. 8; pp. e18272 - n/a |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.04.2024
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1582-1838 1582-4934 1582-4934 |
| DOI | 10.1111/jcmm.18272 |
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| Abstract | The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse library of novel small compounds meticulously designed to specifically target the c‐Myc/Max complex. We conducted in vitro examinations of novel c‐Myc inhibitors across a spectrum of cancer cell lines, including PANC1 (pancreatic adenocarcinoma), MCF7 (breast carcinoma), DU‐145 (prostate carcinoma), and A549 (lung cancer). The initial analysis involved a 25 μM dose, which enabled the identification of potent anticancer compounds effective against a variety of tumour types. We identified c‐Myc inhibitors with remarkable potency, featuring IC50 values as low as 1.6 μM and up to 40 times more effective than the reference molecule in diminishing cancer cell viability. Notably, c‐Myc‐i7 exhibited exceptional selectivity, displaying 37‐fold and 59‐fold preference for targeting prostate and breast cancers, respectively, over healthy cells. Additionally, we constructed drug‐likeness models. This study underscores the potential for in vitro investigations of various tumour types using novel c‐Myc inhibitors to yield ground‐breaking and efficacious anticancer compounds. |
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| AbstractList | The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse library of novel small compounds meticulously designed to specifically target the c‐Myc/Max complex. We conducted in vitro examinations of novel c‐Myc inhibitors across a spectrum of cancer cell lines, including PANC1 (pancreatic adenocarcinoma), MCF7 (breast carcinoma), DU‐145 (prostate carcinoma), and A549 (lung cancer). The initial analysis involved a 25 μM dose, which enabled the identification of potent anticancer compounds effective against a variety of tumour types. We identified c‐Myc inhibitors with remarkable potency, featuring IC50 values as low as 1.6 μM and up to 40 times more effective than the reference molecule in diminishing cancer cell viability. Notably, c‐Myc‐i7 exhibited exceptional selectivity, displaying 37‐fold and 59‐fold preference for targeting prostate and breast cancers, respectively, over healthy cells. Additionally, we constructed drug‐likeness models. This study underscores the potential for in vitro investigations of various tumour types using novel c‐Myc inhibitors to yield ground‐breaking and efficacious anticancer compounds. The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse library of novel small compounds meticulously designed to specifically target the c-Myc/Max complex. We conducted in vitro examinations of novel c-Myc inhibitors across a spectrum of cancer cell lines, including PANC1 (pancreatic adenocarcinoma), MCF7 (breast carcinoma), DU-145 (prostate carcinoma), and A549 (lung cancer). The initial analysis involved a 25 μM dose, which enabled the identification of potent anticancer compounds effective against a variety of tumour types. We identified c-Myc inhibitors with remarkable potency, featuring IC50 values as low as 1.6 μM and up to 40 times more effective than the reference molecule in diminishing cancer cell viability. Notably, c-Myc-i7 exhibited exceptional selectivity, displaying 37-fold and 59-fold preference for targeting prostate and breast cancers, respectively, over healthy cells. Additionally, we constructed drug-likeness models. This study underscores the potential for in vitro investigations of various tumour types using novel c-Myc inhibitors to yield ground-breaking and efficacious anticancer compounds. The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse library of novel small compounds meticulously designed to specifically target the c-Myc/Max complex. We conducted in vitro examinations of novel c-Myc inhibitors across a spectrum of cancer cell lines, including PANC1 (pancreatic adenocarcinoma), MCF7 (breast carcinoma), DU-145 (prostate carcinoma), and A549 (lung cancer). The initial analysis involved a 25 μM dose, which enabled the identification of potent anticancer compounds effective against a variety of tumour types. We identified c-Myc inhibitors with remarkable potency, featuring IC50 values as low as 1.6 μM and up to 40 times more effective than the reference molecule in diminishing cancer cell viability. Notably, c-Myc-i7 exhibited exceptional selectivity, displaying 37-fold and 59-fold preference for targeting prostate and breast cancers, respectively, over healthy cells. Additionally, we constructed drug-likeness models. This study underscores the potential for in vitro investigations of various tumour types using novel c-Myc inhibitors to yield ground-breaking and efficacious anticancer compounds.The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse library of novel small compounds meticulously designed to specifically target the c-Myc/Max complex. We conducted in vitro examinations of novel c-Myc inhibitors across a spectrum of cancer cell lines, including PANC1 (pancreatic adenocarcinoma), MCF7 (breast carcinoma), DU-145 (prostate carcinoma), and A549 (lung cancer). The initial analysis involved a 25 μM dose, which enabled the identification of potent anticancer compounds effective against a variety of tumour types. We identified c-Myc inhibitors with remarkable potency, featuring IC50 values as low as 1.6 μM and up to 40 times more effective than the reference molecule in diminishing cancer cell viability. Notably, c-Myc-i7 exhibited exceptional selectivity, displaying 37-fold and 59-fold preference for targeting prostate and breast cancers, respectively, over healthy cells. Additionally, we constructed drug-likeness models. This study underscores the potential for in vitro investigations of various tumour types using novel c-Myc inhibitors to yield ground-breaking and efficacious anticancer compounds. |
| Author | Yıldırım, Sümbül Kocabaş, Fatih Mermer, Arif |
| AuthorAffiliation | 2 Graduate School of Natural and Applied Sciences Yeditepe University Istanbul Turkey 1 Department of Genetics and Bioengineering, Faculty of Engineering Yeditepe University Istanbul Turkey 3 Institute for Diabetes and Cancer Helmholtz Diabetes Center, Helmholtz Center Neuherberg Germany 5 Experimental Medicine Application and Research Center University of Health Sciences Istanbul Turkey 6 UR22722, LABCİS, Faculty of Science and Technology University of Limoges Limoges France 4 Department of Biotechnology University of Health Sciences Istanbul Turkey |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38568057$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.2174/1568009618666180905100608 10.1016/j.otohns.2004.02.015 10.1016/j.ccell.2019.10.001 10.1038/s41392-021-00500-y 10.3390/cells10112916 10.1007/s10637-020-01018-w 10.1080/15384047.2021.2017223 10.2174/1568009620666201016121005 10.1016/j.cellsig.2010.11.023 10.2174/1389450117666160401124624 10.1158/1535-7163.MCT-07-0005 10.1126/sciadv.abh3635 10.1016/j.ctrv.2021.102154 10.1002/jhet.3635 10.1038/s41598-020-64888-3 10.1002/slct.201802677 10.1080/07391102.2023.2239909 10.1016/j.prp.2022.153851 10.1016/j.bmcl.2012.10.013 10.1016/j.gene.2023.147425 10.1080/10428194.2023.2275532 10.1016/j.molliq.2022.119264 10.1016/j.tetlet.2008.12.107 10.1038/sj.onc.1206641 |
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| Copyright | 2024 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | anti‐cancer ultrasonication Max c‐Myc rhodanine |
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| SubjectTerms | Adenocarcinoma anti‐cancer Breast cancer Breast carcinoma c-Myc protein Cancer therapies Cell cycle Cell growth Cell Line Cell Nucleus Cell Survival Cell viability Chemotherapy c‐Myc Ethanol Fourier transforms Humans Lung cancer Lung carcinoma Male Max Myc protein Original Pancreatic cancer Pancreatic carcinoma Pancreatic Neoplasms Prostate cancer Prostate carcinoma Proteins Radiation rhodanine Tumor cell lines Tumorigenesis Tumors ultrasonication |
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| Title | Development, synthesis and validation of improved c‐Myc/Max inhibitors |
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