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A team of researchers, led by Giorgio Cozza from the Department of Molecular Medicine at the University of Padua, has unveiled an unexpected "second identity" of ivacaftor, a drug known for treating cystic fibrosis. The study, titled "Beyond CFTR: Ivacaftor's Role in Restoring Cellular Redox Balance and Preventing Ferroptosis," has been published in the journal Redox Biology.
To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
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The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
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The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
In addition to the Department of Molecular Medicine, the study involved collaboration from the Departments of Pharmaceutical Sciences and Chemical Sciences at the University of Padua through biological validation by Michela Rubin, Ilaria Artusi, and Valentina Bosello Travain, biochemical and lipidomic analysis by Monica Rossetto, Antonina Gucciardi, Maria Luisa di Paolo, and Giovanni Miotto, and computational atomic-level approach by Davide Zeppilli and Laura Orian. José Pedro Friedmann Angeli from the University of Würzburg, a world expert on ferroptosis, also contributed to the research.
The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
In addition to the Department of Molecular Medicine, the study involved collaboration from the Departments of Pharmaceutical Sciences and Chemical Sciences at the University of Padua through biological validation by Michela Rubin, Ilaria Artusi, and Valentina Bosello Travain, biochemical and lipidomic analysis by Monica Rossetto, Antonina Gucciardi, Maria Luisa di Paolo, and Giovanni Miotto, and computational atomic-level approach by Davide Zeppilli and Laura Orian. José Pedro Friedmann Angeli from the University of Würzburg, a world expert on ferroptosis, also contributed to the research.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
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The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
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A team of researchers, led by Giorgio Cozza from the Department of Molecular Medicine at the University of Padua, has unveiled an unexpected "second identity" of ivacaftor, a drug known for treating cystic fibrosis. The study, titled "Beyond CFTR: Ivacaftor's Role in Restoring Cellular Redox Balance and Preventing Ferroptosis," has been published in the journal Redox Biology.
To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
In addition to the Department of Molecular Medicine, the study involved collaboration from the Departments of Pharmaceutical Sciences and Chemical Sciences at the University of Padua through biological validation by Michela Rubin, Ilaria Artusi, and Valentina Bosello Travain, biochemical and lipidomic analysis by Monica Rossetto, Antonina Gucciardi, Maria Luisa di Paolo, and Giovanni Miotto, and computational atomic-level approach by Davide Zeppilli and Laura Orian. José Pedro Friedmann Angeli from the University of Würzburg, a world expert on ferroptosis, also contributed to the research.
The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
In addition to the Department of Molecular Medicine, the study involved collaboration from the Departments of Pharmaceutical Sciences and Chemical Sciences at the University of Padua through biological validation by Michela Rubin, Ilaria Artusi, and Valentina Bosello Travain, biochemical and lipidomic analysis by Monica Rossetto, Antonina Gucciardi, Maria Luisa di Paolo, and Giovanni Miotto, and computational atomic-level approach by Davide Zeppilli and Laura Orian. José Pedro Friedmann Angeli from the University of Würzburg, a world expert on ferroptosis, also contributed to the research.
The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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A team of researchers, led by Giorgio Cozza from the Department of Molecular Medicine at the University of Padua, has unveiled an unexpected "second identity" of ivacaftor, a drug known for treating cystic fibrosis. The study, titled "Beyond CFTR: Ivacaftor's Role in Restoring Cellular Redox Balance and Preventing Ferroptosis," has been published in the journal Redox Biology.
To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
In addition to the Department of Molecular Medicine, the study involved collaboration from the Departments of Pharmaceutical Sciences and Chemical Sciences at the University of Padua through biological validation by Michela Rubin, Ilaria Artusi, and Valentina Bosello Travain, biochemical and lipidomic analysis by Monica Rossetto, Antonina Gucciardi, Maria Luisa di Paolo, and Giovanni Miotto, and computational atomic-level approach by Davide Zeppilli and Laura Orian. José Pedro Friedmann Angeli from the University of Würzburg, a world expert on ferroptosis, also contributed to the research.
The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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To understand the discovery, one must imagine our cells "under siege." In various pathological states, in addition to cystic fibrosis, cells undergo severe oxidative stress: it is as if their membranes "rust" due to unstable molecules called free radicals. When this lipid damage becomes unsustainable, a violent form of cell death called ferroptosis is triggered.
The study demonstrates for the first time that ivacaftor, beyond its known primary mechanism, acts as a true chemical "scavenger": it intercepts and directly neutralises the free radicals attacking lipids, blocking the chain reaction that would lead to cell death. Unlike many antioxidants that fail to act efficiently on lipids and are rapidly consumed, ivacaftor shows remarkable resilience, remaining active and protecting cells for days. Additionally, the drug helps restore the cell's natural antioxidant defences. This protective ability works even in cells that do not express the primary target (CFTR), suggesting that ivacaftor's antioxidant effect extends beyond cystic fibrosis and could one day be used to treat other diseases characterised by severe oxidative stress.
"Our study is an example of how discovering the hidden potential of an already approved and clinically safe molecule is beneficial. This phenomenon is called drug repurposing, which allows us to incredibly accelerate the timeline for new therapeutic applications, optimising resources that would otherwise take decades to develop from scratch," comments Giorgio Cozza, coordinator of the study. "But the strength of this work also lies in the robustness of the multidisciplinary approach that dissected the mechanism of action from the macroscopic to the atomic level."
In addition to the Department of Molecular Medicine, the study involved collaboration from the Departments of Pharmaceutical Sciences and Chemical Sciences at the University of Padua through biological validation by Michela Rubin, Ilaria Artusi, and Valentina Bosello Travain, biochemical and lipidomic analysis by Monica Rossetto, Antonina Gucciardi, Maria Luisa di Paolo, and Giovanni Miotto, and computational atomic-level approach by Davide Zeppilli and Laura Orian. José Pedro Friedmann Angeli from the University of Würzburg, a world expert on ferroptosis, also contributed to the research.
The research was supported by the Cystic Fibrosis Research Foundation – ETS and the PNRR spoke 7 Biocomputing CN3.
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DO: gestione
