MitoQ--a mitochondria-targeted antioxidant.
Identifieur interne : 000794 ( Ncbi/Merge ); précédent : 000793; suivant : 000795MitoQ--a mitochondria-targeted antioxidant.
Auteurs : Joseph S. Tauskela [Canada]Source :
- IDrugs : the investigational drugs journal [ 1369-7056 ] ; 2007.
English descriptors
- KwdEn :
- Alzheimer Disease (prevention & control), Animals, Anti-Inflammatory Agents, Non-Steroidal (adverse effects), Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Antioxidants (adverse effects), Antioxidants (pharmacology), Antioxidants (therapeutic use), Antiparkinson Agents (adverse effects), Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Apoptosis (drug effects), Clinical Trials as Topic, Friedreich Ataxia (prevention & control), Hepatitis C (drug therapy), Humans, Mitochondria (drug effects), Mitochondria (metabolism), Myocardial Reperfusion Injury (prevention & control), Neuroprotective Agents (adverse effects), Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Organophosphorus Compounds (adverse effects), Organophosphorus Compounds (pharmacology), Organophosphorus Compounds (therapeutic use), Oxidative Stress (drug effects), Parkinson Disease (drug therapy), Ubiquinone (adverse effects), Ubiquinone (pharmacology), Ubiquinone (therapeutic use).
- MESH :
- chemical , adverse effects : Anti-Inflammatory Agents, Non-Steroidal, Antioxidants, Antiparkinson Agents, Neuroprotective Agents, Organophosphorus Compounds, Ubiquinone.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal, Antioxidants, Antiparkinson Agents, Neuroprotective Agents, Organophosphorus Compounds, Ubiquinone.
- drug effects : Apoptosis, Mitochondria, Oxidative Stress.
- drug therapy : Hepatitis C, Parkinson Disease.
- metabolism : Mitochondria.
- prevention & control : Alzheimer Disease, Friedreich Ataxia, Myocardial Reperfusion Injury.
- chemical , therapeutic use : Anti-Inflammatory Agents, Non-Steroidal, Antioxidants, Antiparkinson Agents, Neuroprotective Agents, Organophosphorus Compounds, Ubiquinone.
- Animals, Clinical Trials as Topic, Humans.
Abstract
MitoQ is an orally active antioxidant that has the ability to target mitochondrial dysfunction. The agent is currently under development by Antipodean Pharmaceuticals Inc in phase II clinical trials for Parkinson's disease and liver damage associated with HCV infection. MitoQ has demonstrated encouraging preclinical results in numerous studies in isolated mitochondria, cells and tissues undergoing oxidative stress and apoptotic death. MitoQ aims to not only mimic the role of the endogenous mitochondrial antioxidant coenzyme Q10 (CoQ10), but also to augment substantially the antioxidant capacity of CoQ to supraphysiological levels in a mitochondrial membrane potential-dependent manner. MitoQ represents the first foray into the clinic in an attempt to deliver an antioxidant to an intracellular region that is responsible for the formation of increased levels of potentially deleterious reactive oxygen species. Results from the clinical trials with MitoQ will have important repercussions on the relevance of a mitochondrial-targeted approach.
PubMed: 17642004
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 001074
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pubmed:17642004Le document en format XML
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<country xml:lang="fr">Canada</country>
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<term>Animals</term>
<term>Anti-Inflammatory Agents, Non-Steroidal (adverse effects)</term>
<term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term>
<term>Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)</term>
<term>Antioxidants (adverse effects)</term>
<term>Antioxidants (pharmacology)</term>
<term>Antioxidants (therapeutic use)</term>
<term>Antiparkinson Agents (adverse effects)</term>
<term>Antiparkinson Agents (pharmacology)</term>
<term>Antiparkinson Agents (therapeutic use)</term>
<term>Apoptosis (drug effects)</term>
<term>Clinical Trials as Topic</term>
<term>Friedreich Ataxia (prevention & control)</term>
<term>Hepatitis C (drug therapy)</term>
<term>Humans</term>
<term>Mitochondria (drug effects)</term>
<term>Mitochondria (metabolism)</term>
<term>Myocardial Reperfusion Injury (prevention & control)</term>
<term>Neuroprotective Agents (adverse effects)</term>
<term>Neuroprotective Agents (pharmacology)</term>
<term>Neuroprotective Agents (therapeutic use)</term>
<term>Organophosphorus Compounds (adverse effects)</term>
<term>Organophosphorus Compounds (pharmacology)</term>
<term>Organophosphorus Compounds (therapeutic use)</term>
<term>Oxidative Stress (drug effects)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Ubiquinone (adverse effects)</term>
<term>Ubiquinone (pharmacology)</term>
<term>Ubiquinone (therapeutic use)</term>
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<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term>
<term>Antioxidants</term>
<term>Antiparkinson Agents</term>
<term>Neuroprotective Agents</term>
<term>Organophosphorus Compounds</term>
<term>Ubiquinone</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term>
<term>Antioxidants</term>
<term>Antiparkinson Agents</term>
<term>Neuroprotective Agents</term>
<term>Organophosphorus Compounds</term>
<term>Ubiquinone</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Mitochondria</term>
<term>Oxidative Stress</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Hepatitis C</term>
<term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term>
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<term>Friedreich Ataxia</term>
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<term>Antioxidants</term>
<term>Antiparkinson Agents</term>
<term>Neuroprotective Agents</term>
<term>Organophosphorus Compounds</term>
<term>Ubiquinone</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Clinical Trials as Topic</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">MitoQ is an orally active antioxidant that has the ability to target mitochondrial dysfunction. The agent is currently under development by Antipodean Pharmaceuticals Inc in phase II clinical trials for Parkinson's disease and liver damage associated with HCV infection. MitoQ has demonstrated encouraging preclinical results in numerous studies in isolated mitochondria, cells and tissues undergoing oxidative stress and apoptotic death. MitoQ aims to not only mimic the role of the endogenous mitochondrial antioxidant coenzyme Q10 (CoQ10), but also to augment substantially the antioxidant capacity of CoQ to supraphysiological levels in a mitochondrial membrane potential-dependent manner. MitoQ represents the first foray into the clinic in an attempt to deliver an antioxidant to an intracellular region that is responsible for the formation of increased levels of potentially deleterious reactive oxygen species. Results from the clinical trials with MitoQ will have important repercussions on the relevance of a mitochondrial-targeted approach.</div>
</front>
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<Title>IDrugs : the investigational drugs journal</Title>
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<ArticleTitle>MitoQ--a mitochondria-targeted antioxidant.</ArticleTitle>
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<Abstract><AbstractText>MitoQ is an orally active antioxidant that has the ability to target mitochondrial dysfunction. The agent is currently under development by Antipodean Pharmaceuticals Inc in phase II clinical trials for Parkinson's disease and liver damage associated with HCV infection. MitoQ has demonstrated encouraging preclinical results in numerous studies in isolated mitochondria, cells and tissues undergoing oxidative stress and apoptotic death. MitoQ aims to not only mimic the role of the endogenous mitochondrial antioxidant coenzyme Q10 (CoQ10), but also to augment substantially the antioxidant capacity of CoQ to supraphysiological levels in a mitochondrial membrane potential-dependent manner. MitoQ represents the first foray into the clinic in an attempt to deliver an antioxidant to an intracellular region that is responsible for the formation of increased levels of potentially deleterious reactive oxygen species. Results from the clinical trials with MitoQ will have important repercussions on the relevance of a mitochondrial-targeted approach.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tauskela</LastName>
<ForeName>Joseph S</ForeName>
<Initials>JS</Initials>
<AffiliationInfo><Affiliation>National Research Council, Institute for Biological Sciences, Synaptic Pathophysiology Group, Ottawa, ON K1A 0R6, Canada. joseph.tauskela@nrc-cnrc.gc.ca</Affiliation>
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