Fipamezole (JP‐1730) is a potent α2 adrenergic receptor antagonist that reduces levodopa‐induced dyskinesia in the MPTP‐lesioned primate model of Parkinson's disease
Identifieur interne : 004085 ( Main/Exploration ); précédent : 004084; suivant : 004086Fipamezole (JP‐1730) is a potent α2 adrenergic receptor antagonist that reduces levodopa‐induced dyskinesia in the MPTP‐lesioned primate model of Parkinson's disease
Auteurs : Juha-Matti Savola [Finlande] ; Michael Hill [Royaume-Uni] ; Mia Engstrom [Finlande] ; Hannele Merivuori [Finlande] ; Siegfried Wurster [Finlande] ; Steven G. Mcguire [Royaume-Uni] ; Susan H. Fox [Royaume-Uni] ; Alan R. Crossman [Royaume-Uni] ; Jonathan M. Brotchie [Royaume-Uni, Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-08.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- Adrenergic alpha-2 Receptor Antagonists, Adrenergic alpha-Antagonists (pharmacology), Adrenergic alpha-Antagonists (therapeutic use), Animal, Animals, Antagonist, Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Antiparkinson agent, Binding, Competitive (drug effects), Callithrix, Chemotherapy, Dyskinesia, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (etiology), Female, Imidazole derivatives, Imidazoles (pharmacology), Imidazoles (therapeutic use), Indans (pharmacology), Indans (therapeutic use), JP‐1730, Levodopa, Levodopa (adverse effects), Levodopa (therapeutic use), Male, Mechanism of action, Monkey, Parkinson disease, Parkinsonian Disorders (drug therapy), Radioligand Assay, Rats, Receptors, AMPA (drug effects), Receptors, Adrenergic (drug effects), Receptors, Dopamine (drug effects), Receptors, GABA (drug effects), Receptors, Histamine (drug effects), Receptors, N-Methyl-D-Aspartate (drug effects), Receptors, Serotonin (drug effects), Toxicity, Treatment, dyskinesia, marmoset, α2-Adrenergic receptor, α2‐adrenergic.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , drug effects : Receptors, AMPA, Receptors, Adrenergic, Receptors, Dopamine, Receptors, GABA, Receptors, Histamine, Receptors, N-Methyl-D-Aspartate, Receptors, Serotonin.
- chemical , pharmacology : Adrenergic alpha-Antagonists, Imidazoles, Indans.
- chemical , therapeutic use : Adrenergic alpha-Antagonists, Antiparkinson Agents, Imidazoles, Indans, Levodopa.
- chemical : Adrenergic alpha-2 Receptor Antagonists.
- drug effects : Binding, Competitive.
- drug therapy : Dyskinesia, Drug-Induced, Parkinsonian Disorders.
- etiology : Dyskinesia, Drug-Induced.
- Animals, Callithrix, Female, Male, Radioligand Assay, Rats.
Abstract
Previous studies in the MPTP‐lesioned primate model of Parkinson's disease have demonstrated that α2 adrenergic receptor antagonists such as idazoxan, rauwolscine, and yohimbine can alleviate L‐dopa–induced dyskinesia and, in the case of idazoxan, enhance the duration of anti‐parkinsonian action of L‐dopa. Here we describe a novel α2 antagonist, fipamezole (JP‐1730), which has high affinity at human α2A (Ki, 9.2 nM), α2B (17 nM), and α2C (55 nM) receptors. In functional assays, the potent antagonist properties of JP‐1730 were demonstrated by its ability to reduce adrenaline‐induced 35S‐GTPγS binding with KB values of 8.4 nM, 16 nM, 4.7 nM at human α2A, α2B, and α2C receptors, respectively. Assessment of the ability of JP‐1730 to bind to a range of 30 other binding sites showed that JP‐1730 also had moderate affinity at histamine H1 and H3 receptors and the serotonin (5‐HT) transporter (IC50 100 nM to 1 μM). In the MPTP‐lesioned marmoset, JP‐1730 (10 mg/kg) significantly reduced L‐dopa–induced dyskinesia without compromising the anti‐parkinsonian action of L‐dopa. The duration of action of the combination of L‐dopa and JP‐1730 (10 mg/kg) was 66% greater than that of L‐dopa alone. These data suggest that JP‐1730 is a potent α2 adrenergic receptor antagonist with potential as an anti‐dyskinetic agent in the treatment of Parkinson's disease. © 2003 Movement Disorder Society
Url:
DOI: 10.1002/mds.10464
Affiliations:
- Canada, Finlande, Royaume-Uni
- Angleterre, Finlande occidentale, Grand Manchester
- Manchester, Turku
- Université de Manchester
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Le document en format XML
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Brotchie</name><affiliation wicri:level="4"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Manchester Movement Disorder Laboratory, 1.124 Division of Neuroscience, School of Biological Sciences, University of Manchester, Manchester</wicri:regionArea><placeName><settlement type="city">Manchester</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Manchester</region></placeName><orgName type="university">Université de Manchester</orgName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Current Address: Toronto Western Research Institute, Toronto Western Hospital, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-08">2003-08</date><biblScope unit="vol">18</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="872">872</biblScope><biblScope unit="page" to="883">883</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3D136688F336226CEC2D8EB2B195C0725A059625</idno><idno type="DOI">10.1002/mds.10464</idno><idno type="ArticleID">MDS10464</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenergic alpha-2 Receptor Antagonists</term><term>Adrenergic alpha-Antagonists (pharmacology)</term><term>Adrenergic alpha-Antagonists (therapeutic use)</term><term>Animal</term><term>Animals</term><term>Antagonist</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Antiparkinson agent</term><term>Binding, Competitive (drug effects)</term><term>Callithrix</term><term>Chemotherapy</term><term>Dyskinesia</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Female</term><term>Imidazole derivatives</term><term>Imidazoles (pharmacology)</term><term>Imidazoles (therapeutic use)</term><term>Indans (pharmacology)</term><term>Indans (therapeutic use)</term><term>JP‐1730</term><term>Levodopa</term><term>Levodopa (adverse effects)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Mechanism of action</term><term>Monkey</term><term>Parkinson disease</term><term>Parkinsonian Disorders (drug therapy)</term><term>Radioligand Assay</term><term>Rats</term><term>Receptors, AMPA (drug effects)</term><term>Receptors, Adrenergic (drug effects)</term><term>Receptors, Dopamine (drug effects)</term><term>Receptors, GABA (drug effects)</term><term>Receptors, Histamine (drug effects)</term><term>Receptors, N-Methyl-D-Aspartate (drug effects)</term><term>Receptors, Serotonin (drug effects)</term><term>Toxicity</term><term>Treatment</term><term>dyskinesia</term><term>marmoset</term><term>α2-Adrenergic receptor</term><term>α2‐adrenergic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, AMPA</term><term>Receptors, Adrenergic</term><term>Receptors, Dopamine</term><term>Receptors, GABA</term><term>Receptors, Histamine</term><term>Receptors, N-Methyl-D-Aspartate</term><term>Receptors, Serotonin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adrenergic alpha-Antagonists</term><term>Imidazoles</term><term>Indans</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adrenergic alpha-Antagonists</term><term>Antiparkinson Agents</term><term>Imidazoles</term><term>Indans</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Adrenergic alpha-2 Receptor Antagonists</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Binding, Competitive</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Female</term><term>Male</term><term>Radioligand Assay</term><term>Rats</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Animal</term><term>Antagoniste</term><term>Antiparkinsonien</term><term>Chimiothérapie</term><term>Dyskinésie</term><term>Fipamézole</term><term>Imidazole dérivé</term><term>JP-1730</term><term>Lévodopa</term><term>Mécanisme action</term><term>Parkinson maladie</term><term>Récepteur α2-adrénergique</term><term>Singe</term><term>Toxicité</term><term>Traitement</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous studies in the MPTP‐lesioned primate model of Parkinson's disease have demonstrated that α2 adrenergic receptor antagonists such as idazoxan, rauwolscine, and yohimbine can alleviate L‐dopa–induced dyskinesia and, in the case of idazoxan, enhance the duration of anti‐parkinsonian action of L‐dopa. Here we describe a novel α2 antagonist, fipamezole (JP‐1730), which has high affinity at human α2A (Ki, 9.2 nM), α2B (17 nM), and α2C (55 nM) receptors. In functional assays, the potent antagonist properties of JP‐1730 were demonstrated by its ability to reduce adrenaline‐induced 35S‐GTPγS binding with KB values of 8.4 nM, 16 nM, 4.7 nM at human α2A, α2B, and α2C receptors, respectively. Assessment of the ability of JP‐1730 to bind to a range of 30 other binding sites showed that JP‐1730 also had moderate affinity at histamine H1 and H3 receptors and the serotonin (5‐HT) transporter (IC50 100 nM to 1 μM). In the MPTP‐lesioned marmoset, JP‐1730 (10 mg/kg) significantly reduced L‐dopa–induced dyskinesia without compromising the anti‐parkinsonian action of L‐dopa. The duration of action of the combination of L‐dopa and JP‐1730 (10 mg/kg) was 66% greater than that of L‐dopa alone. These data suggest that JP‐1730 is a potent α2 adrenergic receptor antagonist with potential as an anti‐dyskinetic agent in the treatment of Parkinson's disease. © 2003 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Canada</li><li>Finlande</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Finlande occidentale</li><li>Grand Manchester</li></region><settlement><li>Manchester</li><li>Turku</li></settlement><orgName><li>Université de Manchester</li></orgName></list><tree><country name="Finlande"><region name="Finlande occidentale"><name sortKey="Savola, Juha Atti" sort="Savola, Juha Atti" uniqKey="Savola J" first="Juha-Matti" last="Savola">Juha-Matti Savola</name></region><name sortKey="Engstrom, Mia" sort="Engstrom, Mia" uniqKey="Engstrom M" first="Mia" last="Engstrom">Mia Engstrom</name><name sortKey="Merivuori, Hannele" sort="Merivuori, Hannele" uniqKey="Merivuori H" first="Hannele" last="Merivuori">Hannele Merivuori</name><name sortKey="Wurster, Siegfried" sort="Wurster, Siegfried" uniqKey="Wurster S" first="Siegfried" last="Wurster">Siegfried Wurster</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Hill, Michael" sort="Hill, Michael" uniqKey="Hill M" first="Michael" last="Hill">Michael Hill</name></region><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><name sortKey="Crossman, Alan R" sort="Crossman, Alan R" uniqKey="Crossman A" first="Alan R." last="Crossman">Alan R. Crossman</name><name sortKey="Crossman, Alan R" sort="Crossman, Alan R" uniqKey="Crossman A" first="Alan R." last="Crossman">Alan R. Crossman</name><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name><name sortKey="Mcguire, Steven G" sort="Mcguire, Steven G" uniqKey="Mcguire S" first="Steven G." last="Mcguire">Steven G. Mcguire</name></country><country name="Canada"><noRegion><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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