Odapipam - CAS 131796-63-9
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Dopamine Receptor
Odapipam is a potent dopamine D1 antagonist.
Brife Description:
dopamine D1 antagonist
NNC 756; (5S)-8-chloro-5-(2,3-dihydro-1-benzofuran-7-yl)-3-methyl-1,2,4,5-tetrahydro-3-benzazepin-7-ol
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1.MK-801-induced dystonia in cebus monkeys.
Madsen M;Lublin H Clin Neuropharmacol. 1998 Nov-Dec;21(6):333-8.
MK-801 (dizocilpine), a noncompetitive N-methyl-D-aspartate antagonist, induces dystonia in monkeys at doses of 0.08 mg/kg. This syndrome was tested with the dopamine D1 receptor antagonist NNC 756, the DA D2 receptor antagonist raclopride, the atypical antipsychotic clozapine, the dopamine D1 receptor agonist SKF 81297, the dopamine D2/D3 receptor agonist quinpirole, the anticholinergic biperiden, amphetamine, and the benzodiazepine midazolam in 7 Cebus apella monkeys previously treated with dopaminergic agents. NNC 756 (0.004 and 0.01 mg/kg), raclopride (0.004 and 0.01 mg/kg), SKF 81297 (0.3 and 0.6 mg/kg), quinpirole (0.1 and 0.2 mg/kg), amphetamine (0.25 and 0.5 mg/kg), and biperiden (0.125 and up to 1.0 mg/kg), had no significant effect on MK-801-induced dystonia. In contrast, both clozapine (2.0 mg/kg) and midazolam (0.4 and 1.0 mg/kg) reduced the dystonia caused by MK-801. Dystonia induced by dopamine D1 and D2 antagonists is easily antagonized by biperiden and dopamine agonists, whereas these drugs had no significant effect on MK-801-induced dystonia. It has been proposed that dystonia may be caused by a sudden drop in the output from the basal ganglia that is primarily GABAergic.
2.Long-term treatment with low doses of the D1 antagonist NNC 756 and the D2 antagonist raclopride in monkeys previously exposed to dopamine antagonists.
Lublin H;Gerlach J;Mørkeberg F Psychopharmacology (Berl). 1994 Apr;114(3):495-504.
Eight Cebus apella monkeys previously exposed to D1 and D2 antagonists were treated subcutaneously for 8 weeks with the D1 antagonist NNC 756 (0.01 mg/kg), followed by a wash-out period of 4 weeks and treatment with the D2 antagonist raclopride for 8 weeks (end doses 0.01 mg/kg). NNC 756 induced no dystonia, while marked dystonia was induced by raclopride. Mild tolerance to the dystonia-inducing effect of raclopride slowly developed. Both drugs induced significant sedation and mild bradykinesia. Sedation induced by NNC 756 was stronger than that of raclopride, while no differences were found regarding bradykinesia. The sedative effect of both NNC 756 and raclopride increased over time during chronic treatment. No changes in bradykinesia developed. No significant dyskinesia was induced by NNC 756, while raclopride significantly induced both acute and tardive oral dyskinesia. Furthermore, raclopride-induced acute dyskinesia worsened during chronic treatment. Concomitant treatment with NNC 756 tended to reduce the D1 agonist SKF 81297-induced dyskinesia and grooming, while concomitant treatment with raclopride increased SKF 81297-induced dyskinesia and tended to decrease SKF 81297-induced grooming.
3.Dopamine receptor occupancy in vivo: behavioral correlates using NNC-112, NNC-687 and NNC-756, new selective dopamine D1 receptor antagonists.
Nielsen EB;Andersen PH Eur J Pharmacol. 1992 Aug 14;219(1):35-44.
The ability of dopamine D2, mixed D1/D2 and selective D1 receptor antagonists, including NNC-112, NNC-687, NNC-756, to inhibit the in vivo binding of [3H]SCH 23390 or [3H]raclopride to dopamine receptors was studied in mice and rats. Furthermore, the dopamine-antagonistic effects of these drugs were also studied in various behavioral models. Significant levels of in vivo receptor blockade were required for antagonism of typical dopamine agonist-mediated behaviors. However, fewer D1 than D2 receptors had to be blocked to produce similar antagonistic effects. Thus, there may be a greater receptor reserve for D2 receptors than for D1 receptors.
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CAS 131796-63-9 Odapipam

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