altinicline-maleate has been researched along with Parkinson-Disease* in 2 studies
1 trial(s) available for altinicline-maleate and Parkinson-Disease
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Randomized placebo-controlled study of the nicotinic agonist SIB-1508Y in Parkinson disease.
This randomized, placebo-controlled, 5-week Phase II trial evaluated the safety and tolerability of SIB-1508Y, a selective alpha4beta2 nicotinic acetylcholine receptor agonist, in 77 individuals with early Parkinson disease. Lightheadedness was a common dosage-related adverse effect at higher dosages, leading to frequent dosage reduction, drug discontinuation, and eventual trial redesign. A maximally tolerated dosage of 10 mg daily was identified. No antiparkinsonian or cognitive-enhancing effects were demonstrated in this trial. Topics: Aged; Antiparkinson Agents; Dizziness; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Nicotinic Agonists; Parkinson Disease; Pyridines; Pyrrolidines; Treatment Outcome | 2006 |
1 other study(ies) available for altinicline-maleate and Parkinson-Disease
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Interactions between a novel cholinergic ion channel agonist, SIB-1765F and L-DOPA in the reserpine model of Parkinson's disease in rats.
SIB-1765F, a novel nicotinic acetylcholine receptor agonist, was tested for its efficacy in attenuating reserpine-induced hypolocomotion in rats. SIB-1765F was administered alone or in combination with L-DOPA and its effects were compared to those of nicotine, d-amphetamine and amantadine in the same conditions. Consistent with previous reports, reserpine-induced hypolocomotion was reversed by L-DOPA (plus benserazide), d-amphetamine and amantadine in a dose-dependent manner and the effect of L-DOPA in reserpine-treated rats was potentiated by amantadine. SIB-1765F also increased the locomotor activity of reserpine-treated rats and potentiated the effect of L-DOPA on reserpine-induced hypolocomotion. The onset of potentiation of L-DOPA by SIB-1765F was rapid (< 5 min) compared to the onset of potentiation by amantadine (> 105 min). Interestingly, nicotine did not attenuate reserpine-induced hypolocomotion nor did it affect the action of L-DOPA on reserpine-treated rats. Biochemical analysis of levels of dopamine and its metabolites, dihydroxyphenylacetic and homovanillic acid, indicated that, in contrast to amphetamine, SIB-1765F did not inhibit dopamine reuptake. The effect of SIB-1765F in reserpine-treated rats was attenuated by alpha-methyl-p-tyrosine, implying that SIB-1765F acts by releasing dopamine from both reserpine-insensitive and reserpine-sensitive pools. Our findings demonstrate that nicotinic acetylcholine receptor agonists may offer a new therapeutic approach to the symptomatic treatment of the motor deficits in patients with Parkinson's disease. Topics: Amantadine; Animals; Antiparkinson Agents; Corpus Striatum; Dextroamphetamine; Dopamine; Ion Channels; Levodopa; Male; Motor Activity; Nicotinic Agonists; Olfactory Pathways; Parkinson Disease; Pyridines; Pyrrolidines; Rats; Rats, Sprague-Dawley; Reserpine | 1997 |