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Friday, July 24, 2015

Pioglitazone 'Unlikely' to Slow Parkinson's


July 23, 2015
The diabetes drug pioglitazone is unlikely to modify progression in early Parkinson's disease (PD), new results from a phase 2 study suggest.
The authors, the NINDS Exploratory Trials in Parkinson Disease investigators, led by Tanya Simuni, MD, Northwestern University, Chicago, Illinois, conclude, "Further study of pioglitazone in a larger trial in patients with Parkinson's disease is not recommended."
The FS-ZONE study, published in the August issue of The Lancet Neurology, was a futility study, which the authors describe as "phase 2 clinical trials designed to identify and eliminate compounds that have low likelihood of being efficacious in definitive efficacy studies by comparing the primary outcome measure in the treatment group versus placebo to a prespecified threshold value."
For the study, 210 patients with early PD were randomly assigned to one of three groups: pioglitazone 15 mg/day, pioglitazone 45 mg/day, or placebo. The primary outcome was the change in the total Unified Parkinson's Disease Rating Scale (UPDRS) score between baseline and 44 weeks.
The primary analysis showed that pioglitazone at 45 mg/day showed a mean difference in UPDRS score of –1.12, which was deemed to be futile. The pioglitazone dose of 15 mg/day showed a –1.83 difference in UPDRS score, which was not futile in the primary analysis, but sensitivity analyses and secondary outcome measures suggested that this dose was also futile.
The authors note that pioglitazone was chosen for testing because it had shown neuroprotective effects in tissue culture and animal models.
"Unfortunately, this is another study in which animal models were not predictive of efficacy in human beings," they write, adding that toxin animal models may not reflect Parkinson's disease pathogenesis.
Is UPDRS Best Endpoint? 
In an accompanying editorial, Fabrizio Stocchi, Institute for Research and Medical Care, Rome, Italy, points out that there are some concerns about the sensitivity of the UPDRS in patients with mild disease.
But Dr Simuni and coauthors argue that the UPDRS "is the best validated measure and the one that has extensive data showing its sensitivity to change in early Parkinson's disease."
They add, "Consistent findings for all secondary outcomes, which included a spectrum of validated measures of quality of life, disability, and cognitive impairment, support an absence of biological effect rather than a failure to capture and measure an effect."
Serum and urine biomarkers also failed to show a separation of the active treatment groups from placebo.
"The finding that both clinical and biological markers failed to move is disappointing, but solidifies the conclusion that pioglitazone is not promising for further testing in early Parkinson's disease," the authors conclude.
They note that 12 other possible neuroprotectant agents have been recommended by an expert committee for clinical testing. Most have entered phase 2 studies and 4 have completed phase 3 studies, but all studies have been negative so far.
Given these disappointing results, the researchers suggest that "neuroprotection might not be feasible unless we intervene at the premotor stage of the disease."
The study was funded by the National Institute of Neurological Disorders and Stroke. Dr Simuni reports that he received personal fees from Acadia, Abbvie, Allergan, Eli Lilly, Harbor, Ibsen, Merz, UCB Pharma, and US World Meds; received grants, personal fees, honorarium, consulting fees, and educational grant support from and was a speaker for GE Medical and TEVA; received consulting fees from and was an advisory board member and speaker for IMPAX; received personal fees and consulting fees from and was a speaker for Lundbeck; and received research funding from Auspex, Biotie, Civitas, National Institutes of Health, and Michael J. Fox Foundation during the conduct of the study. Dr Stocchi reports he has received honoraria and research grants from Novartis, Teva, UCB, GlaxoSmithKline, Boehringer Ingelheim, IMPAX, Lundbeck, Merck, and Britannia.
Lancet Neurol. 2015;14:795-803, 780-781. Abstract Editorial
http://www.medscape.com/viewarticle/848572?src=wnl_edit_tpal

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