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New Drug Slows Decline In Mild Alzheimer's Cases


 

SAN JUAN, P.R. – R-flurbiprofen, one of a new class of selective amyloid-β42-lowering drugs, shows some promise at higher doses in delaying cognitive and functional declines associated with Alzheimer's disease, according to phase II trial data presented at the annual meeting of the American Association for Geriatric Psychiatry.

“Subjects with mild AD on the high dose (800 mg) showed a reduced rate of decline on all of the primary outcome measures,” said Dr. Daniel D. Christensen, a psychiatrist and neurologist at the University of Utah, Salt Lake City. This selective amyloid-β 42-lowering agent (SALA) is thought to be an allosteric modulator of γ-secretase.

The proof-of-concept study involved 207 patients with mild to moderate Alzheimer's disease (AD), and was conducted in Canada and the United Kingdom. The trial was sponsored by the drug's developer, Myriad Pharmaceuticals Inc. Dr. Christensen also is a consultant/speaker for the company.

Patients were randomized to receive twice-daily doses of 400 mg R-flurbiprofen, 800 mg R-flurbiprofen, or placebo. The placebo-controlled portion of the trial lasted for 12 months. All trial participants who were stable on anticholinesterase drugs for at least 3 months prior to the study were allowed to continue with them. Patients were assessed using the Alzheimer's Disease Assessment Scale, cognitive section (ADAS-cog), the Alzheimer's Disease Cooperative Study Activities of Daily Living (ADCS-ADL), and the Clinical Dementia Rating (CDR) sum of box score.

“There was essentially no response in the moderate patients,” said Dr. Christensen. For this reason, the researchers limited their analysis to patients with mild AD (those with a Mini-Mental State Examination score of at least 20). Of the patients who had mild Alzheimer's, 46 received placebo, 36 received 400 mg R-flurbiprofen, and 48 received 800 mg R-flurbiprofen.

In terms of ADAS-cog scores, those who received 400 mg R-flurbiprofen had essentially the same response as those on placebo. Those taking the higher dose of R-flurbiprofen showed a 34% effect size at 12 months, though this was not statistically significant. “This basically means that we prevented 34%–about a third–of the respective decline” seen in the other two groups, Dr. Christensen said.

Those in the 800-mg group showed an effect size of 45% at 12 months, as measured by the ADCS-ADL, though this did not reach statistical significance. The 400-mg dose appeared to have an intermediate effect on daily function. There was little difference at 12 months between the placebo group and those in the 400-mg group in global function, as measured by the CDR. The effect size for the 800-mg group was 36%, though this did not reach statistical significance.

In an exploratory analysis, the researchers found a significant relationship between plasma concentration and response. A total of 29 patients (60% of those in the 800-mg group) had drug plasma concentrations greater than 75 μg/mL.

Both dosing regimens were generally well tolerated, Dr. Christensen said. The numbers of discontinuations attributable to adverse events were comparable among the placebo group and the two active treatment groups. Transient eosinophilia, mild anemia, blood pressure elevation, lower respiratory tract infections, and mild rashes occurred more frequently in the active treatment groups.

Patients in Canada were allowed to participate in a follow-on study after 12 months. Of the 106 patients eligible, 86 enrolled for an additional 12 months; 62 had mild AD. Of the mild-AD patients, 20 had previously been in the placebo group and were randomized to receive either 400 mg or 800 mg R-flurbiprofen twice daily.

A phase III trial is now underway in the United States.

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