Myriad Genetics' Follow-on Study of Flurizan Demonstrates Continued Benefit in Alzheimer's Disease
Flurizan Continues to Slow Decline in Cognition, Behavior and Daily Activities through 21 Months
The data suggest that during the follow-on period from months 12 to 21, the benefit of Flurizan on the measures of Alzheimer's disease increases in terms of both effect size and significance, the longer patients remain on Flurizan. The efficacy of Flurizan in the first 12 months of the Phase 2 was measured as the difference between the rates of decline, or slopes, of the treated groups and the placebo group. In the follow-on study, because the placebo group has been randomized into the treatment arms, Myriad is measuring the difference between the slopes of the treated groups and the slope of the placebo group during the first 12 months, extended through 21 months. The statistical significance of the resulting difference in slopes, or the effect size, is computed as a p value.
As measured by the performance of activities of daily living (ADCS-ADL), by patients taking 800 mg of Flurizan BID, there was a 52% effect size compared with the projected slope of the placebo at 21 months, with a significant value of p=0.029. In terms of the patient's global function at 21 months, the CDR-sb scale showed a 75% effect size, with a value of p=0.0007, also significant. These data suggest that there is a substantial benefit from Flurizan on activities of daily living and global function, and that the benefit is increasing over time. The effect of Flurizan in improving cognitive decline, as measured on the ADAS-cog scale, has also increased, as shown by the effect size of 60% at 21 months. All three of the measures suggest sustained benefit from Flurizan in patients with mild Alzheimer's disease.
Flurizan belongs to a new class of drug candidates known as Selective Amyloid beta-42 Lowering Agents (SALAs). Flurizan lowered levels of Abeta42 in cellular assays and animal models. Abeta42 is the primary constituent of senile plaque that accumulates in the brain of patients with Alzheimer's disease. It is thought to be the key initiator of Alzheimer's disease, since Abeta42 has the greatest tendency to aggregate, cause neuronal damage and initiate amyloid deposits in the brain.
Other news from the department research and development
Get the life science industry in your inbox
From now on, don't miss a thing: Our newsletter for biotechnology, pharma and life sciences brings you up to date every Tuesday and Thursday. The latest industry news, product highlights and innovations - compact and easy to understand in your inbox. Researched by us so you don't have to.