Biogen Idec announced Friday detailed results from a Phase Ib study showing that aducanumab reduced amyloid plaque in the brain of patients with prodromal or mild Alzheimer's disease and also slowed cognitive decline. "This is the first time an investigational drug for Alzheimer's disease has demonstrated a statistically significant reduction on amyloid plaque as well as a statistically significant slowing of clinical impairment in patients with prodromal or mild disease," remarked chief medical officer Alfred Sandrock.
"Either result alone would have been exciting, but to see them both in the same study makes it even more exciting," commented Sandrock. In December last year, Biogen Idec said it would start a Phase III programme for aducanumab, also known as BIIB037, based on results from the trial. Sandrock confirmed Friday that the company is "advancing the aducanumab clinical programme to Phase III with plans to initiate enrollment later this year." Shares in the drugmaker jumped as much as 10 percent on the news.
The PRIME study is evaluating several doses of aducanumab in patients with prodromal or mild Alzheimer's disease, with results from a pre-specified interim analysis presented at the International Conference on Alzheimer's and Parkinson's Diseases and Related Neurological Disorders including data for 166 patients. Biogen Idec noted that treatment with aducanumab at doses of 3 milligrams per kilogram and 10 milligrams per kilogram led to significant reductions in amyloid plaque at week 54 of 0.139 and 0.266, respectively, as measured using a composite standardised uptake value ratio (SUVR). The company added that the reduction of amyloid plaque in the 1 milligram per kilogram arm was not significant, while data from the 6 milligram per kilogram arm will become available at a later date. According to the drugmaker, in comparison, the SUVR in the placebo arm was "virtually unchanged."
Further results showed that for the Clinical Dementia Rating sum of boxes (CDR-SB) measure of cognition, aducanumab demonstrated a significant 71 percent reduction at a dose of 10 milligrams per kilogram. Analysts previously said they were looking for 20 percent to 30 percent reductions to qualify as a success. Specifically, patients in the placebo group worsened by an average of 2.04 at one year as measured by the CDR-SB, while the decline was 0.59 in the 10 milligrams per kilogram arm. On another measure of cognition called MMSE, results for aducanumab showed declines of 0.75 in the 3 milligram per kilogram arm and 0.58 in the 10 milligram per kilogram, which were significantly slower than 3.14 at one year in the placebo group.
Biogen Idec CEO George Scangos noted that the company screened patients for the trial to exclude those with other forms of dementia misdiagnosed as Alzheimer's disease. "We imaged every patient coming into study, so we knew that every patient had Alzheimer's disease and plaque," Scangos said, adding "it's hard to think of a reason why these data are not representative of the actual activity of the drug."
Safety results showed that in carriers of the ApoE4 gene, the incidence of amyloid-related imaging abnormalities of oedema (ARIA-E) was 55 percent in the 10 milligrams per kilogram arm, while 35 percent of patients in this group discontinued treatment. In ApoE4 non-carriers, the incidence of ARIA-E was 17 percent in the 10 milligrams per kilogram arm, with discontinuations of 8 percent in these patients. Biogen Idec added that headache occurred in 22 percent of patients receiving aducanumab compared to 5 percent in the placebo groups.
Biogen Idec licensed aducanumab from Neurimmune in 2007. The human recombinant monoclonal antibody targets aggregated forms of beta amyloid including soluble oligomers and insoluble fibrils deposited into the amyloid plaque in the brain of patients with Alzheimer's disease.
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