The premise being evaluated by these three pharmaceuticals is that the amyloid-beta plaques, found in the brains of Alzheimer's patients, are the cause of the disease; therefore if the plaques can be removed or prevented from forming, this could make a significant improvement in patient functioning and slow declining abilities. The three products are solanezumab, aducanumab, and verubecestat and act as antibodies to eliminate and/or prevent plaques. SOLANEZUMAB
In 2015 Lilly reported that solanezumab slowed symptoms of disease progression by two years. As reported in March 2016, “In two previous trials of solanezumab, pharmaceutical company Lilly used both a cognitive test and a functional measurement to track the response of people with both mild and moderate Alzheimer’s disease. Both trials failed to show significant benefits over placebo in either measure.” “However, Lilly noticed that participants with mild Alzheimer’s seemed to do better than controls in the cognitive portion of the testing, says Eric Siemers, a neurologist employed by Lilly.” Final data from a clinical trial targeting 2,100 patients with early Alzheimer’s is expected in 2017. It is anticipated that this product will be targeted to those with mild Alzheimer’s.
http://www.sciencemag.org/news/2016/03/why-big-change-lilly-s-alzheimer-s-trial-not-evidence-its-drug-has-failed-again
ADUCANUMAB
“Alzheimer’s disease (AD) is characterized by deposits of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain.” A hypothesis that is being tested is that if the plaques can be prevented from forming – or can be removed after forming - this would slow clinical decline in patients with Alzheimer’s disease. Reported in Nature, September 2016, these results have been experienced in a one year trial using infusions of aducanumab (only 165 participants) and they are moving into phase III trials now. “Should the slowing of clinical decline be confirmed in ongoing phase 3 clinical trials, it would provide compelling support for the amyloid hypothesis.” Made by Biogen.
http://www.nature.com/nature/journal/v537/n7618/full/nature19323.html
VERUBECESTAT
In Nov. 2016 Merck released information on the success of their brain plaque inhibitor verubecestat, shown to remove amyloid plaques that are prominent in Alzheimer’s disease in the brains of rats, monkeys, and humans. There may even be a possibility that it could prevent amyloid plaques from forming. The limited testing has so far produced no negative side effects.
There are now “two trials testing long-term outcomes in patients (taking verubecestat). The first involves roughly 2,000 patients with mild to moderate Alzheimer's for 18 months. The second has around 1,500 participants with early signs of Alzheimer's (as indicated by amyloid plaques revealed in positron emission tomography (PET) brain scans), for two years.
Solanezumab, aducanumab and verubecestat are all now in “phase III clinical trials (on humans) to assess their efficacy, effectiveness and safety, but the results are promising, experts say.”
https://www.scientificamerican.com/article/new-alzheimer-s-drug-clears-milestone-in-human-clinical-trial1/
In 2015 Lilly reported that solanezumab slowed symptoms of disease progression by two years. As reported in March 2016, “In two previous trials of solanezumab, pharmaceutical company Lilly used both a cognitive test and a functional measurement to track the response of people with both mild and moderate Alzheimer’s disease. Both trials failed to show significant benefits over placebo in either measure.” “However, Lilly noticed that participants with mild Alzheimer’s seemed to do better than controls in the cognitive portion of the testing, says Eric Siemers, a neurologist employed by Lilly.” Final data from a clinical trial targeting 2,100 patients with early Alzheimer’s is expected in 2017. It is anticipated that this product will be targeted to those with mild Alzheimer’s.
http://www.sciencemag.org/news/2016/03/why-big-change-lilly-s-alzheimer-s-trial-not-evidence-its-drug-has-failed-again
ADUCANUMAB
“Alzheimer’s disease (AD) is characterized by deposits of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain.” A hypothesis that is being tested is that if the plaques can be prevented from forming – or can be removed after forming - this would slow clinical decline in patients with Alzheimer’s disease. Reported in Nature, September 2016, these results have been experienced in a one year trial using infusions of aducanumab (only 165 participants) and they are moving into phase III trials now. “Should the slowing of clinical decline be confirmed in ongoing phase 3 clinical trials, it would provide compelling support for the amyloid hypothesis.” Made by Biogen.
http://www.nature.com/nature/journal/v537/n7618/full/nature19323.html
VERUBECESTAT
In Nov. 2016 Merck released information on the success of their brain plaque inhibitor verubecestat, shown to remove amyloid plaques that are prominent in Alzheimer’s disease in the brains of rats, monkeys, and humans. There may even be a possibility that it could prevent amyloid plaques from forming. The limited testing has so far produced no negative side effects.
There are now “two trials testing long-term outcomes in patients (taking verubecestat). The first involves roughly 2,000 patients with mild to moderate Alzheimer's for 18 months. The second has around 1,500 participants with early signs of Alzheimer's (as indicated by amyloid plaques revealed in positron emission tomography (PET) brain scans), for two years.
Solanezumab, aducanumab and verubecestat are all now in “phase III clinical trials (on humans) to assess their efficacy, effectiveness and safety, but the results are promising, experts say.”
https://www.scientificamerican.com/article/new-alzheimer-s-drug-clears-milestone-in-human-clinical-trial1/
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