Taking a break from PPACA analysis, I'm going to examine an Alzheimmer's drug that failed its pivotal trial last week. That drug is solanezumab from Eli Lilly. Upon announcement of the failed trial, Eli Lilly's stock dropped 11%.
Solanezumab is a monoclonal antibody which aims to prevent or reduce amyloid plaque in the braid. Amyloid plaque is thought to be a cause or effect of Alzheimmer's disease. The drug attaches to free amyloid protein to prevent it from joining together with other protein to form plaque.
I didn't follow this drug carefully, but it appears that it had failed two previous trials, so expectations may have already been tempered and priced into the stock. Those two trials suggested that Solanezumab may have a positive effect in patients with mild dementia. These results were the design of Eli Lilly's Phase III trial for solanezumab.
Unfortunately, patients treated with the drug did not experience a statistically significant decrease in cognitive impairment, the primary endpoint for the clinical trial.
But, even in this failure there are important learnings for alzheimmer's treatment. The clinical experience of Solanezumab suggests that by the time amyloid shows up on brain scans, it may be too late for amyloid plaque reduction to improve a patient's cognitive abilities. Thus, the effects of the disease and the resulting dementia may have set in much earlier.
If that's true, then Alzheimmer's research could go into two directions:
1) Earlier detection. If the plaque is found in its very early stages and removed, can dementia be avoided? --> Can we use liquid biopsy and genomic testing to identify early stage Alzheimmer's disease?
2) Regeneration of brain cells involved in cognitive abilities. The amyloid plaque may just be an effect of Alzheimmer's disease. --> Can we use stem cell therapy to regenerate the appropriate places in the brain?
Of course, a variety of other approaches are being studied:
Source: Eli Lilly Alzheimmer's Drug Fails in Trials
Solanezumab is a monoclonal antibody which aims to prevent or reduce amyloid plaque in the braid. Amyloid plaque is thought to be a cause or effect of Alzheimmer's disease. The drug attaches to free amyloid protein to prevent it from joining together with other protein to form plaque.
Unfortunately, patients treated with the drug did not experience a statistically significant decrease in cognitive impairment, the primary endpoint for the clinical trial.
But, even in this failure there are important learnings for alzheimmer's treatment. The clinical experience of Solanezumab suggests that by the time amyloid shows up on brain scans, it may be too late for amyloid plaque reduction to improve a patient's cognitive abilities. Thus, the effects of the disease and the resulting dementia may have set in much earlier.
If that's true, then Alzheimmer's research could go into two directions:
1) Earlier detection. If the plaque is found in its very early stages and removed, can dementia be avoided? --> Can we use liquid biopsy and genomic testing to identify early stage Alzheimmer's disease?
2) Regeneration of brain cells involved in cognitive abilities. The amyloid plaque may just be an effect of Alzheimmer's disease. --> Can we use stem cell therapy to regenerate the appropriate places in the brain?
Of course, a variety of other approaches are being studied:
- Gantenerumab (Roche): amyloid plaque reducer for people who haven't shown symptoms yet
- BACE inhibitors: block an enzyme required for amyloid plaque production
- Crenezumab (Genentech): passive immunity monoclonal antibodies for alpha beta peptides
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| Amyloid Beta Peptide |
Source: Eli Lilly Alzheimmer's Drug Fails in Trials
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