The experimental drug, solanezumab, an injectable humanized monoclonal IgG1 antibody directed against Aβ peptides, is garnering a lot of attention for it's potential disease modifying effects for patients at risk of Alzheimer's disease. Current treatments may modify symptoms associated with the disorder but none are approved for actual disease modification or delayed on-set of symptoms. Previous clinical trials reported negative results and seemed to doom the drug and similar formulations. Now there may be interesting clinical trial results being released at the upcoming July conference.
So what gives?
A quick google search reveals the interest from news and finance channels. As estimates in Alzheimer's and dementia healthcare costs are quoted in excess of 600 billion dollars a year the enthusiasm is anticipated if not perhaps a little premature.
June 12 (Reuters) - The Alzheimer's Association may not offer an early look at highly sought clinical trial data on an experimental drug from Eli Lilly and Co after news of the impending release led to a jump in the company's shares.
Modeling applied to Phase 3 solanezumab data in patients with mild to moderate AD
What is visible from the graphic below--the phase 3 solanezumab data sustains the difference between the mean change in the "early start" and "delayed start" cohorts. An interesting finding worthy of anticipating the latest results from the EXPEDITION safety and efficacy studies and other data sets attempting to differentiate between potential disease modifying effects and attenuation of symptoms.
Application to Phase 3 Randomized Clinical Trial Data
We applied the analytical methodologies we propose in this paper to data from patients with mild AD in Phase 3 studies for solanezumab, a humanized monoclonal antibody, for the treat- ment of AD. EXPEDITION and EXPEDITION2 (ClinicalTrials.gov numbers NCT00905372 and NCT00904683) were Phase 3, 18-month, placebo-controlled studies investigating the efficacy and safety of solanezumab in patients with mild to moderate AD.