Thanks for that. Someone else referenced it as well and I was able to peruse pieces and parts of the data.
My first thought was for the poor meeces getting electrocuted in the name of science and then being decapitated. Ouch.
Beyond that, one thing I like to do is look into the drugs that are chosen for comparison in these type of papers. I begin with the assumption that the comparison drugs are chosen for a good reason. Sometimes it's helpful, to me anyway, to look at those drugs efficacy and side effects for hints that might translate to the main drug.
"The main purpose of the present study was to analyze ANAVEX2-73 effects on Tau pathology and Aß accumulation, by comparison with the reference and selective s1 receptor agonist PRE-084 (Su et al, 1991) and the muscarinic ligand xanomeline,
I seen quite a lot of speculation here that Anavex has a greater chance of success than the ~99% failure rate of Alzheimer's drugs because they are pursuing a unique approach to Alzheimer's. But looking into xanomeline seems to indicate that outside of subtle nuances the MOA of Anavex was tried and apparently was unsuccessful due to side effects with xanomeline.
" Efficacy of xanomeline in Alzheimer disease: cognitive improvement measured using the Computerized Neuropsychological Test Battery (CNTB)." "The cognitive efficacy of the M1-selective muscarinic agonist xanomeline in mild-to-moderate Alzheimer disease (AD) was measured using the Computerized Neuropsychological Test Battery (CNTB) and the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog) in this 17-center, double-blind, placebo-controlled study. Three hundred forty-three patients were randomly assigned to receive 25, 50, or 75 mg xanomeline tartrate or placebo three times daily (t.i.d.) for 24 weeks, followed by placebo for 4 weeks in a single-blind washout phase"
I suppose the argument will be made that A2-73 is "better" than xanomeline for reasons X,Y and Z and although that may be correct I believe at the very least this indicates that A2-73's approach to Alzheimer's is not as unique or untested as many here apparently believe.
"So how useful will M1 and M4 agonists be? That is the big question. I was working in the field when Eli Lilly was trying to get a selective M1 agonist (xanomeline) going, and selectivity in that receptor family is not easy to attain. The side effects will hammer you if you’re not, though, which in the end is what happened with Lilly. They did come up with some clinical data to suggest that the mechanism might be useful in Alzheimer’s before the whole program wiped out, though, which is what brought Heptares back around for another try."
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