Not very concise ramblings and thus hard to comment on specially.
Not sure how the author of the post can come to the conclusions that Anavex might have dropped AD.
I would just give that a pass and look for posts with considered arguments and by that I don’t mean we got this or possessing special understanding of the uniqueness of A2-73.
Anavex themselves do not understand anywhere near fully the MoA of A2-73, but they have planned and are executing current trials based on all they could learn from their’s and other’s pre- and clinical work to date.
As investors we have made our bets for the outcome of current trials. The AD P2b/3 trial will readout late 2022 no matter any ramblings.
Of course one should keep looking out for new approaches, Anavex isn’t and won’t be the only game in town.
Wow! Carl was really well prepared for the question on Anavex. A little too perfectly worded. I think it shows some people really want to take Anavex down.
1) No understanding of the MoA. 2) Side effects? 3) AD indication being dropped? 4) SIGMAR1 receptor might wear out.
All of these points are subjective and some are more far fetched than others but it's clear, Carl has put some thought behind what he might say negatively about Anavex. Given that, it's a pretty weak list of points.
thinks there is only one piece of research on MOA...what about all the Wayne state studies? The extensive genomic analysis? The numerous OLE tests over many years? Most of all the myszy studies! Plus other articles that have been posted here over the years
Side effects? 273 has hardly any over years of use.
From your post: "Perhaps not all may hold true; it's been about 7 months since I have reviewed AVXL. For the record, I am not saying I don't give AVXL's approach a chance, look at their Parkinson's data."
7 months is a long time to make a such a negative statement about Anavex.
Here's a quote from TGD at the H.C. Wainwright 23rd Annual Global Investment Conference last month...at the 12:40 minute mark:
"But the most important distinction of A2-73 and the entire platform of sigma-1 activation is that we've now been able to learn, very recently, that sigma-1 activation goes even further upstream into the nucleus...and its been able to show that it prevents cellular stress before and after RNA translation.
So in regards to that, chromatin remodeling is restored, as well as post-translation proteins - which are toxic - are prevented, by preventing toxic RNA to be expressed into toxic proteins. So only healthy proteins are expressed by expressing healthy RNA".
This is a bunch of BS. Of course, everyone has the goods. There is no way of knowing without clinical trials and there is certainly alot of research data on A2-73, Sigma 1 agonists, and the use of muscarinic receptors. Tough nut to crack...
Noone knows the Golden answer, yet... only time and money will tell.