RE:RE:Seeking Alpha piece on RVX....I enjoyed all three Seeking Alpha articles. The writer is clearly very knowledgeable in this space and does a very good job presenting a balanced opinion.
There were two things that truly caught my eye in the latest SA article - items I had not known from other sources:
SURPRISE TIDBIT # 1. The existence of a new journal article. This article apparently provides the data from the mouse studies of years ago. You'l recall of course that Resverlogix tends to be a fortress when it comes to their data. We only get little pieces here and there. Although I have only seen the summary of this new journal article, it seems to indicate that they are providing therein a great deal of information about the old animal studies completed years ago. This information of course will give researchers a lot of background into understanding how RVX-208 works and does not work. Interesting.
SURPRISE TIDBIT #2. The latest Seeking Alpha article indicates that the apoA-1 trend in the data from ASSURE was "completely absent":
Resverlogix has previously set out to prove that RVX-208 causes apoA1 levels to increase (apoA1 is needed for making, HDL, i.e. the "good" cholesterol). The results were not really clearly positive, although there was a trend in some of the trials, but the trend was - at least in my eyes - more or less completely absent in the ASSURE trial results.
Read more at https://www.stockhouse.com/companies/bullboard/t.rvx/resverlogix-corp#P1mdHFDtxhmcOm8e.99
This was news to me.
What is interesting about all of this is the following:
If you go back to the mouse studies (under SURPRISE TIDBIT #1 above), you'll see that they had the same result in those mouse studies years ago: ApoA1 did not rise. Here's what that article says about apoA-1:
"no significant changes in plasma apoA-I were observed"
LINK: https://www.atherosclerosis-journal.com/article/S0021-9150(14)01238-6/abstract?cc=y?cc=y
So my question is this: Does apoA-1 matter? If the drug doesn't raise https://www.atherosclerosis-journal.com/article/S0021-9150(14)01238-6/abstract?cc=y?cc=y (and if they knew about that years ago), why did they keep touting apoA-1 for all these years?
I recall reading that apoA-1 is a transient molecule (my wording), meaning that it doesn't stay around for long in the blood. It either gets flushed or transforms into something else (HDL).
Thus, I'm left wondering: Does ApoA1 matter that much?
Anyone out there have some insight on this???