Cassandra X, This was a post from my future as

Cassandra X,

This was a post from my future as you will see above in the message board. I'm glad somebody else thought of angiogenesis.

Like Diddy asked about CCR5 overexpression, I'm uncertain if the mere presence of CCR5 halts angiogenesis, or the over expression of CCR5. If one does not have CCR5 is the angiogenesis effect void?

This reminds me of 2019 when Cytodyn used to talk about 4 MOAs not just one. I asked a few times if the board knew all four - I think I could list only 3. Somebody "mocked" me slightly saying they were all 4 related to the 1 idea of CCR5 - or upstream of the other 3 MOAs.

But I swear, we used to talk about 4 MOAs.

1. CCR5 Antagonism
2. Halting angiogenesis
3. Halting Tumor Metastasis - circulating tumor cells
4. Halting De-mylation of nerve cells - MS, Parkinsons, Alzheimers

Not sure I have those correct...

5. Possibly adding crossing the BBB as an MOA

MY QUESTION:

Are all of our MOAs (as previously promoted) now all the result of the CCR5/CCL5 axis?

Follow-up question, does Leronlimab cross the blood brain barrier only as a passenger on a cell that has CCR5 receptors on it's surface and Leronlimab has bound to the CCR5 receptors, OR, can Leronlimab cross a healthy blood brain barrier on it's own (free floating) in the circulatory system?

Is it possible that Leronlimab unbinded to CCR5 receptor (free-floating) can only cross a leaky BBB such as in Alzheimers, Covid, AIDS, or OLD-Age????