the way it effectively blocks CCR5, but yet allows some of its functions to still occur.
That is what co-inventor Dr. Maddon and Cytodyn claimed for years but I believe that to be wrong. Cytodyn removed that statement from their website sometime in 2021.
When I first started studying leronlimab and CCR5 I accepted that as fact. But the effects on diseases outside of HIV didn't make sense. In 2020 I figured out that leronlimab must bind to the N terminus. All chemokines that bind to CCR5 also bind to the N terminus and as a large molecule it would also block all of those chemokines from binding. Which is a wonderful thing or otherwise leronlimab would not work as effectively on so many diseases.
I proposed my theory that the other CCR receptors that also bind the chemokines that leronlimab binds and those chemokines elevate alongside CCR5. The elevation of those chemokines and other CCR receptors and the blocking of CCR5 brings the immune system to a normal state. This has never been studied and I wish someone would. Proof of this would show the FDA why leronlimab is an immunomodulator rather than an immunosuppressant.