Quote:Not sure what was so bad about sub-q and having LL bind to all CCR5 at 100% RO because we've been doing that very safely for 8 years w/o any ASE. So why is it so important not to have it bind to all the CCR5 in the body?
The only difference would be a greater chance that leronlimab would maintain 100% receptor occupancy. It might also mean that less than 700mg could be used to get 100% RO.
The summary mentions the two cured HIV patients. But a total cure is not what they are trying to achieve they are targeting a functional cure. A functional cure is considered maintaining a viral load under the amount of virus that will be transmissible or which hinder the immune system. That amount is 50 copies per ml or less. Leronlimab already acts as a functional cure in quite a large percentage of patients. In combo therapy with leronlimab 81% of patients were less than 50 c/ml which I believe was 350mg. In monotherapy I believe it was 91% or 92% of patients that were under 50 c/ml at 700mg.
Quote:When LL binds, it allows CCR5 to function in the same way it was prior to it's binding.
Once again that is incorrect. That came from Paul Maddon back in 1999 when they only knew of 3 chemokines that bound to CCR5. The only one he tested was CCL5 (RANTES) and leronlimab blocked that. He later came to the conclusion that leronlimab did not affect other chemokines binding because there were no signals of immunosuppression. But we now know that leronlimab boosts the immune system through other means. All CCR5 chemokines bind to the N terminus, leronlimab binds to the N terminus blocking it, therefore chemokines do not bind to leronlimab occupied CCR5.
If leronlimab did not block chemokines binding to CCR5 you would not see the anti-inflammatory effects. You would also not see the downregulation of chemokines that has been proven since 1999.
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