Cytodyn Inc (CYDY)

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My logic however for LL was that since it blocks CCR5 in lungs etc., the organs should not attract CCL5 in the LL patients as much as it would in placebo patients, and therefore we should find a significantly greater % reduction of CCL5 in LL patients than in placebo patients. This clearly is not the case.

Think I got it mixed up. Watched part of Dr. Been's video on the MOA again:

The damaged cell in the lungs releases CCL5 which becomes the attractor for the immune cells (by binding to their CCR5 receptors) causing the immune cells to pile into the lungs or other organs. Leronlimab's action is to block CCR5 in the immune cells which prevents them from getting attracted by the CCL5 feed. The idea that CCL5 should become less because of Leronlimab is likely a misunderstanding on my part.

For the breast cancer case, Dr. Been says that about 50% of breast cancer cells develop CCR5 on them, making them prone to travel outside of that region and infecting cancer onto other regions in body. By blocking the CCR5 receptors in these cancer cells, they become like "sitting ducks" unable to travel and spread elsewhere, at which point the Chemotherapy can attack them and kill them right there. That is the MOA. (Add: in the case of Holly Kennedy, her cancer may have already spread to other parts and reached a critical stage beyond the help of LL.)

However in this case it is curious that we seemed to do better for patients who had <50% CCR5 expression. Ideally if the above MOA is correct, LL should make the biggest impact on patients with high CCR5 % since it supposedly blocks those cells etc. Of course all this is anecdotal and we also don't know whether the patients in the SG arm of the SG trial had predominantly <50% CCR5 (thus skewing their results favorably).