Invisioner, The manner in which CCR5 is targete

Invisioner,

The manner in which CCR5 is targeted makes a huge, if not complete, difference in efficacy and side effects.

I have looked, but not yet seen, information on the new Takeda CCR5 therapeutic.

The previous CCR5 blockers (revisiting some previous discussions) are allosteric modifiers. They attach to the CCR5 receptor on an arm of the transmembrane protein, modifying its function. This has potentially bad (side effects) implications, as the modification blocks desirable functions.

Leronlimab, to this point, is unique, in that it blocks binding of CCL5/RANTES through receptor binding site occupancy. There may be other similar molecules under development, but I am not yet aware of any.

Leronlimab is, at this point, in a class by itself.

The fact that others are trying to duplicate leronlimab, even as it waits approval, is extraordinarily positive.

I had a conversation tonight about the news of competitors chasing CCR5 mAbs with my wife. The anxiety induced by competitive imitators is normal, but a great indicator that Cytodyn and its supporters are on the right track.

All IMO as always.