Quote:

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Leronlimab does not dislodge chemokines that are already bound to CCR5. It binds to empty CCR5 receptors blocking any other binding.

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Competitive antagonists (Leronlimab) bind to receptors, (CCR5), at the same binding site (active site) as the endogenous ligand or agonist, (CCL5), but without activating the receptor. (Leronlimab is a Competitive Antagonist)
Agonists and antagonists "compete" for the same binding site on the receptor. Once bound, an antagonist will block against binding. Sufficient concentrations of an antagonist, (700mg dosing), will displace the agonist from the binding sites , resulting in a lower frequency of receptor activation. The level of activity of the receptor will be determined by the relative affinity of each molecule for the site and their relative concentrations . High concentrations of a competitive agonist will increase the proportion of receptors that the agonist occupies, higher concentrations of the antagonist will be required to obtain the same degree of binding site occupancy.[16]

That came from here:
https://en.wikipedia.org/wiki/Receptor_antago...ompetitive