Hi, I believe you are drawing the wrong conclusions from this passage. As a note, I will say I only looked at your current passage and if you feel there is better content to make your point I would be happy to look at it.

This passage describes the fact that binding to CCR5 is not the only prerequisite to inhibiting HIV entry. This is not uncommon, different compounds often cause different effects on the receptors they bind too. They also conclude that based on the evidence, ECL (extracellular loop) 2 is most important for inhibiting viral entry. This also is not uncommon, as ECL2 often shows some of the most important amino acids involved in receptor activation and consequently inhibition.

What this paper is saying is that binding to CC5 is not enough, as evidenced by the many compounds that bind and do not inhibit entry.

HOWEVER, there are a few that do inhibit entry and by looking at those (including leronlimab) we can conclude that what makes them unique is their activity at ECL2. Therefore, from this passage I would say this is speaking to the complexity of the problem that only a couple compounds, leronlimab included have overcome.

As I said, I would be happy to look at any other literature you find. I have spent a great deal of time in early drug discovery and can navigate their waters fairly quickly.