There may be another problem, but it would take time to tease it out. There are at least two proteases in the viral genome. Both contain a cysteine residue, and I not sure that people are using the same terminology when discussing them, which is what is taking up my time to figure out. If we compare inhibitors of protease A and rank them on the basis of calculated or (preferably) measured affinity, that is fine. If we start comparing an inhibitor of protease A to an inhibitor of protease B, things get more complex. For example, I am very doubtful that one should compare docking energies between two compounds binding to two different receptors.
EDT
Based partially on this
link, my preliminary assessment is that the main protease is the one that is described as chymotrypsin-like. It is also the target of the new Pfizer drug. Therefore, it is OK for Dr. Campbell to focus on it, although the other protease might also be a worthwhile target.
EDT2
I remember taking a shallow dive into the following question a few months ago: Does the size of the molecule introduce a bias in the calculated affinity in a docking experiment? I found some references which suggested that the answer was yes, but that there were ways to compensate for this bias. Given that the sizes of ivermectin, remdesivir, etc. are different, ideally one should factor this into a comparison.