So it appears. The CCR5 protein itself is relatively large, so that there multiple areas to which antibodies can attach to alter its function. The allosteric modulators, i.e. maravorac, bind to a portion of the protein altering its function. This has proved useful in rheumatoid arthritis, but apparently not Covid.

Leronlimab directly inhabits the CCR5 binding site, stopping its response to the CCL5. It is just luck that this is effective to stop the cytokine storm, as it would appear that no one appreciated the role of CCL5 / RANTES until the work of Dr Patterson to elucidate the mechanism by which leronlimab helped a number of the Montefiore EIND patients, all of whom would likely have died without leronlimab.

I’m doubt that anyone gets a Nobel in medicine for one paper, but he may deserve it.