Thank you for sharing CTMedic. I learned long ago that leronlimab did not activate the immune function of the receptor but this dives a bit deeper and adds some great color.

To reciprocate, and this may be obvious to some but is something I have been digging into as of late, is the safety of leronlimab vs. maraviroc. So, we all know that maraviroc is metabolized in the liver via CYP450. These are a group of enzymes that are involved in the clearance and breakdown of products in our bodies. It's believed that the hepatoxicity comes from this breakdown process wherein a toxic intermediary is produced.

What I recently learned is that maraviroc is a substrate for P-glycoprotein. What is that? It's like a mini protein pump that takes the contents from the inside of the cell and transports them outside the cell. Interestingly enough this phenomena is believed to play a part in drug resistance as the cell will pump out drugs intended to destroy the cell therefore rendering the drug less effective. And this is also the reason there are more likely to be drug-drug interactions with maraviroc. As this process is activated, maraviroc can then interact with other drugs in the body.

In comparison, being a monoclonal antibody, leronlimab is basically chopped up into amino acids and excreted. This article has more details if you are curious https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5613179/

It is important to note that maraviroc has definitely been studied a lot more in depth than leronlimab. But I do find it informative to do as you have done and understand the biological underpinnings of the two drugs. The "why" if you will. Thanks again for sharing!