So, I am not 100% sure what the maraviroc difference is that causes the side effects...I have always assumed it's the triggering of the receptor's immune repsponse? But I could be off on that. Would be awesome to get confirmation from one of the many microbiology experts on this board.

To confirm what you have stated however, maraviroc does inhibit CCL3, CCL4 and CCL5

From https://www.sciencedirect.com/topics/agricult.../maraviroc

Quote:

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Maraviroc is the first FDA-approved inhibitor of CCR5 that prevents binding of all three of the receptors' ligands (CCL3, CCL4, and CCL5)

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As for the source of the leronlimab info, it's taken from Cytodn's website

https://www.cytodyn.com/about-cytodyn

Quote:

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What Makes Leronlimab Different
Leronlimab is a unique humanized monoclonal antibody. Leronlimab prevents HIV from using the CCR5 receptor as an entry gateway for healthy cells; preclinical research has also shown that Leronlimab blocks calcium channel signaling of the CCR5 receptor when present on the cancer cell surface. Calcium channel signaling of the CCR5 receptor is a crucial component to the spread of metastatic cancer.

Due to its selectivity and target specific mechanism of action, Leronlimab allows chemokine binding (CCL3, CCL4) at therapeutic doses and does not have agonist activity of the CCR5 receptor (it does not activate the immune function of the receptor). This target specificity separates Leronlimab from other CCR5 antagonists. Other advantages of Leronlimab include improved safety profile, longer half-life, and less frequent dosing.

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Thank you for the pointer to the maraviroc study! Will be interesting to see how their covid trial plays out.