Ha, so many articles, but the quote was from the one you posted from Nature 2004 regarding increased mortality in MS for CCR5d32 homozygotes. So thank you!

Regarding whether leronlimab can bind to other CCRs, I didn't think it did, but haven't seen that studied in particular. I do have a question for someone like ohm that I/we have been pondering elsewhere: maraviroc and leronlimab both bind and inhibit CCR5 (at different locations on the receptor), so why does maraviroc seem to have so many more side effects? Does maraviroc have liver toxicity because it has "off-target" effects on other CCRs or other targets, but leronlimab does not (i.e. it is more specific for CCR5)?

It's interesting that M binds "deep in the receptor pocket" and LL binds at the ECL2 and N-terminal locations. One may be an allosteric modulator and the other a competitive inhibitor of the receptor.

Also, CYDY used to claim that leronlimab still allows the "normal function" of chemokine signaling so that's why it had no/few side effects. That doesn't seem to be the case, as that's the whole premise of using LL as an immunomodulator, it blocks RANTES/CCL5 binding to CCR5, right?

It's all pretty complicated, so thanks to anyone who can help me/us sort it all out.