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I am a little confused about this... My understanding was that if your primary tumor expressed CCR5 then leronlimab would be appropriate to use. And whether or not your tumor expressed CCR5 was based on organ and/or indication--which (from memory) included colon, TNBC, glio, and prostate cancers. Aceparker's experience of being rejected for the basket trial confirms this, at least from what was known back then.

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Around 2020 or so I postulated that leronlimab may have benefit even if there was not a heavy increase in CCR5 on tumor cells as long as there was an increase in CCR5 elsewhere. You would still see a decrease in Tregs, an increase in killer T-cells, an effect on PD-1/PD-L1 and other tumor protectants and a decrease in angiogenesis. Greater effects when CCR5 highly expressed on the tumor or in the tumor microenvironment and lesser elsewhere.

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I have a question right off the bat--anyone know if leronlimab would work on common cancer mutations like KRAS or EFRG?

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The negative effects of those mutations cause and increase in both. Leronlimab lowers EFGR and RAS which KRAS induces.