Appreciate the response and information, even though I think I'll probably have to read that between 5 and 10 times to grasp it to whatever degree my puny brain is able!
Your last comments get to the train of thought that I'm working through. Studies are currently being done using Keytruda and CCR5 inhibitors (maraviroc, in particular). Preclinical data from circa 2012 suggests that this is likely to be effective, but Merck doesn't have the IP to use maraviroc (commercially) to inhibit cancer metastasis. That makes Merck an obvious candidate for partnership, etc. However, Eli Lilly just bought LOXO (and Vitrakvi), and has indicated an interest in continuing to expand its oncology program but doesn't like the CAR-T approach. It apparently wants some diversity and broad usefulness in its assets. I'm wondering if CCR5 inhibitors would pair well with Vitrakvi, or other drugs in the LOXO pipeline, which would potentially make EL another player on our little stage.
While PD-1 and PD-L1 inhibitors work on breaking the bond, their direction and place of action is different and as such PD1 inhibitors are more effective and Ketruda is really leading.
PD1 inhibitors unleash T cells by taking off checks which allow to identify cancer cells and kill them. So they are more effective but also have more side effects
PDL1 inhibitors act on cancer cells and expose them but do not unleash T cells so they are less effective at least currently
Question - where CCR5 fit into this MOA and how it is supposed to enhance the PD1 results?