Thank you for asking the question Ken, and even better was the response. Like Kant, I expect to see similar PD-L1 results across all cancers that over-express CCR5 due to the MOA. In the early Dr. Pestell days, they were targeting specific cancers due to the over-expression of CCR5. For TNBC, CCR5 was over-expressed in 95% of patients. I don’t recall what CRC was, but they are targeting it for a reason and it further supports potential AA due to limited treatment options and how ineffective ICIs are for MSS CRC.

Additionally, this brings Dr. Patterson’s statement to mind about how elegant of a molecule leronlimab is in the repolarization of macrophages and activating immune responses in so many different and deadly diseases. As ohm and now the company has shown, turning cold tumors hot due to PD-L1 increase is just another elegant benefit to this amazing molecule!

The challenge I see in getting this approved across so many different cancers quickly is getting the FDA to recognize the biomarkers such as CTC, CAML, and PD-L1 levels as surrogate endpoints instead of separate trails for each indication. I’m hopeful both Creatv MicroTech and the company are working with the FDA to get these biomarkers recognized and approved as surrogate endpoints, but not sure the extent of this process. Is Creatv MicroTech technology approved for these biomarkers or is a novel approach still in development? I’m patiently waiting for additional CRC trial sites to be added and enrollment to ramp up…and extremely optimistic where we are headed!