Having looked closer at the detail in the patent application...

Having looked closer at the detail in the patent application document and claims, CellPryme-A, which we know from this information uses the mechanism of action of PTX-200, inhibits the AKT pathways and/or PH-domains. But it is done in what seems to be a unique way - not as a separate molecule drug in the same way that targeted therapies like checkpoint inhbitors are administered. The manufactured immune cells of choice are cultured in a medium of the AKT-pathway / PH-domain inhibitor. Essentially, the cells are primed to suppressing T-regs, expanding the immune cell proliferation and break down the .

According to the patent info, yes, the immune cells are enhanced with CellPryme 18 hrs prior to being administered. However, what defines CP-A as a neoadjuvant is the stage at which those cells are administered (ie. prior to the main treatment). It seems to me that CP-A can be administered at any stage of a patient's treatment.... before, during or after the main treatment. Where Car-T therapy is the main treatment, is CP-A defined as a neoadjuvant or an adjuvant?

https://www.cancercenter.com/community/blog/2019/01/whats-the-difference-adjuvant-and-neoadjuvant-therapies

Perhaps the FDA regulations are restricting CP-A use as an adjuvant treatment at this juncture in clinical trials. It would make sense to do so given that it has not yet been tested in the clinic. It looks as though a separate IND is required for CP-A and therefore, to be used alongside Car-T for example, we need a partner to get it into the clinic.

Somehow, I think @hottod knows just how simple things sound in theory but in practice (when it comes to getting biotech stuff into the clinic) they ain't so simple. Time that the FDA caught up with the speed at which science is moving and accept that combination therapy is the way forward! Mind you, my interpretation of what is going on with CP-A could be way off the mark, so by all means (lol) correct me if I have it all skewed.