Marker Therapeutics Inc (MRKR)

[poods]

Here's my take on the results:
Group A - This is a select group of pancreatic cancer patients who are responding to chemo either with SD or PR when they are treated with multi-TAA. The CR is impressive as these are quite rare with chemo and we had a small number of patients treated. Further tumor shrinkage was seen in several patients while on the combined treatment which is also encouraging but Multi-TAA effect is not proven.
Group B - Most impressive here is the patient with SD for a prolonged period following progression on chemo. Probably a multi-TAA effect but not proven
Group C - A bit early to claim any clinical benefit I think

Now to what i consider the best evidence the treatment is working. Antigen/epitope spreading was observed in the responding patients. They did not tell us whether this occurred in non responding patients but perhaps this will be addressed on Monday. What this tells us is that Multi-TAA induced an immune response against the tumor that subsequently induced recognition and response to at least several other non targeted antigens. This is proof that the treatment is doing what it is designed to do - enhance the immune response against pancreatic cancer. Now it's a matter of how to further build on that response. I noted that all the patients who responded developed a response to non targeted WT-1, which is highly expressed in pancreatic cancer and is induced by chemotherapy of various types. Would the addition of WT-1 to the mix induce more responses? Also checkpoint blockade (anti-PD1/CTLA4) can enhance responses and modify the TME. Hyaluronidase might also be synergistic in this setting.

Bottom line: There are many ways we can go from here but we have proof of concept that Multi-TAA produces an immune response to pancreatic cancer in addition to hematological cancers. It carries no side effects and is relatively cheap, so it can be easily deployed in combinations. I'm looking forward to Monday's presentation and to any future plans.