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learningcurve2020

05/12/22 9:48 AM

#32089 RE: GoIrish1776 #32088

.29 is a number we keep seeing. Hmm

hanscott

06/03/22 2:34 PM

#32118 RE: GoIrish1776 #32088

Gorlish, you're absolutely correct that a lot can go on in the body to alter the effectiveness of any therapy.

A perfect example is check point inhibition - where regulatory T cells and macrophages inhibit the immune cells from attacking the cancer. That's why I'd love to see collaborative clinical studies with our therapy and check point inhibitors other companies are having some success with. But such collaborations might depend on MRKR having good results in PII studies before other companies will team up with us (just speculation).

The dose dependent response data in slide 29 does give them hope. But really it's the overall improvements in the new T cell production process are the key to the optimism:

1) the 9 day production improvements, bc this shorter window enables MRKR to find and treat relapsing patients MUCH earlier using the up to 1 million-fold more sensitive method of MRD+/- criteria compared to using Frank Relapse (%5 circulating blast/stem cells, changes in other white blood cell counts - at this point the cancer is getting well established again, and likely has produced more immune-escaping clones by the time you see these gross signs of relapse under a microscope). This is critically important because they can catch and treat the relapse before it becomes insurmountable, so are much more likely to produce MRD negative CR.

2). IIRC the new T cell production process produces ~6000 vs 4000 antitumor T cell clones per batch over the old Baylor method. So that's a 50% increase in diversity of unique T cells to attack the cancer over the old protocol.

3) Higher specificity for tumor cell antigens in the new process over the old Baylor approach.

4) using the 100-200Mil T cell dose vs 50Mil max T cell dose of the old Baylor protocol.


This is off the top of my head, I might be forgetting something.