The following interview with Dan Shelly I suspect is the big clue as to the reason for PTX discontinuing our collaboration with MDA.
https://www.cgtlive.com/view/dan-shelly-phd-developing-allogeneic-adaptable-car-platform
The fact is that AML is a blood cancer that Car-T hasn't been able to crack yet. Part of that reason is AML expresses a multitude of different protein antigens, not just a few, as DS explains. Each patient's cancer is different and won't express the same antigens or the same mutating antigens either. Therefore, whilst CD-33, CLL-1 and 1 x intracellular antigen may be an ideal target combination in some instances, it won't be for all.
CD-33 and CLL-1 are the most commonly expressed antigens that present on the outside of AML cells, so are an obvious choice to target (for a start). MDA has a library of TCR-like binders. Allogeneic "off-the-shelf" cells may be the only way to attack AML across a host of different patients. It could be that we have garnered valuable pre-clinical data (which is confidential given the proprietary nature of MDA's technology)... enough to know that allo is the (only) way to go against AML. That data may be enough to see our OmniCAR trial in AML proceed once the FDA accepts that "off-the-shelf" cells are a safe source... OR the TGA here in Aust lead the way, which is a possibilty.
Its clear from the narratives going on in the media (Dan, Bec and Steve) that getting our OmniCAR trials into the clinic are being dictated by pre-emptive interpretations of what the evolving regulatory parameters are going to be in the near future. Getting an allo AML trial into the clinic via the FDA would be hard at this juncture, however, our other two trials probably suit autologous cell manufacturing and should be easy enough to get approval. I wonder if allogeneic cell manufacturing could be more readily approved in Aust? If so, lets lead the way!!!
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