The way I see the current state of play is that both CellPryme...

The way I see the current state of play is that both CellPryme and OmniCAR have required more pre-clinical optimisation than I think anyone anticipated. CellPryme is proving itself to be the more adaptable or implementable with each pre-clinical study. It is the simpler of the two technologies by far. The latest in-vivo tests carried out in humanised mice may be what gets CellPryme over the line now. "Phenotyping" seems to be the most commonly referenced and discussed topic in cell therapy today.

Whilst scaleability and high recovery were achieved in our OmniCAR testing with TF... the % of OmniCAR cells fell away when armed with SpyTag (or binder) when using the non-viral delivery method. So, more work looks to be done on that front. IMO, the worst case scenario is that if the non-viral method is to be implemented (for reasons of scaleability and cost) then OmniCAR may only be viable as a vehicle for sequential targetting. Arming OmniCAR with multiple binders for simultaneous targeting may only be possible using Lentiviral delivery. I don't know but that's my interpretation. With that said, OmniCAR still retains its merits for making Car-T therapy controllable - it can be switched on and off, directed towards its target/s and dosing levels can be titrated up and down.

OmmiCAR in the AML arena has already been flagged as the most suitable universal candidate for that indication.... however, only when the multitude of antigens expressed by AML have binders available and only when allogeneic cell manufacturing becomes an accepted norm. So, the likelihood of OmniCAR for AML patients in the clinic is way off. As for OmniCAR clinical trials in solid tumours, GBM or any other indicaton for that matter, I think its realistic to say it won't be happening without further optimisation or being pursued using Lentivirus method of delivery. So, either way, clinical trials are on the backburner (well, at least our "in-house" Car-T programs are) by the looks of it.

Our targeted therapies still provide scope on more than just one level. Both PTX-100 and 200 have proven safety and efficacy in the clinic. Its the mechanism of action in both as small molecule drugs that could well offer promise beyond the particular types of cancer PTX has pursued. Whilst our PTX-200 data in AML has been really impressive, recruitment has fizzled due to the number of equally effective drugs concurrently in the clinic (competing for recruitment). With that said, we have data from earlier trials in breast and ovarian cancer. The data supports PTX-200 is a viable AKT-pathway inhibitor which, when combined with chemo or possibly cell therapy, makes PTX-200 a potential candidate for a third-party combo drug or even a monotherapy. This is what Dan Shelly alluded to in a Linkedin post. It also applies to PTX-100 as a RAS-pathway inhibitor - it has applicability beyond TCL and stable disease was achieved (albeit for a far shortened period of time before disease progression occured). There is the possiblity that PTX-100 could work as effectively in other cancer types given higher doses. At 2000m/g, the drug proved safe.... and we don't know the limit as yet.

So, all in all, there is no complete dud in our repertoire but the front runners are definitely now PTX-100 and CellPryme. And, who knows, the co. may come out with something entirely unexpected. At the very least, a CellPryme customer would be nice. We need some score on the board, FGS!