RE:RE:RE:RE:RE:RE:News out 👀 That last paragraph makes no rational sense to me. If you are getting PoC then you are getting it from TH1902. How can you make the call that "docetaxel is not good enough" if it's giving you what you want or need? If you're not getting what you want or need from this drug then how can you know that it's the docetaxel that's the weakest link? This is just more wishful thinking by JFM. Again he believes he can diagnose the situation with absolutely no supporting data. I mean there is a scenario where the data is 'meh' but pinning the cause of that to docetaxel would be a leap of faith and I don't think serious investors do that. If the company announced a halt to TH1902 and a 'strategic shift' to another construct that would be such a negative signal, I expect Soleus would be straight out of the door.
Either TH1902 succeeds and keeps moving forward or they face something far greater than merely "delays" for the SORT1 platform. We already recognize they have so little outside support for the potential of this program, their ability to generate more would vanish.
Anyway none of this is on the agenda atm so no real need to spend time on this nonsense.
jfm1330 wrote: The big takeaway from this poster is the fact that cancer stages don't matter much for many cancers tested. Also, it does not solve anything related to the proof of concept. We are still swimming in hypothetic stuff. As long as we don't have the proof of concept, all that and the preclinical work and any ideas about new PDC could be worthless. It would also have been interesting to know what was the scores all of their different types of grafted tumors on nude mice that they used for preclinical work. This would have given a better understanding of how it could translate to humans. Also, remember that this is in vitro testing where the tissue is chemically treated before and after staining, how would these results correlate with in vivo testing of receptor expression like it is the case with Dotatate Ga68 for example. Also, how would it compare with gene expression testing for sortilin.
Add to that the fact that membrane sortilin can be cleaved to generate soluble sortilin. Another thing is turnaround of outside cell membrane sortilin. We know there is intracellular sortilin related to membrane organelles lile Golgi apparatus and endoplasmic reticulum and there is a recuperation cycle associated with that. So in vitro staining is a snapshot of sortilin presence on the outside cell membrane, while the in vivo process is dynamic with sortilin coming in and going out of the outside membrane. All that to say that this is a very little piece of the puzzle, and not a crtitical one in my view. We desperately want to see data strongly hinting at a proof of concept. I know I insist a lot of that, but it is obviously critical for the whole thing.
Now we have TH1902, a PDC that is a candidate drug, proof of concept gives you a platform. With proof of concept it would no longer be only about TH1902. In other words, if docetaxel is not good enough as a cytotoxic agent, you can go with another one. Yes there would be big delays in that case, but still, you have a valid approach. If the concept is invalid, it's the end of everthing. That's why it would be so important to have that. Until we have this critical milestone, we are in the world of hypotheses. Without proof of concept, total failure of the SORT1+ plarform is a possibility. With proof of concept the question becomes how good can it be? Is TH1902 the best possible PDC out of that platform, etc... I know it's early. I know they cannot answer all the question at once, but at the same time they are so slow in the clinical trial and so secretive