interesting @Mason14 I had somewhat gone down this path before at exploring dose effect on cardio protection but hit a dead end.
More likely MOA1 + MOA2 = CP and one of these MOAs in combo preserves the ACS part of CPACS.
I am not convinced that CP is FTO dependent based on prior announcements. Inhibitors exists to treat cardiotoxicity gene expressions on your list, but Im not aware of any of them resulting in CPACS.
It is therefore plausible that multiple MOA of CPACS will make it near on impossible to replicate. Also unless proved mechanistically the patent office and Pharma will argue ‘Bisantrene’ is simply cardiac friendly.
Race need to know the MOA, in this case. I believe that they already know but we won’t hear about this until the patent is lodged. This is for commercial reasons and fear of being a takeover target.
Moral of the story we need more data, on how the drug works.
My pure speculation, is Aaron knew the MOA
and this went to Brian for validation. If correct then they should have a fairly good idea whether this would translate to the clinic.
For what it’s worth, I think Bisantrene impacts on metabolism of healthy and tumour cells differently in order to facilitate CPACS.
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