I really want to stress these points. There is as much clinical...

I really want to stress these points.

There is as much clinical validation work completed for Bisantrene as a topo2 agent as there is for FTO inhibition.

There is not a single study completed evaluating topo2 inhibition in humans that had clinically relevent responses to Bisantrene. Prior researchers just assumed that it was targeting topo2 because of prior knowledge of anthracyclines and no knowledge of FTO inhibitors (or FTO in general).

The culmination of preclinical data for Bisantrene clearly shows the world leading FTO inhibitory and extremely poor topo2 inhibitory properties of the drug.

It's like saying a car can fly (albeit for the briefest of seconds upon exiting a sharp incline at speed). You are better off using the car for driving (FTO inhibition) and leave the flying for the planes (anthracyclines).

Knowing that there has never been confirmation of the inhibitory target of Zantrene, what do you think the most likely cause of the clinical responses are?

My very educated guess is FTO.