Ann: Compelling Preclinical Breast Cancer Results, page-106

Personally, I would not take that graph and extrapolate differences in FTO concentrations, as true differences may vary between certain cells. The take-away from my post is that FTO is overexpressed in MCF-7 breast cancer cell lines resistant to other therapies and that bisantrene, a potent FTO inhibitor, was found to selectively target these cells better than other drugs. I do not know if this is why bisantrene was more effective in these cell types, but I believe based on association of factors, that it is because bisantrene is inhibiting FTO in MCF-7 cells.

1. I do not know that FTO is the cause for cancer. My understanding the FTO upregulation and overexpression is a result of cells becoming cancerous, which perpetuates cancer cell function and metabolism. Essentially, it's what the cancer cell uses to ensure its growth and survival. From what I can intuit, while bisantrene is an effective FTO inhibitor, which influences drug resistance and sensitivity and cancer cell function and metabolism, it also has cytotoxic properties of its own. This basically means that it has two functions - cancer cell killing and FTO inhibiting (which the latter has a flow-on effect). So, yes, from my understanding, it has two approaches. Happy for discourse.

2. This depends on whether the results are positive or negative. You cannot go to trial without positive preclinical data. If results are negative, it's back to the drawing board. If results are positive, I think RAC will be bought out.

Hope this makes sense.