Speculative M&A Transaction Analysis, page-737

Hey mate.

I think this all comes down to a little confusion between us. Let me explain myself.

I've addressed the publications demonstrating FTO inhibition synergises with cardiotoxic drugs to decrease HCM viability: https://hotcopper.com.au/threads/cardioprotection-thread.7722432/page-444?post_id=73547332

I've explained the difference between FTO inhibitors and Bisantrene in combination with cardiotoxic drugs using a simple model here: https://hotcopper.com.au/threads/cardioprotection-thread.7722432/page-484?post_id=73587478

I've also explained how increased m6A levels (through modulation and focus of METTL complexes) synergises with cardiotoxic drugs to decrease HCM viability here: https://hotcopper.com.au/threads/cardioprotection-thread.7722432/page-506?post_id=73595491

If I knew the cardioprotective mechanism, the statement would likely read: "Bisantrene is a FIC CPACS drug because it targets the FTO protein to effectively combat cancer while providing cardioprotection through the upregulation of CardioX." Apologies for any confusion; I certainly did not intend for readers to interpret that FTO inhibition was driving cardioprotection.

I highly recommend re-reading post #73547332, where I detail the differences between Bisantrene and FTO inhibitors. I highlight that Bisantrene's cardioprotective mechanism appears robust enough to counteract its own FTO-inhibition-associated cardiotoxic synergy when used with cardiotoxic drugs in HCM, which is truly impressive. I also discuss how the cardiotoxic synergy between FTO inhibitors and cardiotoxic drugs may be the ultimate barrier to preventing competition in the CPACS space, where FTO inhibition is the mechanism of action for anti-cancer synergy. In short, Bisantrene could dominate the FTO-inhibitor-specific CPACS market.