The following table is a comprehensive summary of clinical and preclinical evidence evaluating the role of FTO in both approved and unapproved anti-cancer drug classes. This dataset presents an overview of the viability and potential cardiotoxicity of various drug classes in HCM, alongside their potential for synergistic cytotoxic functions when combined with FTO inhibition or knockdown. Notably, FTO inhibition can resensitize cancer cells to drug classes they had previously developed resistance to, thereby enabling more effective cell killing. The dataset underscores the universal nature of FTO inhibition in overcoming chemoresistance, highlighting the enormous clinical and commercial opportunity for Bisantrene. Commercial risk is low as Bisantrene can piggyback off other approved therapies, either synergizing to effectively kill cancer or resensitizing refractory patients to therapy. If the cardioprotective MoA that demonstrated excellent consistency in rescuing HCM from anthracyclines and proteasome inhibitor cardiotoxicity translates to universal cardioprotection across all drug classes, the unique cardiosynergy characteristics of Bisantrene will further reduce commercial competition risk.
Those who have recognised the Bis + Clo + Flu cardiosynergy are ahead of the game. Patients included in the Sheba 2 trial were refractory to Clofarabine and Fludarabine, and both drugs are cardiotoxic as single agents. Non-specific Bisantrene dosing effectively resensitized patients cancer to treatment while also preventing cardiotoxicity associated with antimetabolites.
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