While this paragraph is only a summary of what we already know,...

While this paragraph is only a summary of what we already know, it's still exciting seeing what bisantrene is capable of tackling.

Internal m6A and m7G RNA modifications in hematopoietic system and acute myeloid leukemia
https://journals.lww.com/cmj/fulltext/9900/internal_m6a_and_m7g_rna_modifications_in.1019.aspx

Effective targeted therapeutics against FTO have always been the hotspot field of cancer therapy development in the era of m6A research [Figure 4]. Despite the above-mentioned R-2HG, Meclofenamic acid (MA), a non-steroidal, anti-inflammatory drug, was reported to serve as a highly selective inhibitor of FTO and was proved to suppress glioblastoma cell growth and survival.[72,114] Another identified FTO inhibitor MO-I-500 was shown to inhibit the survival and colony formation of breast cancer cells.[115] FB23 and FB23-2, which also directly bound to FTO, dramatically suppressed proliferation of AML blast cells and promoted the differentiation or apoptosis of AML primary blast cells.[116] CS1(Bisantrene) and CS2 (Brequinara) served as more effective FTO inhibitors.[117] These inhibitors not only decreased the number of LSCs but also significantly inhibited the immune escape of leukemic cells, which was of great clinical value.[117] In addition, Entacapone is an example of drug repurposing. It has demonstrated FTO inhibitory activity in vitro and in vivo, showing clinical potential for treating obesity, diabetes, and other metabolic syndromes by inhibiting the FTO-FOXO1 pathway.[118] Meanwhile, suppression of FTO also act on the immune system in tumor. Knockdown of FTO sensitized melanoma cells to interferon gamma (IFNγ) and sensitized melanoma to anti-programed death-1 (PD-1) therapy in mice, with an increased m6A methylation level in PD-1[119][Figure 4]. This research implicated the possibility that targeting m6A regulators could be used in combination with anti-PD-1 treatment to improve anticancer immunotherapy.