Racura Oncology Presents Bisantrene MYC Data at Frontiers in Cancer Science 2026 Conference

(ASX:RAC) Racura Oncology Limited announced new preclinical data on the MYC-directed mechanism of action of (E,E)-bisantrene, presented as a poster at the Frontiers in Cancer Science (FCS) 2026 Conference in Singapore from 11–13 November 2026. The data demonstrate that (E,E)-bisantrene is the major active isomer of bisantrene capable of stabilizing the G-quadruplex in the MYC gene promoter region, resulting in reduced MYC gene expression and MYC protein levels. In preclinical studies, exposure of (E,E)-bisantrene to blue (440 nm) light reduced its content in solution to approximately 60% after 15 minutes, approximately 40% after one hour, and to an unquantifiable level after four hours. In MDA-MB-231 breast cancer cells, pure (E,E)-bisantrene suppressed MYC gene expression with a half-maximal effective concentration of 277 nM, compared with 514 nM to 1,166 nM for the light-exposed isomer mixtures. Pure (E,E)-bisantrene reduced cancer cell viability with a half-maximal inhibitory concentration of 266 nM, compared with 310 nM to 825 nM for the mixtures. An isomer mixture containing 62% (E,E)-bisantrene stabilized the MYC G-quadruplex significantly less than pure (E,E)-bisantrene at the same concentration, and stabilization was restored when the amount of (E,E)-bisantrene was matched. These findings build on MYC gene expression inhibition data for (E,E)-bisantrene presented at the 2026 American Association for Cancer Research (AACR) Annual Meeting in April 2026. Racura continues to investigate this mechanism through its ongoing research collaboration with Purdue University. The poster, entitled "Light-Induced Isomerization Attenuates (E,E)-Bisantrene G-Quadruplex Binding and MYC Silencing," reports work by Racura scientists and collaborators at the University of Wollongong, Australia. Daniel Tillett, Ph.D., Chief Executive Officer of Racura Oncology, stated that these data confirm (E,E)-bisantrene as the active form stabilizing G-quadruplex structures and inhibiting MYC gene expression, supporting the development of RC220 as a proprietary formulation of (E,E)-bisantrene. RC220 is being clinically developed to target non-canonical G-quadruplex DNA and RNA structures enriched in oncogenic regulatory regions, including promoters, untranslated regions, and highly transcribed loci. (E,E)-bisantrene contains two hydrazone groups that can isomerize, and exposure to light converts it into (E,Z)- and potentially (Z,Z)-isomers. The FCS 2026 data indicate that the (E,E)-isomer is most responsible for MYC G-quadruplex stabilization, MYC suppression, and anticancer activity, supporting Racura's development of RC220 as a proprietary formulation of (E,E)-bisantrene. RC220 is designed to overcome drug solubility issues that prevent safe peripheral intravenous infusion. (E,E)-bisantrene is a clinically validated small molecule anticancer agent that primarily functions via G4-DNA and RNA binding, leading to potent transcriptional silencing of MYC and downstream pathways. G4-binding by (E,E)-bisantrene also inhibits topoisomerase II and telomerase, as well as modulates the m6A RNA pathway. Racura is advancing RC220 in multiple oncology indications, including the EMILI Phase 2b/3 trial in acute myeloid leukemia (AML), the HARNESS Phase 1 trial in combination with osimertinib in mutant EGFR non-small cell lung cancer (EGFRm NSCLC), and the CPACS Phase 1 trial in combination with doxorubicin for solid tumor patients.

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