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BTYNB is a targeted small-molecule inhibitor of **Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)**, an oncofetal RNA-binding protein (RBP) that functions as a molecular driver of immune evasion in certain cancers. In high-grade serous ovarian cancer (HGSC), specifically the C5 molecular subtype, IGF2BP1 accelerates the degradation of IRF1 protein, which subsequently abrogates interferon-gamma signaling and suppresses MHC-I presentation. By inhibiting IGF2BP1, BTYNB restores the interferon regulatory axis, reshapes the immune receptor landscape, and increases T cell infiltration and activation. BTYNB is being investigated for its ability to convert immunologically "cold" tumors into "hot" tumors, demonstrating significant synergy with PD-1 blockade in preclinical models of ovarian cancer.
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