Atsushi Mashimo, Yuta Takamura, Ryuya Ohtani, Maho Takamura-Takioku, Michiko Fujihara, Mayu Kawasaki, Shogo Nakano, Mayuri Inoue, Natsuko Kondo, Yoshinori Sakurai, Hiroki Kakuta
Boron neutron capture therapy requires sustained intracellular 10B accumulation, yet the clinical standard, L-boronophenylalanine (BPA, 1), rapidly effluxes from cells. We explored an intracellular retention strategy by converting borocaptate (BSH, 2) into a nuclear receptor ligand-based conjugate to improve intracellular retention of boron delivery agents. Retinoid X receptor (RXR) ligand scaffolds were selected as a proof-of-concept platform because RXRs are broadly expressed and predominantly nuclear. The lead conjugate CBTF-BSH (3), designed from fluorescent RXR antagonist 5, showed greater intracellular boron retention than 1, consistent with reduced washout. Despite lower total intracellular boron accumulation than 1, 3 decreased colony formation of MCF7 human breast cancer cells after neutron irradiation without detectable RXR degradation. These results support RXR ligand-based conjugate design as a proof-of-concept strategy for improving intracellular boron retention and neutron-induced cytotoxicity, although tumor-selective delivery and the precise retention mechanism require further optimization.