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A series of fluorinated antimony­(V) porphyrins, SbTPP­(OMe)2·PF6, SbTPP­(OTFE)2·PF6, SbT­(4F)­PP­(OMe)2·PF6, SbT­(35F)­PP­(OMe)2·PF6, SbT­(345F)­PP­(OMe)2·PF6, SbT­(4CF3)­PP­(OMe)2·PF6, SbT­(35CF3)­PP­(OMe)2·PF6, and SbT­(35CF3)­PP­(OTFE)2·PF6, have been synthesized with phenyl [P], 4-fluorophenyl [(4F)­P], 3,5-difluorophenyl [(35F)­P], 3,4,5-difluorophenyl [(345F)­P], 4-trifluoromethylphenyl [(4CF3)­P], and 3,5-bis­(trifluoromethyl)­phenyl [(35CF3)­P], in the meso-positions. Additionally, the SbTPP­(OTFE)2·PF6 and SbT­(35CF3)­PP­(OTFE)2·PF6 carry trifluoroethoxy units in their axial-positions. The fluorination on the porphyrin peripherals ranges from zero fluorine atoms in SbTPP­(OMe)2·PF6 to 30 fluorine atoms in SbT­(35CF3)­PP­(OTFE)2·PF6. X-ray crystallography confirmed the structures of the investigated antimony­(V) porphyrins. The absorption spectra depend on the number of fluorine atoms as it is blue-shifted with increasing fluorination. The series also exhibited rich redox chemistry with two reduction processes and one oxidation process. Remarkably, these porphyrins manifested the lowest reduction potentials reported among the main-group porphyrins, which are as low as −0.08 V vs SCE for SbT­(35CF3)­PP­(OTFE)2·PF6. On the contrary, the oxidation potentials were found to be very large, that is equal to 2.20 V vs SCE or even higher for SbT­(4CF3)­PP­(OMe)2·PF6 or SbT­(35CF3)­PP­(OMe)2·PF6 and SbT­(35CF3)­PP­(OTFE)2·PF6, respectively. These unprecedented potentials are due to a combination of two factors: (i) the +5-oxidation state of antimony in the porphyrin cavity and (ii) the presence of the strong electron-withdrawing fluorine atoms on the porphyrin peripherals. Density functional theory (DFT) calculations were used to support the experimental results. The systematic study of antimony­(V) porphyrins, especially their high potentials, make them ideal for the construction of photoelectrodes and excellent electron acceptors for photoelectrochemical cells and artificial photosynthetic systems, respectively, for solar energy conversion and storage applications.

Aberrant self-renewal of leukemia initiation cells (LICs) drives aggressive acute myeloid leukemia (AML). Here, we report that UHRF1, an epigenetic regulator that recruits DNMT1 to methylate DNA, is highly expressed in AML and predicts poor prognosis. UHRF1 is required for myeloid leukemogenesis by maintaining self-renewal of LICs. Mechanistically, UHRF1 directly interacts with Sin3A-associated protein 30 (SAP30) through two critical amino acids, G572 and F573 in its SRA domain, to repress gene expression. Depletion of UHRF1 or SAP30 derepresses an important target gene, MXD4, which encodes a MYC antagonist, and leads to suppression of leukemogenesis. Further knockdown of MXD4 can rescue the leukemogenesis by activating the MYC pathway. Lastly, we identified a UHRF1 inhibitor, UF146, and demonstrated its significant therapeutic efficacy in the myeloid leukemia PDX model. Taken together, our study reveals the mechanisms for altered epigenetic programs in AML and provides a promising targeted therapeutic strategy against AML.