Alexander V. Safronov

Direct observation of bis(dicarbollyl)nickel conformers in solution by fluorescence spectroscopy: an approach to redox-controlled metallacarborane molecular motors.

As a continuation of work on metallacarborane-based molecular motors, the structures of substituted bis(dicarbollyl)nickel complexes in Ni(III) and Ni(IV) oxidation states were investigated in solution by fluorescence spectroscopy. Symmetrically positioned cage-linked pyrene molecules served as fluorescent probes to enable the observation of mixed meso-trans/dl-gauche (pyrene monomer fluorescence) and dl-cis/dl-gauche (intramolecular pyrene excimer fluorescence with residual monomer fluorescence) cage conformations of the nickelacarboranes in the Ni(III) and Ni(IV) oxidation states, respectively. The absence of energetically disfavored conformers in solution--dl-cis in the case of nickel(III) complexes and meso-trans in the case of nickel(IV)--was demonstrated based on spectroscopic data and conformer energy calculations in solution. The conformational persistence observed in solution indicates that bis(dicarbollyl)nickel complexes may provide attractive templates for building electrically driven and/or photodriven molecular motors.

Novel Synthetic Approach to Charge-Compensated Phosphonio- nido-Carboranes. Synthesis and Structural Characterization of Neutral Mono and Bis(Phosphonio) nido-ortho-Carboranes

A number of monosubstituted n-(triphenylphosphonio)-7,8-dicarba-nido-undecaboranes (2a, n = 1; 2b, n = 3; 2c, n = 5; 2d, n = 9) were prepared via a cross-coupling reaction between the tetrabutylammonium iodo-7,8-dicarba-nido-undecaborates (1a-d) and PPh3 in the presence of a Pd(PPh3)4 catalyst. The substitution rate was found to depend on the iodine position in the carborane cage. Under similar conditions, the reaction of 5,6-diiodo- (3) and 9,11-diiodo-7,8-dicarba-nido-undecaborate (5) anions exclusively yielded the monosubstitution products 5-iodo-6-(triphenylphosphonio)-7,8-dicarba-nido-undecaborane (4) and 9-iodo-11-(triphenylphosphonio)-7,8-dicarba-nido-undecaborane (6), respectively. The reaction of tetrabutylammonium 6,9-diiodo-7,8-dicarba-nido-undecaborate (7) exclusively produced the phosphine substitution product in the open face of the nido-carborane, 6-iodo-9-triphenylphosphonio-7,8-dicarba-nido-undecaborane (8). The addition of a base (Cs2CO3, NaH) to the reactions of 3 and 5 with PPh3 afforded the corresponding bis(triphenylphosphonio)-7,8-dicarba-nido-undecaboranes, 9 and 10. Compound 10 was also prepared from 6 using the general procedure. The reaction of the triiodocarborane tetrabutylammonium 5,6,9-triiodo-7,8-dicarba-nido-undecaborate (11) with excess PPh3 in the presence of Cs2CO3 and Pd(PPh3)4 only produced neutral 5-iodo-6,9-bis(triphenylphosphonio)-7,8-dicarba-nido-undecaborane (12); no positively charged tris(phosphonio) species formed. The compositions of all prepared compounds were determined by multinuclear NMR spectroscopy and high-resolution mass spectrometry. The structures of compounds 2c, 6, 8, 9, and 12 were established by the X-ray diffraction analysis of single crystals.

Novel Convenient Synthesis of 10B-Enriched Sodium Borohydride

A convenient and efficient synthesis of (10)B-enriched sodium borohydride [Na(10)BH4] from commercially available (10)B-enriched boric acid [(10)B(OH)3] is described. The reaction sequence (10)B(OH)3 → (10)B(On-Bu)3 → (10)BH3·Et3N → Na(10)BH4 afforded the product in 60-80% yield. The reaction was successfully scaled to hundreds of gram per run.

Boron Neutron Capture Therapy of Cancer as a Part of Modern Nanomedicine

10 B-enriched boron-containing compounds into tumor cells with subsequent irradiation of the tumor tissue by thermal or epithermal neutrons causes tumor damage and death. The mechanism of the tumor cell damage during BNCT is based on the capture-fission reaction between the boron-10 nucleus and a neutron resulting in an α-particle release inside the cell. A successful BNCT therapeutic agent must obey several requirements, most importantly it should (1) selectively accumulate in tumor cells, (2) show certain levels of tumor-to-blood concentration ratios (3 and higher), and (3) provide the therapeutic concentration of 10 B in tumor cells (at least 20 µg of 10 B/g of tumor).