Two new diboranes, 2,6-bis(BMes )mesitylene (1) and 3,3'-bis(BMes )bimesitylene (3), were synthesized. Two-electron reduction of 1 with elemental potassium afforded the C-H activation product [(18-c-6)K(THF) ] ⋅2 bearing a BC four-membered ring as colorless crystals, whereas the reduction of 3 with potassium led to the isolation of [(18-c-6)K(THF) ] ⋅3 as dark blue crystals. Both reduction products were characterized by structural and spectroscopic methods. Electron paramagnetic resonance (EPR) spectroscopy and theoretical calculations revealed that the electron spin density of 3 mainly resides on the two boron nuclei and features a triplet ground state, which was confirmed by superconducting quantum interference device (SQUID) measurements as well as theoretical calculations. 3 represents the first structurally characterized boron-centered diradical with a triplet ground state. In addition, the reactivity of [(18-c-6)K(THF) ] ⋅3 toward PhSeSePh and nBu SnH was investigated, which is consistent with its radical character.

The two new diboranes 1 and 2 connected by a pyrene moiety at the 1,6- and 1,3-positions, respectively, were synthesized, and their two-electron-reduction reactions were investigated. The doubly reduced species 1 ••2– is silent in electron paramagnetic resonance (EPR) and nuclear magnetic resonance (NMR) spectroscopic measurements, suggesting a quasi-quinoidal structure with a diradical character of 1 ••2–, which has a singlet–triplet gap of 6.6 kcal mol–1 as determined by theoretical calculations. In contrast, the reduction product 2 ••2– is EPR active and theoretical calculations indicate that 2 ••2– has an open-shell singlet ground state with a singlet–triplet energy gap of 4.9 kcal mol–1.

The giant muscle protein titin plays important roles in heart function. Mutations in titin have emerged as a major cause of familial cardiomyopathy. Missense mutations have been identified in cardiomyopathy patients; however, it is challenging to distinguish disease-causing mutations from benign ones. Given the importance of titin mechanics in heart function, it is critically important to elucidate the mechano-phenotypes of cardiomyopathy-causing mutations found in the elastic I-band part of cardiac titin. Using single-molecule atomic force microscopy (AFM) and equilibrium chemical denaturation, we investigated the mechanical and thermodynamic effects of two missense mutations, R57C-I94 and S22P-I84, found in the elastic I-band part of cardiac titin that were predicted to be likely causing cardiomyopathy by bioinformatics analysis. Our AFM results showed that mutation R57C had a significant destabilization effect on the I94 module. R57C reduced the mechanical unfolding force of I94 by ∼30–40 pN, accelerated the unfolding kinetics, and decelerated the folding. These effects collectively increased the unfolding propensity of I94, likely resulting in altered titin elasticity. In comparison, S22P led to only modest destabilization of I84, with a decrease in unfolding force by ∼10 pN. It is unlikely that such a modest destabilization would lead to a change in titin elasticity. These results will serve as the first step toward elucidating mechano-phenotypes of cardiomyopathy-causing mutations in the elastic I-band.