Computational studies explain the importance of two different substituents on the chelating bis(amido) ligand for transfer hydrogenation by bifunctional Cp*Rh(III) catalysts

A computational approach (DFT-B3PW91) is used to address previous experimental studies (Chem. Commun. 2009, 6801) that showed that transfer hydrogenation of a cyclic imine by Et3N·HCO2H in dichloromethane catalyzed by 16-electron bifunctional Cp*Rh III(XNC6H4NX') is faster when XNC 6H4NX' = TsNC6H4NH than when XNC6H4NX' = HNC6H4NH or TsNC 6H4NTs (Cp* = η5-C5Me 5, Ts = toluenesulfonyl). The computational study also considers the role of the formate complex observed experimentally at low temperature. Using a model of the experimental complex in which Cp* is replaced by Cp and Ts by benzenesulfonyl (Bs), the calculations for the systems in gas phase reveal that dehydrogenation of formic acid generates CpRhIIIH(XNC 6H4NX'H) via an outer-sphere mechanism. The 16-electron Rh complex + formic acid are shown to be at equilibrium with the formate complex, but the latter lies outside the pathway for dehydrogenation. The calculations reproduce the experimental observation that the transfer hydrogenation reaction is fastest for the nonsymmetrically substituted complex CpRh III(XNC6H4NX') (X = Bs and X' = H). The effect of the linker between the two N atoms on the pathway is also considered. The Gibbs energy barrier for dehydrogenation of formic acid is calculated to be much lower for CpRhIII(XNCHPhCHPhNX') than for CpRh III(XNC6H4NX') for all combinations of X and X'. The energy barrier for hydrogenation of the imine by the rhodium hydride complex is much higher than the barrier for hydride transfer to the corresponding iminium ion, in agreement with mechanisms proposed for related systems on the basis of experimental data. Interpretation of the results by MO and NBO analyses shows that the most reactive catalyst for dehydrogenation of formic acid contains a localized Rh-NH π-bond that is associated with the shortest Rh-N distance in the corresponding 16-electron complex. The asymmetric complex CpRhIII(BsNC6H4NH) is shown to generate a good bifunctional catalyst for transfer hydrogenation because it combines an electrophilic metal center and a nucleophilic NH group

Coordination and oxidative addition of octafluoronaphthalene at a nickel centre: isolation of an intermediate in C-F bond activation

Reaction of [Ni(COD)2] with PEt3 and octafluoronaphthalene yielded the complex [Ni(η2-1,2-C10F8)(PEt3) 2] 1, which was converted thermally into the C - F activation product trans-[NiF(2-C10F7)(PEt3)2] 2. The crystal structure of 1 shows asymmetric η2 coordination with significant distortions of the naphthalene unit compared to the "free" ligand; DFT calculations reproduce the principal features of the geometry

Energetics of halogen bonding of group 10 metal fluoride complexes.

A study is presented of the thermodynamics of the halogen-bonding interaction of C(6)F(5)I with a series of structurally similar group 10 metal fluoride complexes trans-[Ni(F)(2-C(5)NF(4))(PCy(3))(2)] (2), trans-[Pd(F)(4-C(5)NF(4))(PCy(3))(2)] (3), trans-[Pt(F){2-C(5)NF(2)H(CF(3))}(PR(3))(2)] (4a, R = Cy; 4bR = iPr) and trans-[Ni(F){2-C(5)NF(2)H(CF(3))}(PCy(3))(2)] (5a) in toluene solution. (19)F NMR titration experiments are used to determine binding constants, enthalpies and entropies of these interactions (2.4 ≤ K(300) ≤ 5.2; -25 ≤ ΔH(o) ≤ -16 kJ mol(-1); -73 ≤ ΔS(o) ≤ -49 J K(-1) mol(-1)). The data for -ΔH(o) for the halogen bonding follow a trend Ni < Pd < Pt. The fluoropyridyl ligand is shown to have a negligible influence on the thermodynamic data, but the influence of the phosphine ligand is significant. We also show that the value of the spin-spin coupling constant J(PtF) increases substantially with adduct formation. X-ray crystallographic data for Ni complexes 5a and 5c are compared to previously published data for a platinum analogue. We show by experiment and computation that the difference between Pt-X and Ni-X (X = F, C, P) bond lengths is greatest for X = F, consistent with F(2pπ)-Pt(5dπ) repulsive interactions. DFT calculations on the metal fluoride complexes show the very negative electrostatic potential around the fluoride. Calculations of the enthalpy of adduct formation show energies of -18.8 and -22.8 kJ mol(-1) for Ni and Pt complexes of types 5 and 4, respectively, in excellent agreement with experiment

Theoretical study of reaction pathways for the rhodium phosphine-catalysed borylation of C-H bonds with pinacolborane

The reaction mechanism of the rhodium - phosphine catalysed borylation of methyl-substituted arenes using pinacolborane (HBpin) has been investigated theoretically using DFT calculations at the B3PW91 level. Factors affecting selectivity for benzylic vs. aromatic C - H bond activation have been examined. It was found that [Rh(PR3)(2)(H)] is the active species which oxidatively adds the C - H bond leading to an eta(3)-benzyl complex which is the key to determining the unusual benzylic regioselectivity observed experimentally for this catalyst system. Subsequent reaction with HBpin leads to a [Rh(PR3)(2)(eta(3)-benzyl)(H)(Bpin)] complex from which B - C reductive elimination provides product and regenerates the catalyst. The electrophilic nature of the boryl ligand assists in the reductive elimination process. In contrast to Ir(L)(2)(boryl)(3)-based catalysts, for which Ir(III) - Ir(V) cycles have been proposed, the Rh(I) - Rh(III) cycle is operating with the system addressed herein

The reaction of M(CO)3(Ph2PCH2CH2PPh2)(M = Fe, Ru) with parahydrogen: probing the electronic structure of reaction intermediates and the internal rearrangement mechanism for the dihydride products.

The photochemical reaction of Ru(CO)(3)(dppe) and Fe(CO)(3)(dppe)(dppe = Ph(2)PCH(2)CH(2)PPh(2)) with parahydrogen has been studied by in situ-photochemistry resulting in NMR spectra of Ru(CO)(2)(dppe)(H)(2) that show significant enhancement of the hydride resonances while normal signals are seen in Fe(CO)(2)(dppe)(H)(2). This effect is associated with a singlet electronic state for the key intermediate Ru(CO)(2)(dppe) while Fe(CO)(2)(dppe) is a triplet. DFT calculations reveal electronic ground states consistent with this picture. The fluxionality of Ru(CO)(2)(dppe)(H)(2) and Fe(CO)(2)(dppe)(H)(2) has been examined by NMR spectroscopy and rationalised by theoretical methods which show that two pathways for ligand exchange exist. In the first, the phosphorus and carbonyl centres interchange positions while the two hydride ligands are unaffected. A second pathway involving interchange of all three ligand sets was found at slightly higher energy. The H-H distances in the transition states are consistent with metal-bonded dihydrogen ligands. However, no local minimum (intermediate) was found along the rearrangement pathways

Effects of intracellular expression of anti-huntingtin antibodies of various specificities on mutant huntingtin aggregation and toxicity

We have generated eight mAbs (MW1–8) that bind the epitopes polyglutamine (polyQ), polyproline (polyP), or the C terminus of exon 1 in huntingtin (htt) protein. In the brains of Huntington's disease (HD) mouse models, the anti-polyQ mAbs bind to various cytoplasmic compartments, whereas the anti-polyP and anti-C terminus mAbs bind nuclear inclusions containing htt. To use these mAbs as intracellular perturbation agents, we have cloned and expressed the antigen-binding domains of three of the mAbs as single-chain variable region fragment Abs (scFvs). In 293 cells cotransfected with htt exon 1 containing an expanded polyQ domain, MW1, MW2, and MW7 scFvs colocalize with htt exon 1. Moreover, these scFvs coimmunoprecipitate with htt exon 1 in cell extracts. In perturbation experiments, MW7 scFv, recognizing the polyP domains of htt, significantly inhibits aggregation as well as the cell death induced by mutant htt protein. In contrast, MW1 and MW2 scFvs, recognizing the polyQ stretch, stimulate htt aggregation and apoptosis. Therefore, these anti-htt scFvs can be used to investigate the role of the polyP and polyQ domains in HD pathogenesis, and antibody binding to the polyP domain has potential therapeutic value in HD