Kinetics and Thermodynamics of Small Molecule Binding to Pincer-PCP Rhodium(I) Complexes

The kinetics and thermodynamics of the binding of several small molecules, L (L = N-2, H-2, D-2, and C2H4), to the coordinatively unsaturated pincer-PCP rhodium(I) complexes Rh[(t)Bu2(P)CH(2)(C6H3)(CH2PBu2)-Bu-t] (1) and Rh[(Bu2P)-Bu-t(CH2)(2)(CH)(CH2)(2)(PBu2)-Bu-t] (2) in organic solvents (n-heptane, toluene, THF, and cyclohexane-d(12)) have been investigated by a combination of kinetic flash photolysis methods, NMR equilibrium studies, and density functional theory (DFT) calculations. Using various gas mixtures and monitoring by NMR until equilibrium was established, the relative free energies of binding of N-2, H-2, and C2H4 in cyclohexane-d(12) were found to increase in the order C2H4 < N-2 < H-2. Time-resolved infrared (TRIR) and UV-vis transient absorption spectroscopy revealed that 355 nm excitation of 1-L and 2-L results in the photoejection of ligand L. The subsequent mechanism of binding of L to 1 and 2 to regenerate 1-L and 2-L is determined by the structure of the PCP ligand framework and the nature of the solvent. In both cases, the primary transient is a long-lived, unsolvated species (tau = 50 - 800 ns, depending on L and its concentration in solution). For 2, this so-called less-reactive form (LRF) is in equilibrium with a more-reactive form (MRF), which reacts with L at diffusion-controlled rates to regenerate 2-L. These two intermediates are proposed to be different conformers of the three-coordinate (PCP)Rh fragment. For 1, a similar mechanism is proposed to occur, but the LRF to MRF step is irreversible. In addition, a parallel reaction pathway was observed that involves the direct reaction of the LRF of 1 with L, with second-order rate constants that vary by almost 3 orders of magnitude, depending on the nature of L (in n-heptane, k = 6.7 x 10(5) M-1 s(-1) for L = C2H4; 4.0 x 10(6) M-1 s(-1) for L = N-2; 5.5 x 10(8) M-1 s(-1) for L = H-2). Experiments in the more coordinating solvent, THF, revealed the binding of THF to 1 to generate 1-THF, and its subsequent reaction with L, as a competing pathway.