Understanding the Deactivation Pathways of Iridium(III) Pyridine‐Carboxiamide Catalysts for Formic Acid Dehydrogenation

The degradation pathways of highly active [Cp*Ir(κ2‐N,N‐R‐pica)Cl] catalysts (pica=picolinamidate; 1 R=H, 2 R=Me) for formic acid (FA) dehydrogenation were investigated by NMR spectroscopy and DFT calculations. Under acidic conditions (1 equiv. of HNO3), 2 undergoes partial protonation of the amide moiety, inducing rapid κ2‐N,N to κ2‐N,O ligand isomerization. Consistently, DFT modeling on the simpler complex 1 showed that the κ2‐N,N key intermediate of FA dehydrogenation (INH), bearing a N‐protonated pica, can easily transform into the κ2‐N,O analogue (INH2; ΔG≠≈11 kcal mol−1, ΔG ≈−5 kcal mol−1). Intramolecular hydrogen liberation from INH2 is predicted to be rather prohibitive (ΔG≠≈26 kcal mol−1, ΔG≈23 kcal mol−1), indicating that FA dehydrogenation should involve mostly κ2‐N,N intermediates, at least at relatively high pH. Under FA dehydrogenation conditions, 2 was progressively consumed, and the vast majority of the Ir centers (58 %) were eventually found in the form of Cp*‐complexes with a pyridine‐amine ligand. This likely derived from hydrogenation of the pyridine‐carboxiamide via a hemiaminal intermediate, which could also be detected. Clear evidence for ligand hydrogenation being the main degradation pathway also for 1 was obtained, as further confirmed by spectroscopic and catalytic tests on the independently synthesized degradation product 1 c. DFT calculations confirmed that this side reaction is kinetically and thermodynamically accessible. The in situ hydrogenation of the carboxiamide functionality of the ancillary ligand has been identified as the main deactivation pathway of IrIII‐picolinamide catalysts for formic acid dehydrogenation. This was proven by a combined experimental and computational approach, including spectroscopic and catalytic tests on the independently synthesized degradation product with κ2‐N,N‐pyridine‐amine ligand.