(603g) Alkane Dehydrogenation Catalyzed By Brønsted Acidic and Reaction-Derived Carbonaceous Active Sites in Zeolites

Alkane cracking and dehydrogenation rates on aluminosilicate zeolites measured in the presence of H₂ co-feeds and extrapolated to zero turnovers solely reflect protolytic reactions at Brønsted acid sites mediated by carbonium ion-like transition states. In contrast, dehydrogenation rates measured without co-fed H₂ or at nonzero turnovers reflect additional contributions from an extrinsic dehydrogenation function derived from reactants and products. This extrinsic function consists of unsaturated organic residues that catalyze dehydrogenation turnovers by accepting H-atoms from alkanes and recombining them as H₂. Such H-transfer events are kinetically inhibited by H₂ and alkene products, and proceed with barriers that are ~100 kJ mol^-1 lower than dehydrogenation at H⁺ sites. The number and reactivity of extrinsic carbonaceous deposits depend on local concentrations of reactants and products, which vary with alkane and H₂ pressure, bed residence time, and axial mixing. Carbonaceous deposits do not catalyze alkane cracking, whose rate constants rigorously report the state of protons; their invariance with product pressure, residence time and axial mixing confirm that protons remain unoccupied and undisturbed as organic residues change in number, composition, and reactivity. The rates of the reverse reaction (alkene hydrogenation) under H₂-rich conditions inhibit these organic residues; together with formalisms based on non-equilibrium thermodynamics, they confirm that alkane dehydrogenation occurs solely via protolytic routes only at the earliest stages of reaction in the presence of H₂. These findings provide a coherent retrospective view of the root causes of the literature discord about alkane dehydrogenation turnover rates and activation barriers on acidic zeolites. They also prescribe experimental protocols that isolate the kinetic contributions of protolytic dehydrogenation routes, thus ensuring their replication, while suggesting strategies to deposit or remove extrinsic organocatalytic functions that mediate H-transfer reactions.