Computational study of tin-catalyzed Baeyer-Villiger reaction pathways using hydrogen peroxide as oxidant

Density functional theory has been used to study several possible reaction mechanisms for tin-catalyzed Baeyer-Villiger oxidation of the model ketone acetone with hydrogen peroxide. The tin catalyst has been modeled with unconstrained single coordination sphere clusters using a B3LYP/ECP methodology. The Baeyer-Villiger reaction mechanism involves two principal steps: (1) addition of the hydrogen peroxide oxidant and the ketone substrate to form the Criegee intermediate and (2) Baeyer-Villiger rearrangement of the Criegee intermediate to yield the ester product. The Gibbs activation barriers for the addition and rearrangement steps in the noncatalyzed mechanism are 39.8 and 41.7 kcal/mol, respectively. In the absence of solvent coordination, tin activates hydrogen peroxide to produce a tin hydroperoxo (SnOOH) intermediate with a Gibbs activation barrier of 15.4 kcal/mol. Water molecules coordinating the tin active site facilitate proton transfer and lower the Gibbs activation barrier for tin hydroperoxo intermediate formation by 3-7 kcal/mol. The tin-catalyzed Baeyer-Villiger mechanism proceeds through a Criegee intermediate that contains a five-membered chelate ring with the tin center. This intermediate can be generated via two degenerate reaction pathways, one of which involves participation of the tin hydroperoxo intermediate. The Gibbs activation barriers for chelated Criegee intermediate formation are less than 14 kcal/mol. Rearrangement of the chelated Criegee intermediate is the rate-determining step for the tin-catalyzed Baeyer-Villiger mechanism. The Gibbs activation barrier for rearrangement is 24.1 kcal/mol when tin possesses no ligands and 21.4 kcal/mol when a single water ligand coordinates tin. The Lewis acidic tin center assists departure of the hydroxyl leaving group in the transition state for Baeyer-Villiger rearrangement. Increased branching of the migrating a carbon in the ketone substrate reduces the activation barrier for the rate-determining rearrangement step by promoting nucleophilic attack of the peroxo bond.