A biomimetic pathway for vanadium-catalyzed aerobic oxidation of alcohols: evidence for a base-assisted dehydrogenation mechanism.

The first step in the catalytic oxidation of alcohols by molecular O(2), mediated by homogeneous vanadium(V) complexes [LV(V)(O)(OR)], is ligand exchange. The unusual mechanism of the subsequent intramolecular oxidation of benzyl alcoholate ligands in the 8-hydroxyquinolinato (HQ) complexes [(HQ)(2)V(V)(O)(OCH(2)C(6)H(4)-p-X)] involves intermolecular deprotonation. In the presence of triethylamine, complex 3 (X = H) reacts within an hour at room temperature to generate, quantitatively, [(HQ)(2)V(IV)(O)], benzaldehyde (0.5 equivalents), and benzyl alcohol (0.5 equivalents). The base plays a key role in the reaction: in its absence, less than 12% conversion was observed after 72 hours. The reaction is first order in both 3 and NEt(3), with activation parameters ΔH(≠)=(28±4) kJ mol(-1) and ΔS(≠)=(-169±4) J K(-1) mol(-1). A large kinetic isotope effect, 10.2±0.6, was observed when the benzylic hydrogen atoms were replaced by deuterium atoms. The effect of the para substituent of the benzyl alcoholate ligand on the reaction rate was investigated using a Hammett plot, which was constructed using σ(p). From the slope of the Hammett plot, ρ=+(1.34±0.18), a significant buildup of negative charge on the benzylic carbon atom in the transition state is inferred. These experimental findings, in combination with computational studies, support an unusual bimolecular pathway for the intramolecular redox reaction, in which the rate-limiting step is deprotonation at the benzylic position. This mechanism, that is, base-assisted dehydrogenation (BAD), represents a biomimetic pathway for transition-metal-mediated alcohol oxidations, differing from the previously identified hydride-transfer and radical pathways. It suggests a new way to enhance the activity and selectivity of vanadium catalysts in a wide range of redox reactions, through control of the outer coordination sphere.

Mechanism of alcohol oxidation by dipicolinate vanadium(V): unexpected role of pyridine.

Dipicolinate vanadium(V) alkoxide complexes (dipic)V(V)(O)(OR) (OR = isopropoxide (1), n-butanoxide (2), cyclobutanoxide (3), and α-tert-butylbenzylalkoxide (4)) react with pyridine to afford vanadium(IV) and 0.5 equiv of an aldehyde or ketone product. The role of pyridine in the reaction has been investigated. Both NMR and X-ray crystallography experiments indicate that pyridine coordinates to 1, which is in equilibrium with (dipic)V(V)(O)(O(i)Pr)(pyr) (1-Pyr). Kinetic studies of the alcohol oxidation suggest a pathway where the rate-limiting step is bimolecular and involves attack of pyridine on the C-H bond of the isopropoxide ligand of 1 or 1-Pyr. The oxidations of mechanistic probes cyclobutanol and α-tert-butylbenzylalcohol support a two-electron pathway proceeding through a vanadium(III) intermediate. The alcohol oxidation reaction is promoted by more basic pyridines and facilitated by electron-withdrawing substituents on the dipicolinate ligand. The involvement of base in the elementary alcohol oxidation step observed for the dipicolinate system is an unprecedented mechanism for vanadium-mediated alcohol oxidation and suggests new ways to tune reactivity and selectivity of vanadium catalysts.

Aerobic oxidation of lignin models using a base metal vanadium catalyst.

Dipicolinate vanadium(V) complexes oxidize lignin model complexes pinacol monomethyl ether (A), 2-phenoxyethanol (B), 1-phenyl-2-phenoxyethanol (C), and 1,2-diphenyl-2-methoxyethanol (D). With substrates having C-H bonds adjacent to the alcohol moiety (B-D), the C-H bond is broken in pyridine-d(5) solvent, yielding 2-phenoxyacetaldehyde from B, 2-phenoxyacetophenone from C, and benzoin methyl ether from D. In DMSO-d(6) solvent the reaction is slower, and both C-H and C-C bond cleavage products are observed for D. The vanadium(IV) products of these reactions have been identified and characterized. Catalytic oxidation of C and D has been demonstrated using air and (dipic)V(O)O(i)Pr. For both substrates, the C-C bond between the alcohol and ether groups is broken in the catalytic oxidation. 1-Phenyl-2-phenoxyethanol is oxidized to a mixture of phenol, formic acid, benzoic acid, and 2-methoxyacetophenone. The products of oxidation of 1,2-diphenyl-2-methoxyethanol depend on the solvent; in DMSO benzaldehyde and methanol are the major products, while benzoic acid and methyl benzoate are the major products obtained in pyridine solvent. Phenyl substituents on the model complex facilitate the oxidation, with relative rates of oxidation D > C > B.

Aerobic oxidation of pinacol by vanadium(V) dipicolinate complexes: evidence for reduction to vanadium(III).

The reactivity of vanadium complexes bearing the ligand dipicolinic acid (H(2)dipic) with alcohols has been explored. Dipic vanadium complexes are able to catalyze the aerobic oxidative C-C bond cleavage of pinacol. Reaction under anaerobic conditions allowed for isolation of a V(III) mu-oxo dimer, supporting the involvement of V(III) in aerobic oxidation reactions. Stoichiometric oxidation of unactivated aliphatic alcohols has also been observed, with oxidation of cyclobutanol producing cyclobutanone in 93% yield. The absence of ring-opening products in this reaction provides further support for the involvement of V(III) intermediates.

Efficient synthesis of alkyl beta-diketimines.

A general synthesis for the preparation of alkyl N,N'-beta-diketimines has been developed. The method reported here demonstrates the use of dimethyl sulfate for conversion of enaminoketones to beta-diketimines. The reaction can be performed without solvent, providing good yields.

Hydrogen evolution from organic "hydrides".

Benzimidazolines (dihydrobenzimidazoles) are shown for the first time to eliminate hydrogen (H2) by catalyzed reaction with protic compounds.

Lewis base assisted B-H bond redistribution in borazine and polyborazylene.

Lewis bases react with borazine and polyborazylene, yielding borane adducts. In the case of NH3 (l), ammonia-borane (AB) is formed and quantified using NMR spectroscopy against an internal standard. Calculations indicate that the formation of B(NH2)3 may provide the driving force of this redistribution. Given the complexity and expense of currently known spent AB regeneration pathways, it is suggested that this redistribution chemistry be used to recover AB and improve regeneration methods.