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Aldol condensation of n-butanal leads to 2-ethylhexenal, which is further hydrogenated with formation of 2-ethylhexanol, one of the most important industrial plasticizer, solvent and perspective diesel additive.1 Aqueous alkali is typically used as catalyst for aldol condensation of butanal in industry. This leads to large quantities of by-products, corrosion of the equipment and the necessity of additional purification of 2-ethylhexenal. Although basic catalysts are the most frequently used catalysts for aldol condensation. It has been demonstrated this process can be also performed on Lewis acids.2 Recently, Zr-containing zeolites was shown to be efficient catalysts of aldol condensation.3 These material possess unique Lewis acidic properties associated with partially hydrolyzed «open» Zr(OH)(OSi)3 and fully condensed «closed» Zr(OSi)4 Lewis acid sites isolated in siliceous framework.3 The purpose of this study was to elucidate the mechanism of the aldol condensation of butanal over ZrBEA catalysts. The reaction was studied both in integral and differential regimes. In situ FTIR spectroscopy was applied in order to establish the main forms of surface species under operating conditions. Pyridine, 2,6-ditertbutyl-pyridine and CO2 were used as probe molecules for in situ specific poisoning experiments for investigation of reactivity of «open» and «closed» sites of ZrBEA. The analysis of reaction network pointed that the main reaction pathway involves aldol condensation with formation of 2-ethylhexenal, the side reactions involved Cannizzaro disproportionation of butanal leading to butyl butyrate and 4-heptanone, butanol and butyric acid formation via ether hydrolysis. Kinetic data suggested that butanal condensation obeys monomolecular Langmuir-Hinshelwood mechanism with butanal enolization as rate-limiting step. The in situ studies showed that enolic form of butanal is the most abundant on the catalyst surface. The experiments on active sites poisoning showed that pyridine deactivates all Lewis acid sites unselectively, while 2,6-ditertbutyl-pyridine selectively poisons «open» sites. Impact of «open» sites on overall activity was found to be approx. 70% form total reaction rate. Besides that, open sites were shown to interact with CO2 used as acidic poison. In conclusion, the results reveal that a both acidic and basic poison prevents enolization. To account for this observation, the bifunctional acid-base mechanism is proposed.