Probing the Distinct Roles of Zeolite-Confined and External Rh Sites by Selective Poisoning in 1-Hexene Hydroformylation Regioselectivity

Abstract

The selective production of linear aldehydes from long-chain α-olefins using heterogeneous Rh catalysts faces a challenge, as non-selective sites in unconfined environments severely compromise regioselectivity. Herein, we report a strategy to achieve high regioselectivity and activity in 1-hexene hydroformylation by confining atomically dispersed Rh sites within the micropores of a silicalite-1 (S-1) zeolite, followed by the selective poisoning of external Rh sites. A series of Rh@S-1 catalysts with varying loadings were synthesized by an in situ hydrothermal method. Comprehensive characterization (XRD, XPS, STEM) confirmed the successful incorporation of Rh as atomically dispersed species within the MFI framework while preserving the zeolite’s textural properties. In the hydroformylation of 1-hexene, the unpoisoned catalyst exhibited high conversion (98.3%) but poor regioselectivity (n/i = 2.7). The introduction of bulky thiol poisons (DMBT and TPMT), which are size-excluded from the zeolite micropores, selectively passivated the external Rh sites. Consequently, the reaction was confined predominantly to the internal Rh sites, thereby dramatically boosting the n/i ratio to 59.9 and 9.3 for DMBT and TPMT poisoned catalysts, respectively, at a low 1-hexene concentration. The superior regioselectivity achieved with DMBT over TPMT is attributed to its more effective poisoning of pore-mouth Rh sites. However, it also introduced higher diffusion resistance, leading to lower conversion and higher apparent activation energy. Moreover, the catalysts demonstrated excellent recyclability. This work elucidates the decisive roles of confined internal versus unconfined external Rh sites in the atomically dispersed Rh@S-1 catalyst for 1-hexene hydroformylation. This finding provides a key design principle for developing efficient heterogeneous Rh catalysts for long-chain α-olefin hydroformylation.