On the basis of kinetic modeling, this study provides some insight into the hydrogenation kinetics of avermectins B-1a and B-1b (Av(i), i = B-1a and B-1b) with the in situ formed Wilkinson's catalyst from the dinuclear chloro-bridged Rh(I) complex [RhCl(COD)](2) (COD = 1,5-cyclo-octadiene) and triphenylphosphine (Ph3P). More significantly, this paper is the first attempt to derive describing kinetic models. The kinetic behavior was studied in a temperature range of 313-343 K, at a hydrogen pressure of 275.7 kN m(-2). A significant induction period strongly dependent on the temperature was noticed during the in situ generation of the catalytic species. After improving a previous kinetic model describing Wilkinson's hydrogenation catalytic cycle, kinetic models for the in situ synthesis of the catalytic species were developed on the basis of reaction pathways assuming that the COD ligand replacement occurs via substitution by PPh3 or via reductive elimination of COE (COE = cyclo-octene). Estimates of the kinetic parameters characterizing both reaction routes were uncoupled from those of the catalytic cycle steps. Among the rival kinetic models tested, a simple model featuring the PPh3 insertion in the bidentate COD ligand as rate determining step (RDS) and the competitive replacement of the COD ligand by both PPh3 and Avi proved fair enough to describe the synthesis process in the presence of these macrocyclic lactones. A very high activation barrier characterizes the in situ synthesis of the catalytic complexes, and the presence of avermectins in the reaction medium interferes with the course of the catalytic species synthesis due to the formation of too stable intermediate complexes. From these observations, high reaction temperature and the absence of avermectins in the synthesis medium of the species responsible for the catalysis are two necessary conditions for improving the performance of this catalytic hydrogenation system. (c) 2007 Elsevier B.V. All rights reserved.