Intramolecular CâH Activation Reactions of Ru(NHC) Complexes

Article pubs.acs.org/Organometallics

Intramolecular C−H Activation Reactions of Ru(NHC) Complexes Combined with H2 Transfer to Alkenes: A Theoretical Elucidation of Mechanisms and Effects of Ligands on Reactivities Katharina Marie Wenz,† Peng Liu,*,†,‡ and K. N. Houk*,† †

Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095-1569, United States Department of Chemistry, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, United States

‡

S Supporting Information *

ABSTRACT: Recent experimental studies have identified Ru(II) NHC complexes that are highly reactive in the tandem intramolecular C(sp3)−H activation of an N-alkyl substituent to form a metallacycle and transfer hydrogenation of alkenes. These complexes are promising candidates for tandem catalytic processes that depend on a reversible uptake of hydrogen (“borrowing hydrogen catalysis”). We have elucidated the reaction mechanisms by density functional theory calculations and investigated ligand effects on reactivity. The reaction of ruthenium dihydride complex [Ru(H)2(NHC)(CO)(PPh3)2] (1) with ethylene occurs via dissociative ligand exchange to replace one of the phosphine ligands with ethylene, followed by hydride migration and reductive elimination to form a Ru(0) intermediate. Subsequent C−H activation occurs via an oxidative addition mechanism. Bulkier NHC and phosphine ligands facilitate the dissociation of phosphine, which leads to a lower overall barrier. In addition, the N-iPr substituted NHC ligand promotes the C−H oxidative addition/ruthenacyclization due to the release of steric strain caused by the N-iPr group and the substituents on the NHC backbone. The reaction with the monohydride monochloride complex [RuHCl(NHC)(PPh3)2] (2) occurs via ligand exchange and hydride migration to form an alkyl ruthenium(II) complex. The type of phosphine ligand determines whether the subsequent intramolecular C−H activation proceeds via an associative or a dissociative mechanism. In the associative pathway, C−H activation occurs via a concerted σ-bond metathesis mechanism, which directly transfers the hydrogen atom from the C−H bond of the N-alkyl group on the NHC to the alkyl ligand on ruthenium. In the dissociative pathway, C−H activation occurs via stepwise C−H oxidative addition to form a Ru(IV) intermediate followed by reductive elimination of the alkane product.

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INTRODUCTION The low reactivity of C−H bonds makes selective C−H bond activation one of the major challenges in organic chemistry.1 Recent advances in C−H activations with Ir,2 Pd,1b,3 and Rh4 catalysts have led to many efficient C−H functionalization strategies. C−H activation reactions with ruthenium complexes are relatively less developed,5 although ruthenium catalysts have exhibited great reactivity and stability in many important catalytic processes such as olefin metathesis,6 hydrogenation,7 and transfer hydrogenation8 reactions. Interestingly, although only a few examples of Ru-mediated C(sp3)−H activation reactions have been reported;9,5g these processes may take place via several distinct mechanistic pathways (Figure 1)10 including a two-step mechanism involving C−H oxidative addition followed by reductive elimination,11 σ-bond metathesis of an agostic complex (σ-complex assisted metathesis, or σCAM),12 a base-induced electrophilic C−H activation, or a carboxylate-assisted concerted metalation−deprotonation (CMD) mechanism.5a,b,13 © XXXX American Chemical Society

An interesting type of reactivity of Ru(NHC) complexes involves intramolecular C(sp3)−H activation reactions of the N-aryl or N-alkyl groups on the N-heterocyclic carbene (NHC) ligands to generate a five- or six-membered metallacycle complex. This process is one of the key decomposition pathways of ruthenium olefin metathesis catalysts.14 The Grubbs group recently revealed that the products of similar C−H activation reactions of Ru(NHC) complexes are highly Zselective olefin metathesis catalysts.15 Mechanistic studies from the Grubbs and Houk groups indicated a carboxylate-assisted CMD mechanism for this C−H activation.16 Intriguing studies on intramolecular C−H activations of Ru(NHC) hydride complexes were reported by Whittlesey, Williams, and co-workers.17 Alkenes react with dihydride complexes such as [Ru(H)2(NHC)(CO)(PPh3)2] (1), to form alkane and a metallacyclic product (1′) with a new Ru− Received: July 14, 2017

A

DOI: 10.1021/acs.organomet.7b00531 Organometallics XXXX, XXX, XXX−XXX

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Organometallics

regenerated. The C−H activation reactivity is affected by the N-alkyl groups on the NHC ligands. The N,N′-diisopropyl NHC (IiPr2Me2) in complex 1 is more reactive than the N,N′diethyl ligand (IEt2Me2).17b Similar alkene hydrogenation reactions were later reported with ruthenium monohydride monochloride complex 2 (Figure 2b).18,19 The reversible C−H bond cleavage accompanying alkene hydrogenation offers great potential to incorporate such processes into more sophisticated tandem reactions. A wellknown example employing this strategy is the three-step cycle for alkane metathesis, which involves reversible alkane dehydrogenation by iridium catalysts, followed by Mo-catalyzed olefin metathesis and hydrogenation of olefin to yield new alkane molecules (Figure 3b).20 Similarly, the dehydrogenation/hydrogenation cycle with Ru(NHC) complexes has been incorporated into many catalytic processes, which are now called “borrowing hydrogen catalysis”.21 One such example employing the interconversion between 1 and 1′ is a tandem dehydrogenation/Wittig/hydrogenation reaction that allows for the formation of C−C bonds from alcohols (Figure 3a).17b Here, ruthenium complex 1 reacts with cyanoalkenes to form cyanoalkanes and metallacycle complex 1′, followed by transfer hydrogenation from an alcohol to regenerate complex 1 and form an aldehyde. The Macgregor and Whittlesey groups performed computational studies on the intramolecular C−H activations of an Ru(NHC) complexes and explored the base-induced C−H activation pathway.22 A mechanistic study on ligand exchange processes and C−C and C−H oxidative addition with N-aryl substituted NHC ligands was also conducted,23 as well as a comparative analysis of C−X (X = CH3, H, OH, OCH3, NH2, CF3, and F) oxidative addition with these ligands,24 though the latter study used an extremely simplified model system. The mechanism of alkene-promoted C−H activation reactions shown in Figure 2 has not been investigated computationally. In this study we report the mechanisms of the tandem alkene hydrogenation/intramolecular C−H activation reactions of 1 and 2 using the full experimental system. Through our mechanistic investigations we show that dihydride Ru(II) complex 1 and hydride chloride Ru(II) complex 2 react in a different manner. Complex 1 reacts through a dissociative process, with stepwise hydride migration, reductive elimination, and oxidative addition via a Ru(0) intermediate, as proposed in the original experimental paper by the Whittlesey group.17b To

Figure 1. Mechanisms of Ru-mediated C−H activation generally start with the formation of an agostic precomplex. Concerted metalation− deprotonation (CMD) pathways assisted by a carboxylate ligand and an external base are shown in pink and blue, respectively. Stepwise oxidative addition and reductive elimination proceed via the green pathway. σ-Bond metathesis, or σ-complex assisted metathesis (σCAM), proceeds via a trapezoidal transition state (red pathway).

C bond (Figure 2a). Upon hydrogenation or transfer hydrogenation with alcohol, the dihydride complex 1 is

Figure 2. (a) Coupled alkene hydrogenation and intramolecular C−H activation of complex 1 (R = SiMe3). (b) Coupled alkene hydrogenation and intramolecular C−H activation of complex 2 (R = H).17,18

Figure 3. Examples of tandem reactions based on reversible hydrogenation/dehydrogenation cycles. (a) Ru(NHC)-catalyzed tandem alcohol dehydrogenation, Wittig reaction, and alkene hydrogenation; (b) alkane metathesis with an Ir/Mo dual catalysts system. B


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Organometallics the best of our knowledge, C(sp3)−H activation by a Ru(0) complex has only been reported using low-valent [Ru3(CO)12] complexes by Kakiuchi5g and others.25 In contrast, the C−H activation reaction of 2 can either proceed through a reactive Ru(IV) intermediate or a concerted σ-bond metathesis process, depending on whether a dissociative or associative mechanism takes place. Such diversity in mechanistic behavior has previously only been reported in computational studies by Eisenstein et al. on the C−H activation of methane by [Tp(PH3)Ru(CH3)(η2-H-R)] (R = H and CH3; Tp = hydridotris(3,5-dimethylpyrazolyl)borate).26,13f The origins of NHC and phosphine ligand effects on the activity of the Ru catalyst in C−H activation reactions are not fully understood, although electronic effects on the strength of the agostic precomplex have been investigated by Sabo-Etienne et al. using natural bond orbital (NBO) analysis,27 and the influence of anionic ligands on methane C−H activation via σ-bond metathesis with [TpRu(CO)X] (X = CH3, OH, OMe, NH2, and NMe2) complexes has been studied by Gunnoe et al.12c Our computational studies provide a detailed understanding of the electronic and steric effects that determine the mechanisms and reactivity of (NHC) Ru(0) and Ru(II) complexes in coupled intramolecular C(sp3)−H activation and alkene hydrogenation reactions. This opens the pathway for the rational design of tandem ruthenium based catalysts employing C(sp3)−H activation reactions.

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Figure 4. Structure of model complexes 1(IiPr2Me2/PMe3) and 2(IEt2H2/PMe3), and experimental complexes 1(IiPr2Me2/PPh3), 1(IEt2Me2/PPh3) and 2(IiPr2Me2/PPh3).

phosphine ligands dissociates. The mechanism also depends on the association of the alkene substrate and the elimination of the reduced reaction product. As a result, the use of smaller model complexes only provided a rough guide to the most feasible reaction pathways and coordination geometries. Subsequently, the reaction mechanisms of the experimentally used ruthenium complexes 1(IiPr2Me2/PPh3) and 1(IEt2Me2/ PPh3) with ethylene and TMS-CHCH2, as well as that of 2(I iPr2Me2/PPh3) with ethylene, were studied in the computations. The influence of the N-alkyl substituents on the NHC ligand and the effect of a bulkier and more electronrich alkene on the reaction profile will be discussed later in this paper. Figure 5 shows the computed energy profile for the reaction of 1(IiPr2Me2/PPh3) and ethylene to form 1(IiPr2Me2/PPh3)′ and ethane. The DFT calculations indicate that the reaction of 1(IiPr2Me2/PPh3) and ethylene to form 1(IiPr2Me2/PPh3)′ and ethane proceeds through a mechanism with four basic steps shown in Figure 5: (1) dissociative ligand exchange of a phosphine ligand by ethylene, (2) ethylene migratory insertion (hydride migration), (3) reductive elimination of ethane, and (4) oxidative addition of a primary C−H bond of the Nisopropyl group on the NHC ligand to give ruthenacycle product 1(IiPr2Me2/PPh3)′. Recoordination of the second phosphine ligand may occur either before or after the reductive elimination/oxidative addition steps. Octahedral complex 1 (ΔG = 0.0 kcal/mol) is coordinatively saturated, and ligand exchange to replace one of the PPh3 ligands with ethylene is expected to occur through a dissociative pathway via 3 to form 4, which is 6.7 kcal/mol less stable than 1. The most favorable geometry for complex 1 features a trans phosphine arrangement with the two hydride ligands cis to each other. Intermediate 3 is stabilized by an agostic interaction with one of the N-isopropyl groups. The coordination geometry of complex 1 was confirmed by 31P NMR studies in the Whittlesey group.17b By monitoring the exchange reaction of PPh3 for P(pTol)3 they showed that phosphine dissociation occurs rapidly at room temperature which agrees with the very low computed phosphine dissociation energy of 1. One of the hydride ligands in 4 migrates to ethylene to give five-coordinated 16-electron intermediate 6. C−H reductive elimination from intermediate 6 to form agostic Ru(0) intermediate 8 and ethane (7-TS, ΔG⧧=13.7 kcalmol−1) requires a barrier similar to that for hydride migration. Phosphine ligand association occurs after the reductive elimination step to form more stable four-coordinate Ru(0) complex 13. This also stabilizes the subsequent oxidative

COMPUTATIONAL METHODS

All calculations were performed using Gaussian09.28 Geometry optimizations, vibrational frequency, and intrinsic reaction coordinate (IRC) calculations were carried out with B3LYP and a mixed basis set of SDD for Ru and 6-31G(d) for other atoms. A comparison of select geometrical parameters of the optimized geometry of the full experimental system 1(IiPr2Me2/PPh3) with the crystal structure values is given in Table S1. Deviations in computed bond lengths and angles from those in the crystal structure are generally small, around 0.02 Å and 2°, respectively. Deviations in the Ru−P distances are greater, about 0.08 Å. To obtain more reliable values for electronic energies, single-point energy calculations using M06/6-311+G(d,p)− SDD(Ru) and SMD solvation corrections for benzene were performed. On the basis of previous benchmark studies on related ruthenium complexes,29 this level of theory is expected to provide reasonable energetics in the present study, including the dissociation energies of the phosphine ligand and the alkene binding energies of the Ru(NHC) complexes.

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RESULTS AND DISCUSSION Mechanism of the C−H Activation/Transfer Hydrogenation Reaction with Complex 1. We performed DFT calculations to study the possible mechanisms of the reactions of 1 and 2 with ethylene to form ruthenacycles 1′ and 2′, respectively, plus ethane (Figure 2). Octahedral complexes 1 and 1′ are 18-electron species, while five-coordinated 2 and 2′ are 16-electron species. Calculations were initially performed on model system 1(IiPr2Me2/PMe3), with PMe3 instead of PPh3 ligands and ethylene as a substrate to determine the most likely mechanistic pathways (Figure 4). It became apparent that the choice of phosphine ligand influences significantly the barrier heights of all major steps of the reaction. (For full reaction energy profile with the smaller model system 1(IiPr2Me2/PMe3), see Supporting Information.) The mechanism of the reaction is heavily dependent on the ability of the complex to associate and dissociate the phosphine ligands, since the hydride migration step can only take place after one of the C


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Organometallics

Figure 5. M06/6-311+G(d,p)-SDD Gibbs free energy profile for the ethylene hydrogenation and ruthenacyclization of 1(IiPr2Me2/PPh3). The reductive elimination occurs via the dissociative mechanism (7-TS) with one triphenylphosphine ligand bound to the ruthenium. Association of a second phosphine ligand after the reductive elimination renders the oxidative addition step via 14-TS more favorable (blue pathway). Enthalpy values are shown in parentheses.

Figure 6. Optimized structures of (a) hydride migration TS (5-TS), (b) reductive elimination TS (7-TS), and (c) oxidative addition TS (14-TS) with 1(IiPr2Me2/PPh3). Bond lengths are given in Å.

addition transition state in the associative pathway (shown in blue in Figure 5) relative to the dissociative pathway (shown in

red) in which ligand association occurs after oxidative addition. The oxidative addition to the C−H bond of the N-isopropyl D


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Organometallics

Figure 7. M06/6-311+G(d,p)-SDD Gibbs free energy profile for the hydrogenation of TMS-CHCH2 and ruthenacyclization of 1(IiPr2Me2/ PPh3). Only the more favorable dissociative pathway is shown for hydride migration and reductive elimination steps. Association of a second phosphine ligand takes place after the reductive elimination (blue pathway). Enthalpy values are shown in parentheses.

Figure 8. Optimized structures of (a) hydride migration TS (19-TS); (b) reductive elimination TS (21-TS) with 1(IiPr2Me2/PPh3) and TMSCHCH2. Bond lengths are given in Å.

We computed other possible pathways using a model system with a smaller NHC ligand 1(IEt2H2/PMe3), including σ-bond metathesis of the N-Et C−H bond in 3 to give the metallacycle and η2-bound H2. Our calculations indicate that this path requires a much higher activation barrier of 45.3 kcalmol−1. The details are given in the Supporting Information. Effects of Substrate on Reactivity. We explored the effect of the TMS-substituted alkene used in experimental studies by the Whittlesey group on the reaction mechanism compared to the effect of ethylene. The energy profile for the reaction of 1(IiPr2Me2/PPh3) with TMS-CHCH2 is shown

group is rate-determining and requires a barrier of 14.6 kcal/ mol (13 → 14-TS) to form ruthenacycle product 1(IiPr2Me2/ PPh3)′. The product complex with a cis phosphine arrangement is about 6.5 kcal mol−1 more stable than isomeric complex 17 with a trans phosphine arrangement (purple pathway in Figure 5). This is in agreement with the crystal structure of 1(IiPr2Me2/PPh3)′ published by the Whittlesey group which has a cis arrangement of the PPh3 ligands. The optimized structures of the transition states in the preferred reaction pathway are shown in Figure 6. The transition states for the less favorable pathways are shown in the Supporting Information. E


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Organometallics

Figure 9. M06/6-311+G(d,p)-SDD Gibbs free energy profile for the hydrogenation of TMS-CHCH2 and ruthenacyclization of 1(IEt2Me2/ PPh3). Only the more favorable, dissociative pathway is shown for hydride migration and reductive elimination steps. Association of a second phosphine ligand takes place after the reductive elimination (blue pathway). The product then isomerizes to give the complex with trans phosphine arrangement (purple structure). Enthalpy values are shown in parentheses.

reduction of TMS-CHCH2 at 50 °C using 1(IEt2Me2/ PPh3), and 8% conversion was reported using 1(IiPr2H2/ PPh3), as opposed to 45% conversion reported with 1(IiPr2Me2/PPh3)′ under the same conditions.17b Similarly, the bulky iPr group on the NHC ligand also promotes the reaction of monohydride monochloride complex 2 with ethylene (Figure 2b).18 To elucidate the origins of the effects of NHC ligand on reactivity, we computed the energy profile of the reaction of 1(IEt2Me2/PPh3) with TMS-CHCH2. Both the dissociative and associative pathways were computed (Figure 9). The optimized structures of the most favorable transition states in this reaction are shown in the Supporting Information. The use of a less sterically hindered ligand (IEt2Me2) leads to a higher overall barrier of the reaction. The decrease of reactivity is mostly due to the stabilization of the bisphosphine reactant relative to the following TSs and reaction intermediates. This is apparent in the increased phosphine dissociation energy (12.1 kcal mol−1 for 1(IEt2Me2/PPh3) compared to 7.9 kcal mol−1 for 1(IiPr2Me2/PPh3)). The barriers for reductive elimination and oxidative addition steps are also much increased with 1(IEt2Me2/PPh3), as compared to those of the IiPr2Me2-NHC ligated complex. The reductive elimination step (26-TS) proceeds with an activation barrier of 20.4 kcal mol−1, 5 kcal mol−1 higher than that with the IiPr2Me2 ligand. This makes reductive elimination the ratedetermining step for the reaction with 1(IEt2Me2/PPh3). With the IiPr2Me2 ligand, the iPr groups are forced into a rigid conformation by the methyl groups on the NHC backbone. This facilitates the reductive elimination and dissociation of the reduced alkene to form an Ru(0) complex. With the smaller IEt2Me2 ligand, the Ru(II) center in intermediate 25 is less

in Figure 7, and the transition state structures of the hydride migration and reductive elimination TS are shown in Figure 8. The dissociative ligand exchange to replace a phosphine ligand by a TMS-CHCH2 is endergonic by 12.0 kcal mol−1, which is 5.3 kcal mol−1 less favorable compared to the corresponding ligand exchange with ethylene. The alkene coordination in 18 is destabilized by the steric hindrance between the TMS-group and the phosphine coordinated trans to the NHC ligand. Hydride migration is the rate-determining step, with an activation barrier of 17.2 kcal mol−1 (19-TS).30 The barrier for the hydride migration step is significantly influenced by the alkene substrate. The TMS-substituted alkene is more electron-rich than ethylene, and we expected the activation barriers for hydride addition to the CC double bond to be lower. Instead, we find that because the high steric demand of the TMS group and the bulky phosphine ligands on the complex make coordination of the alkene more difficult that the overall activation barrier for hydride migration is increased; the reactivity is lower than that in the reaction with ethylene. The reductive elimination step is less sensitive to the alkene substituent that is β to the metal and the barrier for reductive elimination is less affected (7-TS versus 21-TS). Effects of NHC and Phosphine Ligands on Reactivity. Experiments from the Whittlesey group indicated that bulky Nalkyl groups and methyl substituents on the backbone of the NHC ligand increase the reactivity toward the C−H activation of Ru(NHC) hydride complexes. IiPr2Me2-ligated complex 1(IiPr2Me2/PPh3)′ discussed before is the most active catalyst for the aforementioned tandem Wittig/transfer hydrogenation reaction.17b IEt2Me2-ligated complex 1(IEt2Me2/PPh3) and IiPr2H2-ligated complex 1(IiPr2H2/PPh3) showed a reduced activity toward the tandem hydrogenation/C−H activation reaction: Only 15% conversion was reported in the catalytic F


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Organometallics

Table 1. Release of Unfavorable Steric Interactions between N,N′-iPr (R1/R4) and the NHC Backbone Methyl Groups (R2/R3) in the Oxidative Addition Stepa

intermediate (A) entry

NHC ligand

1 2

IEt2Me2 IiPr2Me2

oxidative addition TS

R1/R4

R2/R3

d(R1−R2)

d(R2−R3)

d(R3−R4)

d(R1−R2)

d(R2−R3)

d(R3−R4)

ΔG⧧

Et Pr

Me Me

2.21 2.15

2.22 2.10

2.30 2.12

2.48 2.20

2.23 2.15

2.23 2.17

17.9 14.6

i

a The shortest H−H distances between these groups, d(R1-R2), d(R2-R3), and d(R3-R4),are given in Å. Gibbs free energy barriers (ΔG⧧) are in kcal mol−1 and are with respect to intermediate A.

Figure 10. M06/6-311+G(d,p)−SDD Gibbs free energy profile for ethylene hydrogenation and ruthenacyclization of 2(IiPr2Me2/PPh3). The associative mechanism (blue) proceeds via a rate-determining σ-bond metathesis step (37-TS). The more favorable dissociative pathway (red) proceeds via consecutive oxidative addition (42-TS) and reductive elimination (44-TS). Free energy profile for a higher energy σ-bond metathesis mechanism is included in the Supporting Information. Enthalpy values are shown in parentheses.

ruthenacycle product (Table 1, entry 1). The distances between N-iPr and Me, between the two backbone Me groups, and between Me and N′-iPr are only 2.15, 2.10, and 2.12 Å, respectively. All three distances increase noticeably in oxidative addition transition state 14-TS, to 2.20, 2.15, and 2.17 Å, respectively. In contrast, there are no steric clashes with the NEt group in intermediate 30 (Table 1, entry 2). In previous studies, the reactivity of base-induced C−H activation was attributed to the acidity of the C−H bond.9b Here, the effects of acidity is expected to be small in the C−H oxidative addition process. Our analysis of atomic charges shows only small changes in electron density in the oxidative addition step (see the Supporting Information for details). The crystal structure of the product complex 1(IEt2Me2/ PPh3)′ published by the Whittlesey group shows a trans

sterically congested, resulting in a higher barrier of reductive elimination. Similar to the reaction with the IiPr2Me2 ligand, the intramolecular C−H oxidative addition also takes place after the reassociation of a PPh3 ligand (31-TS). The activation barrier for oxidative addition is raised by 3.3 kcal mol−1 in comparison to that of the IiPr2Me2 ligand to give a barrier of 17.9 kcal mol−1 (31-TS). The increased reactivity of the N-iPr substituted ligand in oxidative addition is mainly due to steric effects. With the IiPr2Me2 ligand, the optimized geometries of the intermediate before oxidative addition (13) indicated unfavorable steric repulsions between the N-iPr groups and the methyl groups on the NHC backbone. These steric clashes are diminished in the oxidative addition transition states, where the N-iPr group is rotated toward the metal to form the G


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Organometallics

Figure 11. Computed transition states in the associative and dissociative mechanistic pathways in the reaction of 2(IiPr2Me2/PPh3). (a) Dissociative hydride migration TS (40-TS). (b) Oxidative addition TS (42-TS). (c) Reductive elimination TS (44-TS). (d) Associative hydride migration TS (35-TS) (e) Associative σ-bond metathesis TS (37-TS). Bond lengths are given in Å.

reductive elimination following hydride migration is no longer feasible. This indicates a different mechanism for the reaction with complex 2. As with 1, we first elucidated possible reaction pathways using a smaller model system, 2(IEt2H2/PMe3). The three computed mechanisms, dissociative, associative, and σ-bond metathesis, with this model system can be found in the Supporting Information. On the basis of the calculations with the model system, the dissociative and associative pathways are the most likely reaction pathways and were thus studied with the full experimental system. The σ-bond metathesis pathway, in which the C−H activation precedes hydride migration to the alkene, is very unfavorable with an activation barrier of 47.3 kcal mol−1, and this was not calculated with the experimental system (see Supporting Information for more details). The energy profiles for the associative and dissociative pathways with the experimental system 2(IiPr2Me2/PPh3) are shown in Figure 10. The key transition state structures in these pathways are shown in Figure 11. 2(IiPr2Me2/PPh3) was observed experimentally to be present in three isomeric forms in dichloromethane solution: nonagostic trans-phosphine complex and two agostic complexes, with trans (2(IiPr2Me2/

phosphine arrangement, and our calculations also indicate that in this case the trans phosphine product is about 1.1 kcal mol−1 more stable than the cis phosphine product. This is rather surprising since with 1(IiPr2Me2/PPh3)′ as discussed before the cis phosphine product is formed selectively. This leads to the conclusion that a trans arrangement of phosphine ligands is electronically more favorable, but this is countered in the 1(IiPr2Me2/PPh3)′ complex by the steric interactions between the N-iPr substituents on the NHC ligand and the bulky PPh3 ligands. Interestingly the oxidative addition transition state with trans phosphine arrangement is much higher in energy than is the TS with cis phosphine arrangement discussed above. This does not have an impact on the product complex observed experimentally, since the phosphine dissociation barriers are very low (7.8 and 14.3 kcal mol−1 from the trans phosphine and cis phosphine isomers of 1(IiPr2Me2/PPh3)′, respectively). Mechanism of the C−H Activation/Transfer Hydrogenation Reaction with Complex 2. As shown in Figure 1, ruthenium(II) monohydride monochloride complex 2 reacts with alkenes in a very similar fashion as ruthenium(II) dihydride complex 1 discussed previously. However, when replacing one of the hydride ligands with chloride, the C−H H


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Organometallics Table 2. Computed Relative Energies of Isomers of 2(IiPr2Me2/PPh3) Observed in Solution18

ΔG ΔH (kcal mol−1)

2(IiPr2Me2/PPh3)

2(IiPr2Me2/PPh3)_a

2(IiPr2Me2/PPh3)_b

0.0 0.0

4.3 1.4

5.2 2.9

PPh3)_a) and cis phosphine arrangements (2(IiPr2Me2/PPh3) _b), respectively.18 These were found computationally to be close in terms of free energy and enthalpy, which accounts for all three complexes being observable at room temperature (Table 2). The stabilization by agostic interaction in 2(IiPr2Me2/PPh3)_a and 2(IiPr2Me2/PPh3)_b does seem to be overcompensated by the rise in steric interaction between the backbone methyl and isopropyl substituents and the loss in entropy. It is apparent in the energy profile that C−H activation can either take place via stepwise oxidative addition and reductive elimination or a concerted σ-bond metathesis step which directly transfers the hydride from the NHC alkyl substituent to the alkyl group on ruthenium. In this case, this selectivity is dependent on whether an associative mechanism (blue, with two PPh3 ligands bound to the ruthenium) or dissociative mechanism takes place (red, with one PPh3 ligand bound to the ruthenium). In the associative (blue) pathway, association of ethylene and hydride migration from the ruthenium alkene complex (34) lead to an alkyl ruthenium chloride intermediate (36), which undergoes C−H activation of the N-Et group via σbond metathesis to form ethane and ruthenacycle product 2(IiPr2Me2/PPh3)′. The σ-bond metathesis that activates the N-Et C−H bond and eliminates an ethane is the ratedetermining step in this associative pathway. The relatively high overall barrier (ΔG⧧ = 33.0 kcal mol−1, 37-TS) is in part due to the unfavorable association of an ethylene molecule in the associative pathway. Although complex 2(IiPr2Me2/PPh3) is coordinatively unsaturated, association of an ethylene molecule to form 34 is endergonic by 12.7 kcal mol−1. The more favorable dissociative pathway for this reaction is shown in red in Figure 10. The ligand exchange to replace one PPh3 with an ethylene to form intermediate 39 takes place via an associative pathway involving 18-electron complex 34. The phosphine dissociation from 34 to form 39 is exergonic by 8.7 kcal mol−1. Similarly, the subsequent hydride migration (ΔG⧧ = 13.9 kcal mol−1, 40-TS) is also more favorable with only one phosphine bound to the metal center. Unexpectedly, neither 39 nor alkyl ruthenium chloride intermediate 41 show an agostic interaction, as the agostic stabilization through coordination of a methyl C−H bond of the NHC ligand is counteracted by steric interactions and the associated loss of entropy. After formation of intermediate 41, the C−H activation proceeds through an oxidative addition transition state (42-TS) to form a six-coordinated Ru(IV) intermediate (43). Reductive elimination of ethane (44-TS) then leads to the ruthenacycle product. A σ-bond metathesis TS similar to 42-TS could not be located for this dissociative pathway. Since the oxidative addition intermediate 43 does not have a free coordination site, the corresponding bisphosphine complex is not formed.

In the C−H activation by Ru(II), a base-assisted mechanism is often invoked. Since PPh3 could be available as a base in the dissociative pathway shown in Figure 10, we also investigated the base-assisted metalation-deprotonation of intermediate 41 using PPh3. Our calculations showed that this pathway is very unfavorable with a computed barrier of ΔG⧧ = 60.6 kcal mol−1 (details in the Supporting Information). The low reactivity of this deprotonation pathway is due to the relatively low basicity of PPh3 in benzene. Previous literature reports indicate carboxylates or strong bases, such as IiPr2Me2, KOtBu, or KN(SiMe3)2, are usually required for the base-promoted deprotonation mechanism.22,5a,b,13 We also calculated the reaction mechanism using the smaller model system 2(IEt2H2/PMe3). The basic mechanistic steps for the associative and dissociative pathways are very similar to those discussed above for the experimental system; however, the associative pathway is much more favorable than the dissociative pathway. This is mostly due to the greatly reduced steric hindrance caused by the smaller phosphine ligands (PMe3 instead of PPh3) and the smaller NHC ligand. Details can be found in the Supporting Information.

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CONCLUSION The mechanisms of alkene hydrogenation and intramolecular C(sp3)−H activation reaction of Ru-complexes 1 and 2 have been investigated with density functional theory. The C−H activation of complex 1 occurs via ligand exchange of a phosphine for ethylene, hydride migration, reductive elimination, and oxidative addition steps. The C−H oxidative addition step is rate-determining in the reaction of the experimental ruthenium complex 1(IiPr2Me2/PPh3) with ethylene. NHC ligands with bulkier N-alkyl groups favor the overall reaction by promoting phosphine dissociation and after the reductive elimination step the product dissociation from the metal complex. Bulkier NHC ligands also lead to lower barriers in the C−H oxidative addition (cyclometalation) step, which is accelerated by the additional steric strain caused by the N-alkyl groups and the NHC backbone substituents. The reaction with complex 2 proceeds via a different mechanism, which involves association of ethylene, hydride migration, and intramolecular C−H oxidative addition to form a Ru(IV) intermediate and reductive elimination of ethane. The reductive elimination step is rate-determining. With the smaller PMe3 in place of PPh3, the associative pathway is favored. Instead of the stepwise C−H oxidative addition/reductive elimination mechanism, a rate-determining σ-bond metathesis step directly transfers a hydrogen atom from the C−H bond of the N-alkyl group to the alkyl ligand attached to Ru to form the ruthenacycle product and the alkane. The origin of the different mechanisms between 1 and 2 is due to the ability of dihydride complex 1 to form a Ru(0) I


Article

Organometallics

(c) Ackermann, L. Chem. Rev. 2011, 111, 1315−1345. (d) Yeung, C. S.; Dong, V. M. Chem. Rev. 2011, 111, 1215−1292. (e) McMurray, L.; O’Hara, F.; Gaunt, M. J. Chem. Soc. Rev. 2011, 40, 1885−1898. (f) Engle, K. M.; Mei, T.-S.; Wasa, M.; Yu, J.-Q. Acc. Chem. Res. 2012, 45, 788−802. (2) (a) Mkhalid, I. A. I.; Barnard, J. H.; Marder, T. B.; Murphy, J. M.; Hartwig, J. F. Chem. Rev. 2010, 110, 890−931. (b) Hartwig, J. F. Acc. Chem. Res. 2012, 45, 864−873. (c) Li, L.; Brennessel, W. W.; Jones, W. D. Organometallics 2009, 28, 3492−3500. (d) Davies, D. L.; Donald, S. M. A.; Al-Duaij, O.; Macgregor, S. A.; Pölleth, M. J. Am. Chem. Soc. 2006, 128, 4210−4211. (e) Ishiyama, T.; Miyaura, N. Pure Appl. Chem. 2006, 78, 1369−1375. (3) (a) Desai, L. V.; Hull, K. L.; Sanford, M. S. J. Am. Chem. Soc. 2004, 126, 9542−9543. (b) Rousseaux, S.; Gorelsky, S. I.; Chung, B. K. W.; Fagnou, K. J. Am. Chem. Soc. 2010, 132, 10692−10705. (c) Ritleng, V.; Sirlin, C.; Pfeffer, M. Chem. Rev. 2002, 102, 1731− 1769. (d) Engle, K. M.; Yu, J.-Q. J. Org. Chem. 2013, 78, 8927−8955. (4) (a) Colby, D. A.; Tsai, A. S.; Bergman, R. G.; Ellman, J. A. Acc. Chem. Res. 2012, 45, 814−825. (b) Davies, H. M. L.; Morton, D. Chem. Soc. Rev. 2011, 40, 1857−1869. (c) Davies, H. M. L.; Manning, J. R. Nature 2008, 451, 417−424. (d) Rhinehart, J. L.; Manbeck, K. A.; Buzak, S. K.; Lippa, G. M.; Brennessel, W. W.; Goldberg, K. I.; Jones, W. D. Organometallics 2012, 31, 1943−1952. (5) (a) Ozdemir, I.; Demir, S.; Cetinkaya, B.; Gourlaouen, C.; Maseras, F.; Bruneau, C.; Dixneuf, P. H. J. Am. Chem. Soc. 2008, 130, 1156−1157. (b) Ackermann, L.; Vicente, R.; Althammer, A. Org. Lett. 2008, 10, 2299−2302. (c) Foley, N. A.; Lail, M.; Gunnoe, T. B.; Cundari, T. R.; Boyle, P. D.; Petersen, J. L. Organometallics 2007, 26, 5507−5516. (d) Jun, C. H.; Hwang, D. C.; Na, S. J. Chem. Commun. 1998, 1405−1406. (e) Weissman, H.; Song, X. P.; Milstein, D. J. Am. Chem. Soc. 2001, 123, 337−338. (f) Oi, S.; Fukita, S.; Hirata, N.; Watanuki, N.; Miyano, S.; Inoue, Y. Org. Lett. 2001, 3, 2579−2581. (g) Chatani, N.; Asaumi, T.; Yorimitsu, S.; Ikeda, T.; Kakiuchi, F.; Murai, S. J. Am. Chem. Soc. 2001, 123, 10935−10941. (h) Prokopcová, H.; Bergman, S. D.; Aelvoet, K.; Smout, V.; Herrebout, W.; Van der Veken, B.; Meerpoel, L.; Maes, B. U. W. Chem. - Eur. J. 2010, 16, 13063−13067. (i) Ackermann, L. Org. Lett. 2005, 7, 3123−3125. (j) Padala, K.; Jeganmohan, M. Org. Lett. 2011, 13, 6144−6147. (k) Dastbaravardeh, N.; Kirchner, K.; Schnürch, M.; Mihovilovic, M. D. J. Org. Chem. 2013, 78, 658−672. (l) Dastbaravardeh, N.; Schnürch, M.; Mihovilovic, M. D. Org. Lett. 2012, 14, 3792−3795. (m) Arockiam, P. B.; Bruneau, C.; Dixneuf, P. H. Chem. Rev. 2012, 112, 5879−5918. (n) De Sarkar, S.; Liu, W.; Kozhushkov, S. I.; Ackermann, L. Adv. Synth. Catal. 2014, 356, 1461−1479. (o) Park, B. Y.; Nguyen, K. D.; Chaulagain, M. R.; Komanduri, V.; Krische, M. J. J. Am. Chem. Soc. 2014, 136, 11902−11905. (p) van der Boom, M. E.; Iron, M. A.; Atasoylu, O.; Shimon, L. J. W.; Rozenberg, H.; Ben-David, Y.; Konstantinovski, L.; Martin, J. M. L.; Milstein, D. Inorg. Chim. Acta 2004, 357, 1854−1864. (q) Jazzar, R. F. R.; Macgregor, S. A.; Mahon, M. F.; Richards, S. P.; Whittlesey, M. K. J. Am. Chem. Soc. 2002, 124, 4944−4945. (r) Kakiuchi, F.; Murai, S. Acc. Chem. Res. 2002, 35, 826− 834. (s) Kakiuchi, F.; Kochi, T. Synthesis 2008, 2008, 3013−3039. (t) Murai, S.; Kakiuchi, F.; Sekine, S.; Tanaka, Y.; Kamatani, A.; Sonoda, M.; Chatani, N. Nature 1993, 366, 529−531. (u) Ogiwara, Y.; Tamura, M.; Kochi, T.; Matsuura, Y.; Chatani, N.; Kakiuchi, F. Organometallics 2014, 33, 402−420. (v) Prechtl, M. H. G.; Hölscher, M.; Ben-David, Y.; Theyssen, N.; Milstein, D.; Leitner, W. Eur. J. Inorg. Chem. 2008, 2008, 3493−3500. (w) Algarra, A. G.; Cross, W. B.; Davies, D. L.; Khamker, Q.; Macgregor, S. A.; McMullin, C. L.; Singh, K. J. Org. Chem. 2014, 79, 1954−1970. (6) (a) Trnka, T. M.; Grubbs, R. H. Acc. Chem. Res. 2001, 34, 18−29. (b) Schrock, R. R.; Hoveyda, A. H. Angew. Chem., Int. Ed. 2003, 42, 4592−4633. (c) Vougioukalakis, G. C.; Grubbs, R. H. Chem. Rev. 2010, 110, 1746−1787. (d) Schrock, R. R. Chem. Rev. 2009, 109, 3211−3226. (e) Samojłowicz, C.; Bieniek, M.; Grela, K. Chem. Rev. 2009, 109, 3708−3742. (7) (a) Noyori, R.; Ohkuma, T. Angew. Chem., Int. Ed. 2001, 40, 40− 73. (b) Lee, H. M.; Smith, D. C., Jr.; He, Z.; Stevens, E. D.; Yi, C. S.; Nolan, S. P. Organometallics 2001, 20, 794−797. (c) Louie, J.;

intermediate via reductive elimination of alkane, while in the case of monohydride monochloride complex 2, formation of such Ru(0) complex is not possible. We have shown that the efficiency of hydrogen borrowing strategies with Ru NHC dihydride complexes such as 1 or Ru NHC monohydride monochloride complexes, such as 2, is dependent on a subtle interplay between steric demand of the NHC ligand, and steric demands and electron-donating ability of the phosphine ligands. The first can promote intramolecular oxidative addition reactions as well as facilitate release of the product, while the latter determines whether associative or dissociative pathways are favored.

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ASSOCIATED CONTENT

S Supporting Information *

The Supporting Information is available free of charge on the ACS Publications website at DOI: 10.1021/acs.organomet.7b00531. Complete reference of Gaussian09, comparison of the crystal structure and B3LYP-optimized geometry of 1(IiPr2Me2/PPh3)′, computed transition state structures in the less favorable pathways in the reaction of 1(IiPr2Me2/PPh3) with ethylene, and in the reaction of 1(IEt2Me2/PPh3) with TMS-CHCH2, Gibbs free energy profile and optimized TS structures in the reaction of 1(IiPr2Me2/PMe3), 1(IEt2H2/PMe3), and 2(IEt2H2/PMe3) with ethylene, natural population analysis of oxidative addition educts, TS, and products with 1(IEt2Me2/PPh3) and 1(IiPr2Me2/PPh3), discussion of an alternative reaction pathway involving σ-bond metathesis from 58 and an alternative σ-bond metathesis pathway in the reaction of 2(IEt2H2/PMe3) and a concerted metalation-deprotonation pathway from 41 (PDF) Coordinates of all intermediates and transition states (XYZ)

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AUTHOR INFORMATION

Corresponding Authors

*E-mail: [email protected]. *E-mail: [email protected]. ORCID

Katharina Marie Wenz: 0000-0002-5115-5673 Peng Liu: 0000-0002-8188-632X K. N. Houk: 0000-0002-8387-5261 Notes

The authors declare no competing financial interest.

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ACKNOWLEDGMENTS We are grateful for financial support from the Maersk Oil Research and Technology Center, Doha, Qatar, NSF (CHE1361104 for K.N.H. and CHE-1654122 for P.L.), and a PROMOS fellowship from Albert-Ludwigs-Universität Freiburg and the DAAD to K.M.W. Calculations were performed on the Hoffman2 cluster at UCLA and the Extreme Science and Engineering Discovery Environment (XSEDE), which is supported by the NSF(ACI-1053575).

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REFERENCES

(1) (a) Crabtree, R. H. J. Organomet. Chem. 2004, 689, 4083−4091. (b) Lyons, T. W.; Sanford, M. S. Chem. Rev. 2010, 110, 1147−1169. J


Article

Organometallics Bielawski, C. W.; Grubbs, R. H. J. Am. Chem. Soc. 2001, 123, 11312− 11313. (d) Lund, C. L.; Sgro, M. J.; Cariou, R.; Stephan, D. W. Organometallics 2012, 31, 802−805. (8) (a) Hashiguchi, S.; Fujii, A.; Takehara, J.; Ikariya, T.; Noyori, R. J. Am. Chem. Soc. 1995, 117, 7562−7563. (b) Noyori, R.; Hashiguchi, S. Acc. Chem. Res. 1997, 30, 97−102. (c) Shibahara, F.; Bower, J. F.; Krische, M. J. J. Am. Chem. Soc. 2008, 130, 6338−6339. (d) Moran, J.; Krische, M. J. Pure Appl. Chem. 2012, 84, 1729−1739. (9) Select examples: (a) Gruver, B. C.; Adams, J. J.; Warner, S. J.; Arulsamy, N.; Roddick, D. M. Organometallics 2011, 30, 5133−5140. (b) Foley, N. A.; Gunnoe, T. B.; Cundari, T. R.; Boyle, P. D.; Petersen, J. L. Angew. Chem., Int. Ed. 2008, 47, 726−730. (c) Man, W.-L.; Lam, W. W. Y.; Kwong, H.-K.; Yiu, S.-M.; Lau, T.-C. Angew. Chem., Int. Ed. 2012, 51, 9101−9104. (d) Bergman, S. D.; Storr, T. E.; Prokopcová, H.; Aelvoet, K.; Diels, G.; Meerpoel, L.; Maes, B. U. W. Chem. - Eur. J. 2012, 18, 10393−10398. (e) Schinkel, M.; Wang, L.; Bielefeld, K.; Ackermann, L. Org. Lett. 2014, 16, 1876−1879. (10) Albrecht, M. Chem. Rev. 2010, 110, 576−623. (11) (a) Matsubara, T.; Koga, N.; Musaev, D. G.; Morokuma, K. Organometallics 2000, 19, 2318−2329. (b) Helmstedt, U.; Clot, E. Chem. - Eur. J. 2012, 18, 11449−11458. (12) (a) Perutz, R. N.; Sabo Etienne, S. Angew. Chem., Int. Ed. 2007, 46, 2578−2592. (b) DeYonker, N. J.; Foley, N. A.; Cundari, T. R.; Gunnoe, T. B.; Petersen, J. L. Organometallics 2007, 26, 6604−6611. (c) Ess, D. H.; Gunnoe, T. B.; Cundari, T. R.; Goddard, W. A., III; Periana, R. A. Organometallics 2010, 29, 6801−6815. (13) (a) Flegeau, E. F.; Bruneau, C.; Dixneuf, P. H.; Jutand, A. J. Am. Chem. Soc. 2011, 133, 10161−10170. (b) Lapointe, D.; Fagnou, K. Chem. Lett. 2010, 39, 1118−1126. (c) Ackermann, L.; Vicente, R.; Potukuchi, H. K.; Pirovano, V. Org. Lett. 2010, 12, 5032−5035. (d) Kumar, N. Y. P.; Jeyachandran, R.; Ackermann, L. J. Org. Chem. 2013, 78, 4145−4152. (e) Ackermann, L. Acc. Chem. Res. 2014, 47, 281−295. (f) Boutadla, Y.; Davies, D. L.; Macgregor, S. A.; PobladorBahamonde, A. I. Dalton Trans. 2009, 30, 5820. (g) Davies, D. L.; Macgregor, S. A.; McMullin, C. L. Chem. Rev. 2017, 117, 8649. (14) (a) Hong, S. H.; Chlenov, A.; Day, M. W.; Grubbs, R. H. Angew. Chem., Int. Ed. 2007, 46, 5148−5151. (b) Mathew, J.; Koga, N.; Suresh, C. H. Organometallics 2008, 27, 4666−4670. (c) Poater, A.; Cavallo, L. J. Mol. Catal. A: Chem. 2010, 324, 75−79. (d) Poater, A.; Bahri-Laleh, N.; Cavallo, L. Chem. Commun. 2011, 47, 6674−6676. (e) Leitao, E. M.; Dubberley, S. R.; Piers, W. E.; Wu, Q.; McDonald, R. Chem. - Eur. J. 2008, 14, 11565−11572. (15) (a) Endo, K.; Grubbs, R. H. J. Am. Chem. Soc. 2011, 133, 8525− 8527. (b) Keitz, B. K.; Endo, K.; Patel, P. R.; Herbert, M. B.; Grubbs, R. H. J. Am. Chem. Soc. 2012, 134, 693−699. (16) (a) Cannon, J. S.; Zou, L.; Liu, P.; Lan, Y.; O’Leary, D. J.; Houk, K. N.; Grubbs, R. H. J. Am. Chem. Soc. 2014, 136, 6733−6743. (b) Herbert, M. B.; Suslick, B. A.; Liu, P.; Zou, L. F.; Dornan, P. K.; Houk, K. N.; Grubbs, R. H. Organometallics 2015, 34, 2858−2869. (17) (a) Burling, S.; Mahon, M. F.; Paine, B. M.; Whittlesey, M. K.; Williams, J. M. J. Organometallics 2004, 23, 4537−4539. (b) Burling, S.; Paine, B. M.; Nama, D.; Brown, V. S.; Mahon, M. F.; Prior, T. J.; Pregosin, P. S.; Whittlesey, M. K.; Williams, J. M. J. J. Am. Chem. Soc. 2007, 129, 1987−1995. For reactions employing bidentate phosphine ligands, see: (c) Chilvers, M. J.; Jazzar, R. F. R.; Mahon, M. F.; Whittlesey, M. K. Adv. Synth. Catal. 2003, 345, 1111−1114. (d) Ledger, A. E. W.; Mahon, M. F.; Whittlesey, M. K.; Williams, J. M. J. Dalton Trans. 2009, 6941−6947. (18) Burling, S.; Mas-Marzá, E.; Valpuesta, J. E. V.; Mahon, M. F.; Whittlesey, M. K. Organometallics 2009, 28, 6676−6686. (19) Intramolecular C−H bond activation of similar ruthenium complexes in the absence of alkenes were also reported. See ref 17b and (a) Reade, S. P.; Acton, A. L.; Mahon, M. F.; Martin, T. A.; Whittlesey, M. K. Eur. J. Inorg. Chem. 2009, 2009, 1774−1785. (b) Armstrong, R.; Ecott, C.; Mas-Marza, E.; Page, M. J.; Mahon, M. F.; Whittlesey, M. K. Organometallics 2010, 29, 991−997. (c) Page, M. J.; Mahon, M. F.; Whittlesey, M. K. Dalton Trans. 2011, 40, 7858− 7865. (d) Bramananthan, N.; Mas-Marzá, E.; Fernandéz, F. E.; Ellul,

C. E.; Mahon, M. F.; Whittlesey, M. K. Eur. J. Inorg. Chem. 2012, 2012, 2213−2219. (20) (a) Goldman, A. S.; Roy, A. H.; Huang, Z.; Ahuja, R.; Schinski, W.; Brookhart, M. Science 2006, 312, 257−261. (b) Haibach, M. C.; Kundu, S.; Brookhart, M.; Goldman, A. S. Acc. Chem. Res. 2012, 45, 947−958. (c) Bailey, B. C.; Schrock, R. R.; Kundu, S.; Goldman, A. S.; Huang, Z.; Brookhart, M. Organometallics 2009, 28, 355−360. (21) (a) Hamid, M. H. S. A.; Slatford, P. A.; Williams, J. M. J. Adv. Synth. Catal. 2007, 349, 1555−1575. (b) Dobereiner, G. E.; Crabtree, R. H. Chem. Rev. 2010, 110, 681−703. (c) Guillena, G.; Ramón, D. J.; Yus, M. Chem. Rev. 2010, 110, 1611−1641. (22) Häller, L. J. L.; Page, M. J.; Macgregor, S. A.; Mahon, M. F.; Whittlesey, M. K. J. Am. Chem. Soc. 2009, 131, 4604−4605. (23) Diggle, R. A.; Macgregor, S. A.; Whittlesey, M. K. Organometallics 2008, 27, 617−625. (24) Diggle, R. A.; Kennedy, A. A.; Macgregor, S. A.; Whittlesey, M. K. Organometallics 2008, 27, 938−944. (25) (a) Kulago, A. A.; Van Steijvoort, B. F.; Mitchell, E. A.; Meerpoel, L.; Maes, B. U. W. Adv. Synth. Catal. 2014, 356, 1610− 1618. (b) Pastine, S. J.; Gribkov, D. V.; Sames, D. J. Am. Chem. Soc. 2006, 128, 14220−14221. (c) Li, W.; Huang, X.; You, J. Org. Lett. 2016, 18 (4), 666−668. (d) Dastbaravardeh, N.; Schnürch, M.; Mihovilovic, M. D. Org. Lett. 2012, 14, 1930−1933. (e) Bergman, S. D.; Storr, T. E.; Prokopcová, H.; Aelvoet, K.; Diels, G.; Meerpoel, L.; Maes, B. U. W. Chem. - Eur. J. 2012, 18, 10393−10398. (26) Lam, W. H.; Jia, G.; Lin, Z.; Lau, C. P.; Eisenstein, O. Chem. Eur. J. 2003, 9, 2775−2782. (27) Toner, A.; Gründemann, S.; Matthes, J.; Limbach, H.-H.; Chaudret, B.; Clot, E.; Sabo Etienne, S. Proc. Natl. Acad. Sci. U. S. A. 2007, 104, 6945−6950. (28) Frisch, M. J.; Trucks, G. W.; Schlegel, H. B.; Scuseria, G. E.; Robb, M. A.; Cheeseman, J. R.; Scalmani, G.; Barone, V.; Mennucci, B.; Petersson, G. A.; Nakatsuji, H.; Caricato, M.; Li, X.; Hratchian, H. P.; Izmaylov, A. F.; Bloino, J.; Zheng, G.; Sonnenberg, J. L.; Hada, M.; Ehara, M.; Toyota, K.; Fukuda, R.; Hasegawa, J.; Ishida, M.; Nakajima, T.; Honda, Y.; Kitao, O.; Nakai, H.; Vreven, T.; Montgomery, J. A., Jr.; Peralta, J. E.; Ogliaro, F.; Bearpark, M.; Heyd, J. J.; Brothers, E.; Kudin, K. N.; Staroverov, V. N.; Kobayashi, R.; Normand, J.; Raghavachari, K.; Rendell, A.; Burant, J. C.; Iyengar, S. S.; Tomasi, J.; Cossi, M.; Rega, N.; Millam, J. M.; Klene, M.; Knox, J. E.; Cross, J. B.; Bakken, V.; Adamo, C.; Jaramillo, J.; Gomperts, R.; Stratmann, R. E.; Yazyev, O.; Austin, A. J.; Cammi, R.; Pomelli, C.; Ochterski, J. W.; Martin, R. L.; Morokuma, K.; Zakrzewski, V. G.; Voth, G. A.; Salvador, P.; Dannenberg, J. J.; Dapprich, S.; Daniels, A. D.; Farkas, O.; Foresman, J. B.; Ortiz, J. V.; Cioslowski, J.; Fox, D. J. Gaussian 09, revision D.01; Gaussian, Inc: Wallingford, CT, 2009. (29) (a) Zhao, Y.; Truhlar, D. G. Org. Lett. 2007, 9, 1967−1970. (b) Minenkov, Y.; Occhipinti, G.; Jensen, V. R. J. Phys. Chem. A 2009, 113, 11833−11844. (c) Zhao, Y.; Truhlar, D. G. J. Chem. Theory Comput. 2009, 5, 324−333. (d) Poater, A.; Pump, E.; Vummaleti, S. V. C.; Cavallo, L. J. Chem. Theory Comput. 2014, 10, 4442−4448. (30) The barrier for hydride migration to the β-position to the TMS group is only about 0.8 kcal mol−1 higher than for hydride migration alpha to the TMS group (19-TS). The secondary alkyl ruthenium complex resulting from this step with the TMS group at the α position is about 6.5 kcal mol−1 less stable than the primary alkyl regioisomer with the TMS group at the β position. This is due to the steric repulsions between the TMS substituent and the Ru center. We expect the subsequent C−H reductive elimination from the secondary alkyl ruthenium isomer to the branched silane product is disfavored due to similar steric effects.

K


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