The Origins of Dramatic Differences in Five-Membered vs Six

Jun 3, 2017 - The origin of the unique effectiveness of six-membered chelates on the β-methylene C(sp3)–H activation reactions by Pd(II) catalyst w...
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The Origins of Dramatic Differences in Five-Membered vs SixMembered Chelation of Pd(II) on Efficiency of C(sp3)−H Bond Activation Yun-Fang Yang,† Gang Chen,§ Xin Hong,‡ Jin-Quan Yu,*,§ and K. N. Houk*,† †

Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095, United States Department of Chemistry, Zhejiang University, Hangzhou 310027, China § Department of Chemistry, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, United States ‡

S Supporting Information *

ABSTRACT: The origin of the unique effectiveness of six-membered chelates on the β-methylene C(sp3)−H activation reactions by Pd(II) catalyst was explained with density functional theory. The Pd(II) catalysts that involve five-membered chelates are inactive in this transformation. Computational studies suggest that the C(sp3)−H bond activation is the rate-limiting step in both cases. The C(sp3)−H bond activation with a five-membered chelate is unfavorable by 7.7 kcal/mol compared to the corresponding six-membered chelate with Pd(II). Two factors cause the difference: (1) the dimeric Pd species with five-membered chelation square-planar structure is more stable than that with six-membered chelation by 2.0 kcal/mol; (2) steric repulsion between the ArF group of the substrate and the quinoline group of the acetyl-protected aminomethyl quinoline ligand destabilizes the five-membered chelate transition structure by 5.7 kcal/mol. The six-membered chelate of Pd(II) with an acetyl-protected aminoethyl quinoline ligand orients the ligand away from the ArF group of the substrate and alleviates the steric repulsion.

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INTRODUCTION Transition-metal-catalyzed C−H bond activation and functionalization is a very powerful strategy for C−C bond formation.1 The use of directing groups is one of the most successful strategies to achieve the site selectivity.2 Enantioselective alkyl C(sp3)−H bond activation is a challenge of intense current interest.3 Pd(II) catalysts with chiral monoprotected amino acid (MPAA) have been employed for arylation of relatively reactive cyclopropyl and cyclobutyl C−H bonds via a Pd(II)/Pd(IV) catalytic cycle.4 Various synthetic strategies have been developed to construct complex products from simple prochiral molecules with unreactive C−H bonds.1,2 However, enantioselective methylene C(sp3)−H bond activation reactions are rare.3 Duan and co-workers reported the Pd(II)-catalyzed enantioselective arylation of benzylic β-C(sp3)−H bonds of 8-aminoquinoline amides using chiral phosphoric amides and acids to control the stereoselectivity.5 Challenging substrates with alkyl substituents at the β-position, such as n-propyl and isopropyl, were examined, and the desired products were produced, but with relatively low enantioselectivities and yields.5 Chen and He and co-workers reported the Pd(II)-catalyzed enantioselective arylation of benzylic γ-C(sp3)−H bonds of alkyl amines with the 2,2′-dihydroxy-1,1′-binaphthyl (BINOL) phosphoric acid ligand.6 © 2017 American Chemical Society

We recently reported the chiral acetyl-protected aminoethyl quinoline (APAQ) bidentate ligand-accelerated methylene C(sp3)−H bond activation reactions shown in Scheme 1.7 The origin of the enantioselectivity was also clarified computationally. The APAQ ligand, L34, chelates with palladium through its quinoline nitrogen and deprotonated acetylScheme 1. Ligand-Accelerated Methylene C(sp3)−H Arylation

Received: February 20, 2017 Published: June 3, 2017 8514

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Figure 1. Proposed mechanism for ligand-accelerated methylene C(sp3)−H arylation.

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protected amino group forming a six-membered chelate. This chelation form enables β-methylene C(sp3)−H activation. The achiral analog, L9, is also effective. The Pd(II) catalyst with an acetyl-protected aminomethyl quinoline ligand (L6) can form only a five-membered chelate and is completely inactive in this transformation. We have carried out a detailed computational study to address the mechanism of these transformations and to elucidate differences between ligands forming five-membered or six-membered chelates with Pd(II). The proposed mechanism for APAQ ligand-accelerated methylene C(sp3)−H arylation is shown in Figure 1. Deprotonation of L9 generates palladium complex Int2, which can dimerize to Int1 that is in equilibrium with Int2. Int1 is an off-cycle intermediate. Ligand exchange with the aliphatic amide substrate, accompanied by deprotonation by acetate, generates palladium complex Int3. Subsequent concerted metalation and cleavage of the β-methylene C−H bond by the oxygen of the amide of L9 generates palladacycle Int4. Oxidative addition of ArI on the palladacycle Int4 affords Pd(IV) complex Int6. Reductive elimination from Int6 to Pd(II) complex Int9 forms the C−C bond. Finally, the protonation with HOAc and scavenging of an iodide anion with silver salt Ag2CO3 gives the coupling product and regenerates the palladium acetate catalyst. Ag+ coordination may facilitate previous steps in the cycle, as described later. There are extensive studies of Pd(II)/Pd(IV) analogous redox chemistry in Pd(II)-catalyzed C−H arylation.8 This mechanism was used earlier to explain7 how stereoselectivity is controlled with L34. Here we investigate why L6 with Pd(II) is ineffective as a catalyst.

COMPUTATIONAL DETAILS

All the calculations were carried out with Gaussian 09.9 Geometry optimizations were performed with B3LYP.10 The LANL2DZ +f (1.472) basis set11 with ECP was used for Pd, the LANL2DZ +f (1.611) basis set with ECP was used for Ag, the LANL2DZ basis set with ECP was used for I, and the 6-31G (d) basis set12 was used for other atoms. Frequency analysis was conducted at the same level of theory to verify that the stationary points are minima or saddle points. The single-point energies and solvent effects were computed with the M0613/SDD14-6-311++G(d,p) basis sets by using the SMD solvation model15 (Solvent = Generic, eps = 16.7). The relative Gibbs free energies (at 298.15 K) are given in kcal/mol. Computed structures are illustrated using CYLView.16

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RESULTS AND DISCUSSION Catalytic Palladium Complex. In solution, palladium acetate maintains the trimeric structure in nonpolar organic solvents.17 Ligand exchange with solvents or ligands causes dissociation of the trimeric structure. Figure 2 shows the energetics of various forms of palladium acetate. The trimeric Pd3(OAc)6, Cat1, is more stable than both monomeric and dimeric forms, Cat2 and Cat3, by 15.1 and 4.7 kcal/mol, respectively.18 There are four acetate bridges in dimeric complex Cat3, and each Pd is coordinated by four acetates. Another dimeric complex Cat4 preserves only two acetate bridges, while the other two acetates act as a bidentate ligand to one Pd.19 The amide H of ligand L9/ L6 can be deprotonated by acetate to form homodimeric palladium complex Int1/ Int1b. Int1b is 2 kcal/mol more stable than Int1. This is caused by the difference between the square-planar coordination of five-membered palladacycles and the nonplanar coordination of six-membered palladacycles. The Pd−Pd distances in Int1 and 8515

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Figure 2. Various forms of palladium acetate catalyst and dimeric palladium complexes with ligands L9 and L6. The Pd−Pd distances are shown in Ångströms.

Int1b are 3.46 and 3.16 Å, respectively. The five-membered chelate of Pd(II) forms a stable dimeric species with two acetate bridges and make it less reactive by 2.0 kcal/mol. A similar homodimeric palladium complex with a five-membered palladacycle was reported by Ritter20 and Sanford.21 C(sp3)−H Activation Step. Figure 3 shows the M06 free energy profiles for methylene C(sp3)−H activation reactions with ligands L6 and L9, via five-membered and six-membered chelation of Pd(II), respectively. The homodimeric palladium complex Int1 or Int1b first dissociates to the palladium complex, Int2 or Int2b. The subsequent deprotonation of the substrate by acetate and coordination to form palladium complexes Int3 or Int3b is significantly uphill. The transition structures for cleaving the N−H bonds of the ligands and the substrate by acetate are shown in Figure S1 (Supporting Information). They have lower barriers than those of C(sp3)− H bond activation. Int3b, a five-membered chelate with Pd(II), is much more unfavorable than the corresponding sixmembered chelate Int3 by 4.6 kcal/mol. In C−H activation transition structures TS1 and TS1b, the Pd(II) center is coordinated with the quinoline N and the amide N of the deprotonated ligands as well as the amide N of the deprotonated substrate. The oxygen of the amide of the ligand acts as an intramolecular base to deprotonate the methylene C−H bond and facilitate the Pd−C bond formation.7,22 The

energy difference between TS1 and TS1b is even larger, nearly 6 kcal/mol. With respect to their corresponding resting state, Int1 and Int1b, the barriers for C−H activation via sixmembered chelate and five-membered chelate are 22.1 and 29.8 kcal/mol, respectively. This implies that the reaction via TS1 is ∼105 faster than that via TS1b at room temperature, consistent with the nonreactivity with L6. Structures TS1 and TS1b are shown in Figure 4. The fivemembered chelate with Pd(II) is planar, and the dihedral angle N−Pd−N−C (four atoms marked with green circles in Figure 4) is 28°. This causes close contact between the ArF group of substrate and the quinoline group of the ligand. In TS1b, the distance between the carbon atom on the N substituent of ArF and hydrogen atom at the 8-position of the quinoline group is 2.65 Å, which is smaller the sum of van der Waals radii of C (1.7 Å) and H (1.2 Å). In TS1, the corresponding C−H distance is 2.95 Å. This is because the six-membered chelation of Pd(II) enforces a nonplanar gauche conformation of the ethane unit, which orients the quinoline ring away from the ArF group; the dihedral angle N−Pd−N−C is 54°. The steric repulsion between the ArF group of the substrate and the quinoline group of the ligand appears to be the main cause of the higher C(sp3)−H bond activation barrier. To test this idea, we studied the C(sp3)−H bond activation transition structures, TS1b_py and TS1_py, with ligands N-(pyridin-28516

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Figure 3. Free energy profiles for ligand-accelerated methylene C(sp3)−H activation reactions via five-membered and six-membered chelation with Pd(II).

ylmethyl)acetamide and N-(2-(pyridin-2-yl)ethyl)acetamide, respectively (Figure 5). Here pyridine replaces the quinoline of L6 and L9. In TS1b_py, although the C−H distance is shortened to 2.50 Å, the dihedral angle N−Pd−N−C is 18°, much closer to planar coordination. The energy difference between TS1b_py and TS1_py is 2.6 kcal/mol, that is, significantly smaller than the energy difference of 5.7 kcal/mol between TS1b and TS1. This is due to the smaller size of the pyridine group compared to the quinoline group. For fivemembered chelation, the steric repulsion is alleviated in TS1b_py with the pyridine group compared to TS1b with the quinoline group. With respect to their respective dimeric palladium resting state, Int1_py and Int1b_py, the barriers for C−H activation via six-membered chelate and five-membered chelate are 22.8 and 29.3 kcal/mol, respectively. For sixmembered chelation, the barrier for C−H activation with the pyridine ligand is higher than that with the quinoline ligand by 0.7 kcal/mol. We predict that the six-membered pyridine containing complex (Int1_py) will likely undergo reaction, whereas the five-membered analog (TS1b_py) still has steric hindrance and a high barrier of reaction. This is mainly due to the very favorable dimerization of the catalyst. The experiments also showed low reactivity with a six-membered chelate pyridine ligand (28% yield; detailed information in Scheme S1 of Supporting Information). We also tested various other

modifications of the chelating ligand to verify the origins of reactivity differences (see Figures S2−S5 in Supporting Information). C(sp3)−H Arylation Steps. C(sp3)−H bond activation leads to palladacycle intermediate Int4 or Int4b. As shown in Figure 3, these two intermediates isomerize to more stable species with amide NH coordination, Int5 and Int5b, respectively. Figure 6 shows four possible pathways for subsequent arylation steps, oxidative addition, and reductive elimination. Starting from intermediates Int5/Int5b, the dissociation of ligands L9/L6 provides vacant sites for iodobenzene coordination in both pathways I and II. In pathway I, the silver salt AgOAc, resulting from reaction of Ag2CO3 and HOAc, interacts with iodobenzene to facilitate the oxidative addition and reductive elimination reactions. In pathways III and IV, the intermediates Int5/Int5b reorganize to ligand amide O coordinated species and provide vacant sites for iodobenzene coordination. Silver salt AgOAc is involved in pathway III, as in the case of pathway I. Pathway I with the assistance of AgOAc and without the ligand coordination is the most favorable one. Figure 7 shows the free energy profiles of pathway I for methylene C(sp3)−H arylation reactions. In pathway I, starting from intermediates Int5/Int5b, upon ligand dissociation and iodobenzene coordination, the intermediate IntVI is formed. 8517

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Figure 4. C(sp3)−H bond activation transition structures with ligands L6 and L9. The values not in italics are with respect to the separated reactants. The values in italics are with respect to the resting state dimeric palladium complexes Int1b and Int1. The distances are shown in angströms.

Figure 5. C(sp3)−H bond activation transition structures with pyridine ligands L6_py and L9_py. The values not in italics are with respect to the separated reactants. The values in italics are with respect to the resting state dimeric palladium complexes Int1b_py/Int1_py. The distances are shown in angströms.

coordination sites, which is calculated to be 15.2 kcal/mol. The subsequent iodobenzene coordination gives intermediate IntVI. The dissociative mechanism is less favorable than the associative mechanism. AgOAc interacting with iodobenzene of IntVI leads to a more stable intermediate IntVII. The oxidative addition of iodobenzene to the Pd(II) center via TSII gives Pd(IV) species IntVIII. The subsequent reductive elimination via TSIII leads to IntIX. Finally, protonation with HOAc and exclusion of silver iodide give the final C(sp3)−H arylation product and regenerate the catalyst. In pathway I, the

For the ligand exchange processes on Int5/Int5b, we studied both associative and dissociative mechanisms. In the associative mechanism, the intermediates Int5/Int5b reorganize to ligand amide O coordinated species and provide vacant sites for iodobenzene coordination. This process leads to the formation of Int6 (7.0 kcal/mol)/Int6b (3.0 kcal/mol), as shown in Figures S7 and S8 of Supporting Information. The subsequent dissociation of the ligand gives intermediate IntVI, as shown in Figure 7. In the dissociative mechanism, the dissociation of the ligand leads to a palladacycle intermediate with two vacant 8518

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Figure 6. Four pathways for methylene C(sp3)−H arylation reactions starting from Int5/Int5b.

Figure 7. Free energy profiles of pathway I for methylene C(sp3)−H arylation reactions.

oxidative addition has a barrier of 9.8 kcal/mol and leads to the high valent Pd(IV) intermediate, IntVIII. The subsequent reductive elimination has a barrier of 17.7 kcal/mol, which is 4.4 kcal/mol lower than the barrier for the C−H activation step with the six-membered chelate. The fast reductive elimination will cause only a low concentration and short lifetime of IntVIII. We have also made many attempts to isolate the intermediates without success (see Experimental section in Supporting Information).

Figure 8 shows the transition structures for the oxidative addition and reductive elimination steps. We also studied the three other pathways for the oxidative addition and reductive elimination steps shown in Figure 6. They are all energetically unfavorable compared to pathway I (see Figures S6−S9 in Supporting Information). The favorable pathway for L9-accelerated methylene C(sp3)−H bond arylation reaction is through Int1-Int2-Int3TS1-Int4-Int5-IntVI-IntVII-TSII-IntVIII-TSIII-IntIX-Pro. The largest energy span is from Int1 to TS1, 22.1 kcal/mol. 8519

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Journal of the American Chemical Society *[email protected] ORCID

Yun-Fang Yang: 0000-0002-6287-1640 Xin Hong: 0000-0003-4717-2814 Jin-Quan Yu: 0000-0003-3560-5774 K. N. Houk: 0000-0002-8387-5261 Notes

The authors declare no competing financial interest.

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ACKNOWLEDGMENTS This paper is dedicated to Professor Yun-Dong Wu on the occasion of his 60th birthday. We are grateful to the National Science Foundation of the USA (CHE-1361104), the National Science Foundation under the CCI Center for Selective C−H Functionalization (CHE-1205646), and the Chinese “Thousand Youth Talents Plan” (X.H.) for financial support of this research. Calculations were performed on the Hoffman2 cluster at UCLA and the Extreme Science and Engineering Discovery Environment (XSEDE), which is supported by the National Science Foundation (OCI-1053575).

Figure 8. Transition structures for oxidative addition and reductive elimination. The values not in italics are with respect to the separated reactants, and the values in italics are with respect to the preceding intermediates IntVII or IntVIII. The distances are shown in angströms.

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The favorable pathway for methylene C(sp3)−H bond arylation reactions with ligand L6 is through Int1b-Int2b-Int3b-TS1bInt4b-Int5b-IntVI-IntVII-TSII-IntVIII-TSIII-IntIX-Pro. The largest energy span is from Int1b to TS1b, 29.8 kcal/mol. Therefore, the Pd(II) catalyst with five-membered chelated ligand L6 is completely inactive.

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CONCLUSION We have studied the mechanism of achiral acetyl-protected aminoethyl quinoline ligand (L9)-accelerated methylene C(sp3)−H bond arylation reactions. This six-membered chelate enables β-methylene C(sp3)−H activation. However, the Pd(II) catalyst with an acetyl-protected aminomethyl quinoline ligand (L6) can form only a five-membered chelate and is inactive in this transformation. We have elucidated the difference between five-membered and six-membered chelation with Pd(II). Computational studies suggest that the C(sp3)−H bond activation is likely the rate-limiting step. The C(sp3)−H bond activation with a five-membered chelate with Pd(II) is less favorable than the corresponding six-membered chelate with Pd(II) by 7.7 kcal/mol. With L6, the steric repulsion between the ArF group of the substrate and the quinoline group of the acetyl-protected aminomethyl quinoline ligand introduces 5.7 kcal/mol more to the C(sp3)−H bond activation barrier. The six-membered chelate with Pd(II) with an acetylprotected aminoethyl quinoline ligand orients the ligand away from the ArF group of the substrate and alleviates the steric repulsion. The dimeric Pd species with the five-membered chelate square-planar structure is more stable than that with the six-membered chelation by 2.0 kcal/mol. This also makes the five-membered chelate inactive in this transformation.

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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/jacs.7b01801. More details of experiments and DFT calculations (PDF)

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REFERENCES

(1) (a) Daugulis, O.; Do, H.-Q.; Shabashov, D. Acc. Chem. Res. 2009, 42, 1074. (b) Chen, X.; Engle, K. M.; Wang, D.-H.; Yu, J.-Q. Angew. Chem., Int. Ed. 2009, 48, 5094. (c) Crabtree, R. H. Chem. Rev. 2010, 110, 575. (d) Balcells, D.; Clot, E.; Eisenstein, O. Chem. Rev. 2010, 110, 749. (e) Xu, L.-M.; Li, B.-J.; Yang, Z.; Shi, Z.-J. Chem. Soc. Rev. 2010, 39, 712. (f) Doyle, M. P.; Goldberg, K. I. Acc. Chem. Res. 2012, 45, 777. (g) Brückl, T.; Baxter, R. D.; Ishihara, Y.; Baran, P. S. Acc. Chem. Res. 2012, 45, 826. (h) Hartwig, J. F. J. Am. Chem. Soc. 2016, 138, 2. (2) (a) Colby, D. A.; Bergman, R. G.; Ellman, J. A. Chem. Rev. 2010, 110, 624. (b) Lyons, T. W.; Sanford, M. S. Chem. Rev. 2010, 110, 1147. (c) Colby, D. A.; Tsai, A. S.; Bergman, R. G.; Ellman, J. A. Acc. Chem. Res. 2012, 45, 814. (d) Leow, D.; Li, G.; Mei, T.-S.; Yu, J.-Q. Nature 2012, 486, 518. (3) (a) Davies, H. M. L.; Beckwith, R. E. J. Chem. Rev. 2003, 103, 2861. (b) Giri, R.; Shi, B.-F.; Engle, K. M.; Maugel, N.; Yu, J.-Q. Chem. Soc. Rev. 2009, 38, 3242. (c) Davies, H. M. L.; Manning, J. R. Nature 2008, 451, 417. (d) Liao, K.; Negretti, S.; Musaev, D. G.; Bacsa, J.; Davies, H. M. L. Nature 2016, 533, 230. (4) (a) Shi, B.-F.; Maugel, N.; Zhang, Y.-H.; Yu, J.-Q. Angew. Chem., Int. Ed. 2008, 47, 4882. (b) Wasa, M.; Engle, K. M.; Lin, D. W.; Yoo, E. J.; Yu, J.-Q. J. Am. Chem. Soc. 2011, 133, 19598. (c) Xiao, K.-J.; Lin, D. W.; Miura, M.; Zhu, R.-Y.; Gong, W.; Wasa, M.; Yu, J.-Q. J. Am. Chem. Soc. 2014, 136, 8138. (d) Bonney, K. J.; Schoenebeck, F. Chem. Soc. Rev. 2014, 43, 6609. (e) Chan, K. S. L.; Fu, H.-Y.; Yu, J.-Q. J. Am. Chem. Soc. 2015, 137, 2042. (5) Yan, S.-B.; Zhang, S.; Duan, W.-L. Org. Lett. 2015, 17, 2458. (6) Wang, H.; Tong, H.-R.; He, G.; Chen, G. Angew. Chem., Int. Ed. 2016, 55, 15387. (7) Chen, G.; Gong, W.; Zhuang, Z.; Andrä, M. S.; Chen, Y.-Q.; Hong, X.; Yang, Y.-F.; Liu, T.; Houk, K. N.; Yu, J.-Q. Science 2016, 353, 1023. (8) (a) Dyker, G. Angew. Chem., Int. Ed. Engl. 1994, 33, 103. (b) Zaitsev, V. G.; Shabashov, D.; Daugulis, O. J. Am. Chem. Soc. 2005, 127, 13154. (c) Sehnal, P.; Taylor, R. J. K.; Fairlamb, I. J. S. Chem. Rev. 2010, 110, 824. (d) Xiao, B.; Gong, T.-J.; Xu, J.; Liu, Z.-J.; Liu, L. J. Am. Chem. Soc. 2011, 133, 1466. (9) 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,

AUTHOR INFORMATION

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Journal of the American Chemical Society K. N.; Staroverov, V. N.; Keith, T.; 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, Rev. D.01; Gaussian, Inc.: Wallingford, CT, 2010. (10) (a) Lee, C.; Yang, W.; Parr, R. G. Phys. Rev. B: Condens. Matter Mater. Phys. 1988, 37, 785. (b) Becke, A. D. J. Chem. Phys. 1993, 98, 1372. (c) Becke, A. D. J. Chem. Phys. 1993, 98, 5648. (d) Stephens, P. J.; Devlin, F. J.; Chabalowski, C. F.; Frisch, M. J. J. Phys. Chem. 1994, 98, 11623. (11) (a) Hay, P. J.; Wadt, W. R. J. Chem. Phys. 1985, 82, 299. (b) Ehlers, A. W.; Böhme, M.; Dapprich, S.; Gobbi, A.; Höllwarth, A.; Jonas, V.; Köhler, K. F.; Stegmann, R.; Veldkamp, A.; Frenking, G. Chem. Phys. Lett. 1993, 208, 111. (c) Roy, L. E.; Hay, P. J.; Martin, R. L. J. Chem. Theory Comput. 2008, 4, 1029. (12) (a) Ditchfield, R.; Hehre, W. J.; Pople, J. A. J. Chem. Phys. 1971, 54, 724. (b) Hehre, W. J.; Ditchfield, R.; Pople, J. A. J. Chem. Phys. 1971, 54, 724. (c) Hariharan, P. C.; Pople, J. A. Theor. Chim. Acta. 1973, 28, 213. (13) (a) Zhao, Y.; Truhlar, D. G. Theor. Chem. Acc. 2008, 120, 215. (b) Zhao, Y.; Truhlar, D. G. Acc. Chem. Res. 2008, 41, 157. (14) (a) Dolg, M.; Wedig, U.; Stoll, H.; Preuss, H. J. Chem. Phys. 1987, 86, 866. (b) Andrae, D.; Häußermann, U.; Dolg, M.; Stoll, H.; Preuß, H. Theor. Chem. Acc. 1990, 77, 123. (15) Marenich, A. V.; Cramer, C. J.; Truhlar, D. G. J. Phys. Chem. B 2009, 113, 6378. (16) Legault, C. Y. CYLView, 1.0b; Université de Sherbrooke: Canada, 2009; http://www.cylview.org. (17) (a) Stephenson, T. A.; Morehouse, S. M.; Powell, A. R.; Heffer, J. P.; Wilkinson, G. J. Chem. Soc. 1965, 3632. (b) Skapski, A. C.; Smart, M. L. J. Chem. Soc. D 1970, 658b. (c) Bakhmutov, V. I.; Berry, J. F.; Cotton, F. A.; Ibragimov, S.; Murillo, C. A. Dalton Trans. 2005, 1989. (d) Carole, W. A.; Bradley, J.; Sarwar, M.; Colacot, T. J. Org. Lett. 2015, 17, 5472. (18) Yang, Y.-F.; Cheng, G.-J.; Liu, P.; Leow, D.; Sun, T.-Y.; Chen, P.; Zhang, X.; Yu, J.-Q.; Wu, Y.-D.; Houk, K. N. J. Am. Chem. Soc. 2014, 136, 344. (19) (a) Sanhueza, I. A.; Wagner, A. M.; Sanford, M. S.; Schoenebeck, F. Chem. Sci. 2013, 4, 2767. (20) (a) Powers, D. C.; Xiao, D. Y.; Geibel, M. A. L.; Ritter, T. J. Am. Chem. Soc. 2010, 132, 14530. (b) Powers, D. C.; Ritter, T. Acc. Chem. Res. 2012, 45, 840. (21) Deprez, N. R.; Sanford, M. S. J. Am. Chem. Soc. 2009, 131, 11234. (22) (a) Musaev, D. G.; Kaledin, A.; Shi, B.-F.; Yu, J.-Q. J. Am. Chem. Soc. 2012, 134, 1690. (b) Cheng, G.-J.; Yang, Y.-F.; Liu, P.; Chen, P.; Sun, T.-Y.; Li, G.; Zhang, X.; Houk, K. N.; Yu, J.-Q.; Wu, Y.-D. J. Am. Chem. Soc. 2014, 136, 894. (c) Cheng, G.-J.; Chen, P.; Sun, T.-Y.; Zhang, X.; Yu, J.-Q.; Wu, Y.-D. Chem. - Eur. J. 2015, 21, 11180.

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