We report the synthesis and structural characterization of a dicobalt(III) complex with a μ-OH,μ-O2 core, namely μ-OH,μ-O2-[Co(enN4)]2(X)3 [1(ClO4)3 and 1(BF4)3]. The dinuclear core is cross-linked by two N4 Schiff base ligands that span each cobalt center. The formally Co(III)-Co(III) dimer is formed spontaneously upon exposure of the mononuclear Co(II) complex to air and exhibits a ν(O-O) value at 882 cm(-1) that shifts to 833 cm(-1) upon substitution with (18)O2. The CV of 1(BF4)3 exhibits a reversible {Co(III)-Co(III)}↔{Co(III)-Co(IV)} redox process, and we have investigated the oxidized {Co(III)-Co(IV)} species by EPR spectroscopy (g = 2.02, 2.06; S = 1/2 signal) and DFT calculations.

We report the synthesis of two fluoride bridged cobalt(ii) dimers - [Co(μ-F)(pnN4-PhCl)2(OH2)(MeCN)](BF4)3 (1) and [Co(μ-F)2(pnN4-PhCl)2](BF4)2 (2) - and related complexes derived from propyl-bridged N4 Schiff base plus pyridine ligands. Notably, the bridging fluoride ion(s) emanate from B-F abstraction processes on the BF4 anions in the starting salt, [Co(H2O)6](BF4)2. Two types of bridging motifs are generated - mono-bridged (μ-F) or di-bridged (μ-F)2- synthetically differentiated by the absence or presence of pyridine, respectively, during metalation. The synergistic roles of pyridine and the (ClPh)N4 ligand in promoting B-F abstraction were clarified by the isolation and crystallization of the simple tetrakis-pyridine monomeric complex [Co(py)4(MeCN)2](BF4)2 (4) [no B-F abstraction]; subsequent addition of the (ClPh)N4 ligand to 4 resulted in formation of the dimeric, di-bridged complex 2. Omission of pyridine during metalation resulted in formation of the mono-bridged dimer 1. The bulky chlorophenyl substituents were obligate for B-F abstraction, as metalation of the unsubstituted N4 ligand resulted in the non-fluoride-bridged dimer, [Co(pnN4)3](BF4)4 (3). In magnetic studies, complexes 1 (μeff = 6.24μB, 298 K) and 2 (μeff = 7.70μB, 298 K) both exhibit antiferromagnetic (AFM) coupling, but to different extents. Temperature-dependent magnetic susceptibility measurements (SQUID, 2 → 300 K) reveal that the linearity of the mono-fluoride bridge in 1 [∠Co-F-Co = 159.47(11)°] results in very strong AFM coupling (J = -14.9 cm(-1)). In contrast, the more acute Co2F2 diamond core [∠Co-F-Co = 98.8(2)°, 99.1(2)°] results in a smaller extent of AFM coupling (J = -2.97 cm(-1)). Overall, the results indicate the 'non-innocence' of the BF4 counterion in cobalt(ii) chemistry, and dimers 1 and 2 affirm the effect of the geometry of the bridging fluoride ion(s) in determining the extent of AFM coupling.

We report syntheses and H2 activation involving model complexes of mono-iron hydrogenase (Hmd) derived from acyl-containing pincer ligand precursors bearing thioether (CNS Pre ) or phosphine (CNP Pre ) donor sets. Both complexes feature pseudo-octahedral iron­(II) dicarbonyl units. While the CNS pincer adopts the expected mer-CNS (pincer) geometry, the CNP ligand unexpectedly adopts the fac-CNP coordination geometry. Both complexes exhibit surprisingly acidic methylene C–H bond (reversibly de/protonated by a bulky phenolate), which affords a putative dearomatized pyridinate-bound intermediate. Such base treatment of Fe-CNS also results in deligation of the thioether sulfur donor, generating an open coordination site trans from the acyl unit. In contrast, Fe-CNP maintains a CO ligand trans from the acyl site both in the parent and dearomatized complexes (the −PPh2 donor is cis to acyl). The dearomatized mer-Fe-CNS was competent for H2 activation (5 atm D2(g) plus phenolate as base), which is attributed to both the basic site on the ligand framework and the open coordination site trans to the acyl donor. In contrast, the dearomatized fac-Fe-CNP was not competent for H2 activation, which is ascribed to the blocked coordination site trans from acyl (occupied by CO ligand). These results highlight the importance of both (i) the open coordination site trans to the organometallic acyl donor and (ii) a pendant base in the enzyme active site.

Microbial type II polyketides serve as powerful medicinally relevant agents. These molecules are biosynthesized by polyketide synthases (PKSs) comprised of a core ketosynthase-chain length factor (KS-CLF) and phosphopantetheinylated acyl carrier protein (holo-ACP). While engineering type II PKSs holds potential to unlock sustainable access to diverse bioactive molecules, the inability to obtain cognate type II KS-CLFs andholo-ACPs forin vitrostudies represents a longstanding barrier. Herein, we share how the sequence and structural analysis of theGloeocapsa sp.PCC 7428 ACP allowed us to tune to a requisite weak yet specific interaction with a phosphopantetheinyl transferase to afford theholo-ACP. This, coupled with our ability to heterologously express the cognate KS-CLF in high quantities, unlocked access to polyketide products viain vitromultienzyme assembly. We hope this work inspires future studies of type II PKSs that have previously evaded heterologous expression or have yet to be explored.Abstract Figure