Mechanistic insight into hydroxamate transfer reaction mimicking the inhibition of zinc-containing enzymes

Abstract

A hydroxamate transfer reaction between metal complexes has been investigated by a combination of experimental and theoretical studies. A hydroxamate-bound cobalt(II) complex bearing a tetradentate macrocyclic ligand, [CoII(TBDAP)(CH3C(-NHO)O)]+ (1), is...

Controlling Reactivity through Spin Manipulation: Steric Bulkiness of Peroxocobalt(III) Complexes

“…According to reported mechanistic studies on the nitrile activation reaction with 2 Tb , the initial step involves Co–O bond cleavage with nitrile addition, leading to the formation of an η 1 -superoxo species (Scheme ). ,, The transformation into the η 1 -superoxo species is crucial, as it proceeds through intramolecular attacks between superoxo and nitriles, and undergoes additional reactions including homolytic O–O bond cleavage step to form hydroximatocobalt­(III) species. The transformation to the η 1 -superoxo species has feasible reaction barriers for all spin states excluding the CS singlet state.…”

NMR spectroscopic investigations of transition metal complexes in organometallic and bioinorganic chemistry

“…literature. [267][268][269][270][271][272][273][274] For example, M III (acac) 3 complexes (acac = acetylacetonate) with different transition metal centers exhibit different δ H changes, with the highest shift for Fe III and no shift for Co III . Detailed calculations reveal that Fe(acac) 3 and Co(acac) 3 have S = 5/2 and 0, respectively, consistent with the previous literature (Figure 7c).…”

“…1 H NMR measurements yield two signals of the internal standard with different δ H values, affected by the magnetic susceptibility of paramagnetic molecules in the sample solution. The magnetic susceptibility can be calculated by quantifying the δ H change of the internal standard peaks, providing the number of unpaired electrons which is an indicative of the spin state of the paramagnetic species, as reported in various literature 267–274 . For example, M III (acac) 3 complexes (acac = acetylacetonate) with different transition metal centers exhibit different δ H changes, with the highest shift for Fe III and no shift for Co III .…”

The strongin vitroandvivocytotoxicity of three new cobalt(ii) complexes with 8-methoxyquinoline

“…4,5 In addition, cobalt (Co) is an essential element for life, and the study of Co( ii / iii ) coordination compounds for biological and medical applications has flourished more recently. 6 These activated Co( ii / iii ) complexes include hydroxamatocobalt( ii ) complexes, 7 salicylaldehyde-derivative copper( ii ) complexes, 8 phen-dicarboxylic acid based cobalt( ii ) antitumor drugs, 9 cobalt( ii ) oxoisoaporphine complexes, 10 2-benzimidazolyl-pyridine copper( ii ) complexes, 11 thiosemicarbazone cobalt( ii ) complexes, 1 a ,12 diamidonaphthalene cobalt( ii ) complexes, 13 cobalt dioxolene/isonicotinic compounds, 14 tris(2-pyridylmethyl)amine cobalt pro-drugs, 15 cobalt( ii ) pyridyl complexes, 16 and anthraquinone-type cobalt complexes. 17…”

“…4,5 In addition, cobalt (Co) is an essential element for life, and the study of Co(II/III) coordination compounds for biological and medical applications has flourished more recently. 6 These activated Co(II/III) complexes include hydroxamatocobalt(II) complexes, 7 salicylaldehyde-derivative copper(II) complexes, 8 phen-dicarboxylic acid based cobalt(II) antitumor drugs, 9 cobalt(II) oxoisoaporphine complexes, 10 2-benzimidazolyl-pyridine copper(II) complexes, 11 thiosemicarbazone cobalt(II) complexes, 1a,12 diamidonaphthalene cobalt (II) complexes, 13 cobalt dioxolene/isonicotinic compounds, 14 tris(2-pyridylmethyl)amine cobalt pro-drugs, 15 cobalt(II) pyridyl complexes, 16 and anthraquinone-type cobalt complexes. 17 Many different metal 8-hydroxyquinoline derived compounds can function as important DNA inhibitors, 18 protein synthesis inhibitors, 19 amyloid-β (Aβ) oligomer drugs, 20 photosensitizers, 21 mitochondrial apoptosis related antineoplastic agents, 22 bFGF-mediated angiogenesis specific inhibitors, 23 topoisomerase IIa inhibitors, 24 telomerase inhibitors, 25 cell autophagy inductors, 26 and so on.…”