SPh functionalized bridging-vinyliminium diiron and diruthenium complexes

The SPh functionalized vinyliminium complexes [Fe2{μ-η1:η3-Cγ(R′)Cβ(SPh)CαN(Me)(R)}(μ-CO)(CO)(Cp)2][SO3CF3] [R = Xyl, R′ = Me, 2a; R = Me, R′ = Me, 2b; R = 4-C6H4OMe, R′ = Me, 2c; R = Xyl, R′ = CH2OH, 2d; R = Me, R′ = CH2OH, 2e; Xyl = 2,6-Me2C6H3] are generated in high yields by treatment of the corresponding vinyliminium complexes [Fe2{μ-η1:η3-Cγ(R′)Cβ(H)CαN(Me)(R)}(μ-CO)(CO)(Cp)2][SO3CF3] (1a–e) with NaH in the presence of PhSSPh. Likewise, the diruthenium complex [Ru2{μ-η1:η3-Cγ(Me)Cβ(SPh)CαN(Me)(Xyl)}(μ-CO)(CO)(Cp)2][SO3CF3] (2f) was obtained from the corresponding vinyliminium complex [Ru2{μ-η1:η3-Cγ(Me)Cβ(H)CαN(Me)(Xyl)}(μ-CO)(CO)(Cp)2] (1f). The synthesis of 2c is accompanied by the formation, in comparable amounts, of the aminocarbyne complex [Fe2{μ-CN(Me)(4-C6H4OMe)}(SPh)(μ-CO)(CO)(Cp)2] (3). The molecular structures of 2d, 2e and 3 have been determined by X-ray diffraction studies

Hydride addition at m-vinyliminium ligand obtained from disubstituted alkynes

New μ-vinylalkylidene complexes cis-[Fe2{μ-η1:η3-Cγ(R′)Cβ(R″)CαHN(Me)(R)}(μ-CO)(CO)(Cp)2] (R = Me, R′ = R″ = Me, 3a; R = Me, R′ = R″ = Et, 3b; R = Me, R′ = R″ = Ph, 3c; R = CH2Ph, R′ = R″ = Me, 3d; R = CH2Ph, R′ = R″ = COOMe, 3e; R = CH2 Ph, R′ = SiMe3, R″ = Me, 3f) have been obtained b yreacting the corresponding vinyliminium complexes [Fe2{μ-η1:η3-Cγ(R′)Cβ(R″)CαN(Me)(R)}(μ-CO)(CO)(Cp)2][SO3CF3] (2a–f) with NaBH4. The formation of 3a–f occurs via selective hydride addition at the iminium carbon (Cα) of the precursors 2a–f. By contrast, the vinyliminiumcis-[Fe2{μ-η1:η3-Cγ (R′) = Cβ(R″)Cα = N(Me)(Xyl)}(μ-CO)(CO)(Cp)2][SO3CF3] (R′ = R″ = COOMe, 4a; R′ = R″ = Me, 4b; R′ = Prn, R″ = Me, 4c; Prn = CH2CH2CH3, Xyl = 2,6-Me2C6H3) undergo H− addition at the adjacent Cβ, affording the bis-alkylidene complexes cis-[Fe2{μ-η1:η2-C(R′)C(H)(R″)CN(Me)(Xyl)}(μ-CO)(CO)(Cp)2], (5a–c). The cis and trans isomers of [Fe2{μ-η1:η3-Cγ(Et)Cβ(Et)CαN(Me)(Xyl)}(μ-CO)(CO)(Cp)2][SO3CF3] (4d) react differently with NaBH4: the former reacts at Cα yielding cis-[Fe2{μ-η1:η3-Cγ(Et)Cβ(Et)CαHN(Me)(Xyl)}(μ-CO)(CO)(Cp)2], 6a, whereas the hydride attack occurs at Cβ of the latter, leading to the formation of the bis alkylidene trans-[Fe2{μ-η1:η2-C(Et)C(H)(Et)CN(Me)(Xyl)}(μ-CO)(CO)(Cp)2] (5d). The structure of 5d has been determined by an X-ray diffraction study. Other μ-vinylalkylidene complexes cis-[Fe2{μ-η1:η3-Cγ(R′)Cβ(R″)CαHN(Me)(Xyl)}(μ-CO)(CO)(Cp)2], (R′ = R″ = Ph, 6b; R′ = R″ = Me, 6c) have been prepared, and the structure of 6c has been determined by X-ray diffraction. Compound 6b results from treatment of cis-[Fe2{μ-η1:η3-Cγ(Ph)Cβ(Ph)CαN(Me)(Xyl)}(μ-CO)(CO)(Cp)2][SO3CF3] (4e) with NaBH4, whereas 6c has been obtained by reacting 4b with LiHBEt3. Both cis-4d and trans-4d react with LiHBEt3 affording cis-6a

Stereochemistry of the insertion of disubstituted alkynes into the metal aminocarbyne bond in diiron complexes

Terminal alkynes (HCdropCR') (R'=COOMe, CH2OH) insert into the metal-carbyne bond of the diiron complexes [Fe-2{mu-CN(Me)(R)} (mu-CO)(CO)(NCMe)(Cp)(2)][SO3CF3] (R=Xyl, 1a; CH2Ph, 1b; Me, 1c; Xyl=2,6-Me2C6H3), affording the corresponding mu-vinyliminium complexes [Fe-2{mu-sigma:eta(3)-C(R')=CHC=N(Me)(R)}(mu-CO)(CO)(Cp)(2)][SO3CF3] (R=Xyl, R'=COOMe, 2; R=CH2Ph, R'=COOMe, 3; R=Me, R'=COOMe, 4; R=Xyl, R'=CH2OH, 5; R=Me, R'=CH2OH, 6). The insertion is regiospecific and C-C bond formation selectively occurs between the carbyne carbon and the CH moiety of the alkyne. Disubstituted alkynes (R'CdropCR') also insert into the metal-carbyne bond leading to the formation of [Fe-2{mu-sigma:eta(3)- C(R')=C(R')C=N(Me)(R)}(mu-CO)(CO)(Cp)(2)][SO3CF3] (R'=Me, R=Xyl, 8; R'=Et, R=Xyl, 9; R'=COOMe, R=Xyl, 10; R'=COOMe, R=CH2Ph, 11; R'= COOMe, R=Me, 12). Complexes 2, 3, 5, 8, 9 and 11, in which the iminium nitrogen is unsymmetrically substituted, give rise to E and/or Z isomers. When iminium substituents are Me and Xyl, the NMR and structural investigations (X-ray structure analysis of 2 and 8) indicate that complexes obtained from terminal alkynes preferentially adopt the E configuration, whereas those derived from internal alkynes are exclusively Z. In complexes 8 and 9, trans and cis isomers have been observed, by NMR spectroscopy, and the structures of trans-8 and cis-8 have been determined by X-ray diffraction studies. Trans to cis isomerization occurs upon heating in THF at reflux temperature. In contrast to the case of HCdropCR', the insertion of 2-hexyne is not regiospecific: both [Fe-2{mu-sigma:eta(3)-C(CH2CH2CH3)=C(Me)C=N(Me)(R)} (mu-CO)(CO)(Cp)(2)][SO3CF3] (R=Xyl, 13; R=Me, 15) and [Fe-2{mu-sigma:eta(3)-C(Me)=C(CH2CH2CH3)C=N(Me)(R)}(mu-CO)(CO)(Cp)(2)][SO3CF3] (R=Xyl, 14, R=Me, 16) are obtained and these compounds are present in solution as a mixture of cis and trans isomers, with predominance of the former

Atomically Precise Ni-Pd Alloy Carbonyl Nanoclusters: Synthesis, Total Structure, Electrochemistry, Spectroelectrochemistry, and Electrochemical Impedance Spectroscopy

The molecular nanocluster [Ni36-xPd5+x(CO)46]6- (x = 0.41) (16-) was obtained from the reaction of [NMe3(CH2Ph)]2[Ni6(CO)12] with 0.8 molar equivalent of [Pd(CH3CN)4][BF4]2 in tetrahydrofuran (thf). In contrast, [Ni37-xPd7+x(CO)48]6- (x = 0.69) (26-) and [HNi37-xPd7+x(CO)48]5- (x = 0.53) (35-) were obtained from the reactions of [NBu4]2[Ni6(CO)12] with 0.9-1.0 molar equivalent of [Pd(CH3CN)4][BF4]2 in thf. After workup, 35- was extracted in acetone, whereas 26- was soluble in CH3CN. The total structures of 16-, 26-, and 35- were determined with atomic precision by single-crystal X-ray diffraction. Their metal cores adopted cubic close packed structures and displayed both substitutional and compositional disorder, in light of the fact that some positions could be occupied by either Ni or Pd. The redox behavior of these new Ni-Pd molecular alloy nanoclusters was investigated by cyclic voltammetry and in situ infrared spectroelectrochemistry. All three compounds 16-, 26-, and 35- displayed several reversible redox processes and behaved as electron sinks and molecular nanocapacitors. Moreover, to gain insight into the factors that affect the current-potential profiles, cyclic voltammograms were recorded at both Pt and glassy carbon working electrodes and electrochemical impedance spectroscopy experiments performed for the first time on molecular carbonyl nanoclusters

Anticancer ruthenium(ii) tris(pyrazolyl)methane complexes with bioactive co-ligands

In comparison with RuII-arene compounds, the medicinal potential of homologous RuII-tpm compounds [tpm = tris(pyrazolyl)methane] is underexplored. Pyridine, 4-pyridinemethanol and four functionalized pyridines, synthesized from the esterification of 4-pyridinemethanol with bioactive carboxylic acids (i.e., ethacrynic acid, ibuprofen, flurbiprofen and naproxen), react with the precursor [RuCl(κ3-tpm)(PPh3)2]Cl (1) to afford [RuCl(κ3-tpm)(PPh3)(L)]Cl (2-7, L = pyridine ligand), in 78-91% yields. All products were fully characterized by HR-ESI mass spectrometry, IR and multinuclear NMR spectroscopy and the solid-state structures of two of the complexes, i.e. where L = pyridine and 4-pyridinemethanol, were ascertained by single crystal X-ray diffraction. The {Ru-tpm-PPh3} assembly is stable in D2O and in biological medium (DMEM) at 37 °C, with a tendency to slowly dissociate the pyridine ligand. The antiproliferative activity of the complexes was assessed on the cancerous A2780 and A2780cisR cell lines, and the nontumoral HEK 293T cell line; moreover inhibition assays were carried out on the complexes towards COX-2 and GSTP1 enzymes

Modulating the water oxidation catalytic activity of iridium complexes by functionalizing the Cp*-ancillary ligand: hints on the nature of the active species

The catalytic activity toward NaIO4driven water oxidation of a series of [RCp*IrCl(μ-Cl)]2dimeric precursors, containing tetramethylcyclopentadienyl ligands with a variable R substituent (H,1; Me,2; Et,3;nPr,4; CH2CH2NH3+,5; Ph,6; 4-C6H4F,7; 4-C6H4OH,8; Bn,9), has been evaluated at 298 K and pH = 7 (with phosphate buffer). For each dimer, the effect of changing the catalyst (1-10 μM) and NaIO4(5-40 mM) concentration has been studied. All precursors exhibit a high activity with TOF values ranging from 101 min−1to 393 min−1and TON values being always those expected assuming a 100% yield. The catalytic activity was strongly affected by the nature of the R substituent. The highest TOF values were observed when R was electron-donating and small. The results of multiple consecutive injection experiments suggest that a fragment of the initial C5Me4R, still bearing the R-substituent, remains attached at iridium in the active species, despite the oxidativein situdegradation of the same ligand. The decrease of TOF in the second and third catalytic runs was completely ascribed to a drop of the redox potential caused by the conversion of IO4−into IO3−, according to the Nernst equation. This hypothesis was verified by performing catalytic experiments in which the initial redox potential (ΔE) was deliberately varied by using water solutions of IO4−/IO3−mixtures at different relative concentrations. Consistently, TOFversusΔEplots show that, for a given catalyst, the same TOF is obtained at a certain redox potential, irrespective of the initial reaction conditions used. All seems to indicate that after a short activation period, during which the transformation of the precursors occurs, individual active species for each dimer form and remain the same also after multiple additions of the sacrificial oxidant. It can be speculated that such active species are small iridium clusters bearing R-functionalized likelyO,O-bidentate ligands

Ruthenium(II) Tris-Pyrazolylmethane Complexes in Transfer Hydrogenation Reactions

While ruthenium(II) arene complexes have been widely investigated for their potential in catalytic transfer hydrogenation, studies on homologous compounds replacing the arene ligand with the six-electron donor tris(1-pyrazolyl)methane (tpm) are almost absent in the literature. The reactions of [RuCl(κ3-tpm)(PPh3)2]Cl, 1, with a series of nitrogen ligands (L) proceeded with selective PPh3 mono-substitution, affording the novel complexes [RuCl(κ3-tpm)(PPh3)(L)]Cl (L=NCMe, 2; NCPh, 3; imidazole, 4) in almost quantitative yields. Products 2–4 were fully characterized by IR and multinuclear NMR spectroscopy, moreover the molecular structure of 4 was ascertained by single crystal X-ray diffraction. Compounds 2–4 were evaluated as catalytic precursors in the transfer hydrogenation of a series of ketones with isopropanol as the hydrogen source, and 2 exhibited the highest activity. Extensive NMR experiments and DFT calculations allowed to elucidate the mechanism of the transfer hydrogenation process, suggesting the crucial role played by the tpm ligand, reversibly switching from tri- to bidentate coordination during the catalytic cycle

Human dyskerin binds to cytoplasmic H/ACA-box-containing transcripts affecting nuclear hormone receptor dependence

Background Dyskerin is a nuclear protein involved in H/ACA box snoRNA-guided uridine modification of RNA. In humans, its defective function is associated with cancer development and induces specific post-transcriptional alterations of gene expression. In this study, we seek to unbiasedly identify mRNAs regulated by dyskerin in human breast cancer-derived cells. Results We find that dyskerin depletion affects the expression and the association with polysomes of selected mRNA isoforms characterized by the retention of H/ACA box snoRNA-containing introns. These snoRNA retaining transcripts (snoRTs) are bound by dyskerin in the cytoplasm in the form of shorter 3 ' snoRT fragments. We then characterize the whole cytoplasmic dyskerin RNA interactome and find both H/ACA box snoRTs and protein-coding transcripts which may be targeted by the snoRTs' guide properties. Since a fraction of these protein-coding transcripts is involved in the nuclear hormone receptor binding, we test to see if this specific activity is affected by dyskerin. Obtained results indicate that dyskerin dysregulation may alter the dependence on nuclear hormone receptor ligands in breast cancer cells. These results are paralleled by consistent observations on the outcome of primary breast cancer patients stratified according to their tumor hormonal status. Accordingly, experiments in nude mice show that the reduction of dyskerin levels in estrogen-dependent cells favors xenograft development in the absence of estrogen supplementation. Conclusions Our work suggests a cytoplasmic function for dyskerin which could affect mRNA post-transcriptional networks relevant for nuclear hormone receptor functions