Ring-Opening Polymerization of Lactides by (Pyrazol-1-ylmethyl)pyridine Zn(II) and Cu(II) Complexes: Kinetics, Mechanism and Tacticity Studies

The kinetics, mechanism and polymer microstructure studies of ring-opening polymerization (ROP) of lactides (LA) by Zn(II) and Cu(II) complexes of (pyrazolylmethyl)pyridine ligands, 2-(3,5-dimethylpyrazol-1-ylmethyl)pyridine (L1) and 2-(3,5-diphenylpyrazol-1-ylmethyl)pyridine (L2) is described. The complexes [Zn(Ac)2(L1)] (1), [Cu(Ac)2(L1)] (2), [Zn(Ac)2(L2)] (3) and [Cu2(Ac)4(L2)2] (4) formactive initiators in the ROP of D,L-LA and L-LA monomers. Generally Zn(II) complexes 1 and 3 exhibit higher activities compared to the corresponding Cu(II) complexes 2 and 4. Polymerization kinetics of D,L-LA show higher rates compared to the L-LA reactions. All the polymerization reactions follow pseudo first-order kinetics with respect to monomer while 1 shows second-order dependency on the polymerization reactions. Molecular weights of the polymers range from 813 g mol–1 to 9207 g mol–1 and exhibit relatively narrow molecular weight distributions between 1.2 to 1.6. While poly(D,L-LA) are predominantly atactic, poly(L-LA) are largely isotactic. All polymerization reactions proceed through coordination insertion mechanism followed by hydrolysis of the end groups.KEYWORDS Zinc and copper complexes, lactide, polymerization, kinetics, mechanism.PDF and Supp files attache

(Pyridyl)benzoazole ruthenium(III) complexes: Kinetics of ligand substitution reaction and potential cytotoxic properties

The present work investigates the kinetics of ligand substitution reaction and anticancer activities of the complexes, [{2-(2-pyridyl) benzimidazole} RuCl3] (C1), [{2-(2-pyridyl) benzoxazole} RuCl3] (C2), [{2-(2-pyridyl) benzothiazole} RuCl3] (C3) and [{1-propyl-2- (pyridin-2-yl)-H-benzoimidazole} RuCl3] (C4). The substitution kinetics reaction of the complexes with the three bio-relevant nucleophiles, viz.: thiourea (TU), 1, 3-dimethyl-2-thiourea (DMTU) and 1, 1, 3, 3-tetramethyl-2-thiourea (TMTU) was investigated under pseudo first-order conditions as a function of concentration and temperature using UV–Visible spectrophotometer. The substitution of the coordinated chloride was controlled by the electronic effect. The order of reactivity of the complexes with the nucleophiles is in the form C1 > C2 > C3 > C4 which is in line with the density functional theory (DFT) studies. The complexes showed minimal anticancer activity against the HeLa cell line, which is in contrast to the molecular docking experiments that exhibited stronger DNA binding affinities. © 2018 Elsevier B.V

Structural, DNA/BSA binding interactions and cytotoxicity studies of carboxamide (pyridyl)pyrazine palladium(II) complexes

Reactions of ligands [N2, N3-bis(pyridin-2-yl)pyrazine-2,3-dicarboxamide] (L1), [N2, N3-bis(6-methylpyridin-2- yl)pyrazine-2,3-dicarboxamide] (L2), [N2,N3-bis(4-methylpyridin-2-yl)pyrazine-2,3-dicarboxamide] (L3) and [N2, N3-bis(quinoline-8-yl)pyrazine-2,3-dicarboxamide] (L4) with [PdCl2(NCMe)2] afforded the respective palladium(II) complexes: [Pd2(L1)2Cl2] (Pd1), [Pd2(L2)2Cl2] (Pd2), [Pd2(L3)2Cl2] (Pd3) and [Pd(L4)Cl] (Pd4). Molecular structures of complexes Pd1 and Pd3 are dinuclear containing two bridging bidentate ligand units. The interactions of the palladium complexes (Pd1-Pd4) with calf thymus DNA (CT-DNA) were monitored using UV–Vis and fluorescence spectroscopy and revealed intercalative binding modes, with intrinsic binding constants (Kb) in the order of 106 M1. Bovine serum albumin (BSA) interaction was evaluated using fluorescence techniques and displayed a static quenching mechanism. The cytotoxic effects of the complexes Pd1-Pd4 were examined against human breast cancer cell lines MCF-7 and MDA-MB-231, and human transformed lung cell line MRC5-SV2 (a model of lung cancer) and its parental normal lung fibroblast cell line MRC5. While the complexes Pd1 and Pd4 showed significant to moderate cytotoxicity against MCF-7 (IC50 of 11.2 µM and 61.5 µM, respectively), complexes Pd2 and Pd3 were inactive. All the complexes were inactive against the MDA-MB-231 cell line, and Pd2-Pd4 were inactive against the MRC5-SV2 cell line. Compounds Pd1 exhibited lower cytotoxicity against the normal cell line MRC5

Novel OˆNˆN Pyrazolyl-imine and Imidazolyl-imine Pincer Palladium Complexes as Heck Coupling Catalysts

Five pyrazolyl and imidazolyl compounds, 2,4-di-tert-butyl-6-[2-pyrazol-1-yl-ethylimino-methyl]-phenol (L1), 2,4-di-tert-butyl-6-{[2- (3,5-dimethyl-pyrazol-1-yl)-ethylimino]-methyl}-phenol (L2), 2,4-di-tert-butyl-6-{[2-(1H-imidazol-4-yl)-ethylimino]-methyl}-phenol (L3), 4-tert-butyl-2-{[2-(1H-imidazole-4-yl)-ethylimino]-methly}-phenol (L4) and 2-{[2-(1H-imidazole-4-yl)-ethylimino]-methly}-phenol (L5) were synthesized by condensation of the appropriate 2-hydroxybenzaldehyde and the corresponding alkylamine. Reactions of L1–L5 with either [Pd(NCMe)2Cl2] or [Pd(COD)MeCl] led to in situ deprotonation of the phenolic-OH proton to afford the pincer palladium complexes [Pd(L1)Cl] (1), [Pd(L1)Me] (2), [Pd(L2)Cl] (3), [Pd(L3)Cl] (4),[Pd(L4)Cl] (5) and [Pd(L5)Cl] (6). The tridentate coordination modes of the ligands were confirmed by the solid state structures of 1, 2, 3 and 4.H2O. Complexes 1–6 catalyzed the Heck coupling reactions of iodobenzene and butylacrylate. In addition, complex 4 catalyzed the Heck coupling reaction of butyl acrylate and bromobenzene; giving conversions as high as 70 %.Keywords: Pincer palladium complexes, pyrazolyl-imine, imidazolyl imine, aryl halides, Heck coupling catalyst