1359998-80-3

Upstream product

• 14243-64-2 (triphenylphosphine)gold(I) chloride 
• 1137-68-4 2-(2'-pyridyl)benzimidazole 
• 95-54-5 1,2-diamino-benzene 
• 98-98-6 2-Picolinic acid 
• 1359998-79-0 [(2-(2-pyridyl)benzimidazole)Au(triphenylphosphine)][PF₆] 

Relevant academic research and scientific papers

Combined effect of caspase-dependent and caspase-independent apoptosis in the anticancer activity of gold complexes with phosphine and benzimidazole derivatives

Since the potential anticancer activity of auranofin was discovered, gold compounds have attracted interest with a view to developing anticancer agents that follow cytotoxic mechanisms other than cisplatin. Two benzimidazole gold(I) derivatives containing triphenylphosphine (Au(pben)(PPh3 )) (1) or triethylphosphine (Au(pben)(PEt3 )) (2) were prepared and characterized by standard techniques. X-ray crystal structures for 1 and 2 were solved. The cytotoxicity of 1 and 2 was tested in human neuroblastoma SH-SY5Y cells. Cells were incubated with compounds for 24 h with concentrations ranging from 10 μM to 1 nM, and the half-maximal inhibitory concentration (IC50 ) was determined. 1 and 2 showed an IC50 of 2.7 and 1.6 μM, respectively. In order to better understand the type of cell death induced by compounds, neuroblastoma cells were stained with Annexin-FITC and propidium iodide. The fluorescence analysis revealed that compounds were inducing apoptosis; however, pre-treatment with the caspase inhibitor Z-VAD did not reduce cell death. Analysis of compound effects on caspase-3 activity and reactive oxygen species (ROS) production in SH-SY5Y cells revealed an antiproliferative ability mediated through oxidative stress and both caspase-dependent and caspase-independent mechanisms.

Structure-activity relationships in cytotoxic AuI/Au III complexes derived from 2-(2′-pyridyl)benzimidazole

Gold(I) and gold(III) complexes derived from 2-(2′-pyridyl) benzimidazole (pbiH) were proven to be a promising class of in vitro antitumor agents against A2780 human ovarian cancer cells. In this paper, a comparative electrochemical, UV-vis absorption, and emission spectroscopic investigation is reported on pbiH, the two mononuclear AuIII complexes [(pbi)AuX 2] (X = Cl (1), AcO (2)), the four mononuclear AuI derivatives [(pbiH)AuCl] (3), [(pbiH)Au(PPh3)]PF6 ((4 +)(PF6-)), [(pbi)Au(PPh3)] (5), and [(pbi)Au(TPA)] (6), the three mixed-valence AuIII/AuI complexes [(μ-pbi)Au2Cl3] (7), [(Ph3P) Au(μ-pbi)AuX2]PF6 (X = Cl ((8+)(PF 6-)), AcO ((9+)(PF6-))), and the binuclear AuI-AuI compound [(μ-pbi)Au 2(PPh3)2]PF6 ((10 +)(PF6-)). All complexes feature irreversible reduction processes related to the AuIII/AuI or Au I/Au0 processes and peculiar luminescent emission at about 360-370 nm in CH2Cl2, with quantum yields that are remarkably lower ((0.7-14.5) × 10-2) in comparison to that determined for the free pbiH ligand (31.5 × 10-2) in the same solvent. The spectroscopic and electrochemical properties of all complexes were interpreted on the grounds of time-dependent PBE0/DFT calculations carried out both in the gas phase and in CH2Cl2 implicitly considered within the IEF-PCM SCRF approach. The electronic structure of the complexes, and in particular the energy and composition of the Kohn-Sham LUMOs, can be related to the antiproliferative properties against the A2780 ovarian carcinoma cell line, providing sound quantitative structure-activity relationships and shedding a light on the role played by the global charge and nature of ancillary ligands in the effectiveness of Au-based antitumor drugs.

Synthesis, structural characterization, solution behavior, and in vitro antiproliferative properties of a series of gold complexes with 2-(2′-pyridyl)benzimidazole as ligand: Comparisons of gold(III) versus gold(I) and mononuclear versus binuclear derivatives

A variety of gold(III) and gold(I) derivatives of 2-(2′-pyridyl) benzimidazole (pbiH) were synthesized and fully characterized and their antiproliferative properties evaluated in a representative ovarian cancer cell line. The complexes include the mononuclear species [(pbi)AuX2] (X = Cl, 1; OAc, 2), [(pbiH)AuCl] (3), [(pbiH)Au(PPh3)][PF6] (4-PF6), and [(pbi)Au(L)] (L = PPh3, 5; TPA, 6), and the binuclear gold(I)/gold(I) and gold(I)/gold(III) derivatives [(PPh 3)2Au2(μ2-pbi)][PF6] (10-PF6), [ClAu(μ3-pbi)AuCl2] (7),and [(PPh3)Au(μ3-pbi)AuX2][PF6] (X = Cl, 8-PF6; OAc, 9-PF6). The molecular structures of 6, 7, and 10-PF6 were determined by X-ray diffraction analysis. The chemical behavior of these compounds in solution was analyzed both by cyclic voltammetry in DMF and absorption UV-vis spectroscopy in an aqueous buffer. Overall, the stability of these gold compounds was found to be acceptable for the cellular studies. For all complexes, relevant antiproliferative activities in vitro were documented against A2780 human ovarian carcinoma cells, either resistant or sensitive to cisplatin, with IC50 values falling in the low micromolar or even in the nanomolar range. The investigated gold compounds were found to overcome resistance to cisplatin to a large degree. Results are interpreted and discussed in the frame of current knowledge on cytotoxic and antitumor gold compounds.