41290-68-0

Upstream product

• 14898-67-0 ruthenium(III) chloride trihydrate 
• 67-68-5 dimethyl sulfoxide 
• 118541-65-4 mer-trichlorotris(dimethylsulfoxide)ruthenium(III) 
• 194497-67-1 cis-{RuCl₂(Me₂SO)4} 
• 194497-67-1 trans-RuCl₂(Me₂SO)4 
• 14898-67-0 ruthenium trichloride hydrate 
• 10025-69-1 tin(II) chloride dihdyrate 
• 10049-08-8 ruthenium(III)chloride 
• 63767-78-2 ruthenium trichloride 

Downstream Products

• 31790-57-5 {tris(4,4'-diphenyl-2,2'-bipyridine)ruthenium(II)}Cl₂ 
• 24162-09-2 Ru(phen)₃²⁺ 
• 112220-32-3 RuCl₂(OS(CH₃)2)(CH₃C(CH₂As(C₆H₅)2)3) 
• 67-68-5 dimethyl sulfoxide 
• 103500-17-0 [tris(μ-chloro)bis((triphos)ruthenium(II))] chloride 
• 172703-18-3 trans-RuCl2(κ4-N,N'-bis[o-(dipenylphosphino)benzylidene]-1,2-diaminoethane) 
• 494871-39-5 dichloro [2-(N-(2-hydroxyphenyl)carbamoyl)pyridine]bis(dimethylsulfoxide)ruthenium(II) 
• 1056478-85-3 trans-[ruthenium(II)Cl bis(triphenylphosphane)(C₁₄H₈ON₂CNH₂S)] 

Relevant academic research and scientific papers

Different Bonding Modes for 6-(2-Thienyl)-2,2'-bipyridine at Rutheniuim(II); the Structural Characterization of

The ligand 6-(2-thienyl)-2,2'-bipyridine (HL) forms ruthenium complexes in which it acts as a terdentate N,N,S-donor, a bidentate N,N-donor, and in a deprotonated form a terdentate N,N,C-donor; the complex has been structurally characteri

Synthesis and Characterization of an Epidermal Growth Factor Receptor-Selective RuII Polypyridyl–Nanobody Conjugate as a Photosensitizer for Photodynamic Therapy

There is a current surge of interest in the development of novel photosensitizers (PSs) for photodynamic therapy (PDT), as those currently approved are not completely ideal. Among the tested compounds, we have previously investigated the use of RuII

Preparation method of ruthenium tetra(dimethyl sulfoxide) dichloride metalloorganic compound

The molecular formula of a ruthenium tetra(dimethyl sulfoxide) dichloride metalloorganic compound is RuCl2 (DMSO)4, and the preparation method comprises the following steps: adding dimethyl sulfoxideinto a ruthenium reagent, reacting for 12-48 hours at the temperature of 80-90 DEG C until yellow precipitate appears, filtering to obtain a yellow solid, washing the yellow solid with acetone and diethyl ether respectively, and airing in air to obtain the ruthenium tetra(dimethyl sulfoxide) dichloride metalloorganic compound RuCl2 (DMSO)4 containing the dimethyl sulfoxide ligand. Many ruthenium metal complexes with novel structures and special functional properties can be prepared through the ruthenium tetra(dimethyl sulfoxide) dichloride metalloorganic compound, and more possibilities are provided for design and construction of functional complexes. Good potential application is realized in the aspects of molecular-based magnetic materials, nonlinear optical materials, selective catalysis, molecular recognition, gas adsorption, photoelectric materials and the like.

Tris-heteroleptic ruthenium(II) polypyridyl complexes: Synthesis, structural characterization, photophysical, electrochemistry and biological properties

Three water-soluble tris-heteroleptic ruthenium(II) polypyridyl complexes [Ru(bpy)(phen)(bpg)]2+ (1), [Ru(bpy)(dppz)(bpg)]2+ (2), and [Ru(phen)(dppz)(bpg)]2+ (3) (where bpy = 2,2′-bipyridine, phen = 1,10-phenanthroline, dppz = dipyrido[3,2-a:2′,3′-c] phenazine, bpg = 4b,5,7,7a-tetrahydro-4b,7a-epiminomethanoimino-6H-imidazo[4,5-f] [1,10] phenanthroline-6,13-dione) have been synthesized and characterized. Molecular structures of complexes 1 and 3 are confirmed by single crystal X-ray structure determination. Interaction of complexes 1–3 with DNA is explored by various spectroscopic techniques. The complexes 1–3 show solvent dependent photophysical properties. Complexes 2 and 3 show extensive “molecular light switch” effect for DNA. The complexes 1–3 are low toxic towards HeLa (human cervical cancer) and HL-60 (human promyelocytic leukemia) cell lines. Further, the cellular uptake of complexes 2 and 3 by cells shows that complexes mainly localised on the nucleus of the cells.

Nitro reduction-based fluorescent probes for carbon monoxide require reactivity involving a ruthenium carbonyl moiety

Recently, several arylnitro-based fluorescent CO probes have been reported. The design was based on CO's ability to reduce an arylnitro group for fluorescence turn-on. In this work, we assessed the response of three published arylnitro-based fluorescent C

Synthesis, characterization and biological evaluation of ruthenium flavanol complexes against breast cancer

Four Ru(II) DMSO complexes (M1R-M4R) having substituted flavones viz. 3-Hydroxy-2-(4-methoxyphenyl)-4H-chromen-4-one (HL1), 3-Hydroxy-2-(4-nitrophenyl)-4H-chromen-4-one (HL2), 3-Hydroxy-2-(4-dimethylaminophenyl)-4H–chromen-4-one (HL3) and 3-Hydroxy-2-(4-chlorophenyl)-4H-chromen-4-one (HL4) were synthesized and characterized by elemental analysis, IR, UV–Vis, 1H NMR spectroscopies and ESI-MS. The molecular structures of the complexes were investigated by integrated spectroscopic and computational techniques (DFT). Both ligands as well as their complexes were screened for anticancer activities against breast cancer cell lines MCF-7. Cytotoxicity was assayed by MTT [3-(4, 5-dimethyl thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide] assay. All ligands and their complexes exhibited significant cytotoxic potential of 5–40?μM concentration at incubation period of 24?h. The cell cytotoxicity increased significantly in a concentration-dependent manner. In this series of compounds, HL2 (IC50 17.2?μM) and its complex M2R (IC50 16?μM) induced the highest cytotoxicity.

Synthesis, reactivities and anti-cancer properties of ruthenium(II) complexes with a thiaether macrocyclic ligand

Drug resistance and severe patient side-effects of Pt drugs have spurred research into other metal-based pharmaceuticals and recently Ru complexes have been identified as promising anti-cancer drugs. A series of RuIIcomplexes [RuX2([9]aneS3)(S-dmso)] (X = Cl, Br, I, S-dmso = sulfur-bound dimethylsulfoxide) containing the neutral face-capping sulfur macrocycle ligand, 1,4,7-trithiacyclononane ([9]aneS3) was synthesized, characterized and their substitution reactions and biological activities were investigated. While the iodido complex was not sufficiently soluble for detailed studies, [RuCl2([9]aneS3)(S-dmso)] and [RuBr2([9]aneS3)(S-dmso)] were investigated to determine whether there was a direct relationship between the rates of halido ligand substitution (determined by UV/vis spectroscopy and X-ray absorption spectroscopy) and anti-cancer activities. A two-stage halido substitution process occurred in HEPES buffer (pH 7.4, 310 K). The rate constants for chlorido substitution were a factor of two larger than for the bromido analogue ((4.5 ± 0.2) × 10?4and (1.5 ± 0.1) × 10?4s?1for the chlorido complex and (2.6 ± 0.2) × 10?4and (9.2 ± 0.1) × 10?5s?1for the bromido complex). The corresponding rate constants were a factor of two to three times larger in cell culture media, but the same trends were observed. There was also a third slower reaction in media that had the same rate constant irrespective of the starting complex ((3.6 ± 0.7) × 10?5and (3.9 ± 0.3) × 10?5s?1, respectively). Neither complex exhibited significant cytotoxicity. However, both complexes exhibited anti-invasive properties to highly invasive MDA-MB-231 breast cancer cells. The more reactive chlorido complex was also the most active in the invasion assay when either the cells were treated prior to the addition to collagen matrix, or the top collagen matrix was treated with Ru after adding it to cover the cells and wound.

An efficient route to asymmetrically diconjugated tris(heteroleptic) complexes of Ru(ii)

A highly efficient and versatile route to the preparation of tris(heteroleptic) Ru(ii) polypyridyl complexes is described which permits access to two or more independently conjugatable termini in the final structure. The strategy utilizes the well-known R

[RuCl2(η6-p-cymene)(P*)] and [RuCl 2(κ-P-η6-arene)] complexes containing p -stereogenic phosphines. activity in transfer hydrogenation and interactions with DNA

The preparation of a series of half-sandwich ruthenium complexes, [RuCl2(η6-p-cymene)(P)] (P* = S-PMeRR′) and [RuCl2(κ-P-η6-arene)], containing P-stereogenic phosphines is reported. The borane-protected P-stereogenic phosphines have been obtained by addition of the (H3B)PMe 2R (R = t-Bu (1), Cy (2), Fc (3))/sec-BuLi/(-)-sparteine adduct to benzyl halides, carbonyl functions, and epoxides with yields between 40 and 90% and ee values in the 70-99% range. Those containing an aryl secondary function have been used in the preparation of [RuCl2(η6-p- cymene)(P)] complexes. Borane deprotection has been performed using HBF 4, except for (H3B)PRMe(CH2SiMe2Ph) phosphines, where DABCO was used to avoid partial cleavage of the CH 2-Si bond. In the case of (H3B)P(t-Bu)Me(CH 2C(OH)Ph2) (1l) the dehydrated phosphine was obtained. The tethered complexes were obtained by p-cymene substitution in chlorobenzene at 120 C, except for ferrocenyl-containing complexes, which decomposed upon heating. The presence of substituents in the aryl arm of some of the phosphines introduces new chiral elements in the tethered [RuCl2(κ-P- η6-arene)] compounds. Full characterization of all compounds both in solution and in the solid state has been carried out. Crystal structure determinations of four phosphine-borane molecules confirm the S configuration at the phosphorus atom (1a,e,l and 2d). Moreover, the crystal structure of one p-cymene complex (5i) and four tethered complexes reveal the strain of the compounds with two atoms in the tether (7c,g,l and 8i). Tethering has a marked effect on the catalytic performance transfer hydrogenation of acetophenone and on the nature of hydridic species originating during the activation period. The chiral induction attains 58% ee with complexes with the bulkiest substituents in the pendant arm of the phosphine. Three of the prepared complexes can interact with DNA and present a reasonable cytotoxicity toward cancer cells. Intercalation of the free aromatic pendant arm of the phosphines seems to be fundamental for such interactions.

Inhibition of human prion neuropeptide PrP106-126 aggregation by hexacoordinated ruthenium complexes

Prion disease is a neurodegenerative disorder that can occur among humans and other animals. The aberrant isoform of prion protein PrPSc has been identified as the infectious agent. The neuropeptide PrP106-126 has been widely used as a suitable model to study the biological and physiochemical properties of PrPSc. PrP106-126 shares several physicochemical and biological properties with PrPSc, including cellular toxicity, fibrillogenesis, and membrane-binding affinity. Ruthenium complexes are commonly employed in anti-cancer studies due to their low cellular toxicity. In this study, six hexacoordinated ruthenium complexes with different molecular configurations were used to investigate their effects on PrP106-126 aggregation inhibition. Results revealed that the interaction between the complexes and the peptide included metal coordination and hydrophobic interaction mainly. Those complexes with aromatic structure displayed better inhibitory effects, although they only had a common binding affinity to PrP106-126. This study provided better understanding on the interaction of metal complexes with PrP106-126 and paved the way for potential Ru-based metallodrugs against prion diseases.