600-700| Page 10 of 13 | Chiral phosphine ligands

Cas: 34031-32-8 was involved in experiment | Journal of Medical Microbiology 2021

((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold(cas: 34031-32-8) is a potent inhibitor of selenoenzyme thioredoxin reductase (TrxR), which is involved in defense against oxidative stress.Name: ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold

Evans, Andris;Kavanagh, Kevin A. published 《Evaluation of metal-based antimicrobial compounds for the treatment of bacterial pathogens》 in 2021. The article was appeared in 《Journal of Medical Microbiology》. They have made some progress in their research.Name: ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold The article mentions the following:

A review. Antimicrobial resistance (AMR) is one of the greatest global health challenges of modern times and its prevalence is rising worldwide. AMR within bacteria reduces the efficacy of antibiotics and increases both the morbidity and the mortality associ- ated with bacterial infections. Despite this growing risk, few antibiotics with a novel mode of action are being produced, leading to a lack of antibiotics that can effectively treat bacterial infections with AMR. Metals have a history of antibacterial use but upon the discovery of antibiotics, often became overlooked as antibacterial agents. Meanwhile, metal-based complexes have been used as treatments for other diseases, such as the gold-containing drug auranofin, used to treat rheumatoid arthritis. Metal-based antibacterial compounds have novel modes of action that provide an advantage for the treatment of bacterial infections with resistance to conventional antibiotics. In this review, the antibacterial activity, mode of action, and potential for systemic use of a number of metal-based antibacterial complexes are discussed. The current limitations of these compounds are highlighted to determine if metal-based agents are a potential solution for the treatment of bacterial infections, especially those resistant to conventional antibiotics. To complete the study, the researchers used ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Antioxidants | Cas: 34031-32-8 was involved in experiment

((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold(cas: 34031-32-8) is a gold(I)-phosphine thiolate small molecule described to produce antiinflammatory and antiarthritic effects.Related Products of 34031-32-8

Related Products of 34031-32-8In 2021, Wall, Stephanie B.;Li, Rui;Butler, Brittany;Burg, Ashley R.;Tse, Hubert M.;Larson-Casey, Jennifer L.;Carter, A. Brent;Wright, Clyde J.;Rogers, Lynette K.;Tipple, Trent E. published 《Auranofin-mediated NRF2 induction attenuates interleukin 1 beta expression in alveolar macrophages》. 《Antioxidants》published the findings. The article contains the following contents:

Background: Alveolar macrophages (AMs) are resident inflammatory cells in the lung that serve as early sentinels of infection or injury. We have identified thioredoxin reductase 1 inhibition by gold compounds increases activation of nuclear factor erythroid 2-related factor 2 (NRF2)-dependent pathways to attenuate inflammatory responses. The present studies utilized murine alveolar macrophages (MH-S) to test the hypothesis that the gold compound, auranofin (AFN), decreases interleukin (IL)-1β expression through NRF2-mediated interactions with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway genes and/or increases in glutathione synthesis. Methods: MH-S cells were treated with AFN and lipopolysaccharide (LPS) and analyzed at 6 and 24 h. The Il1b promoter was analyzed by chromatin immunoprecipitation for direct interaction with NRF2. Results: Expression of IL-1β, p-IκBα, p-p65 NF-kB, and NOD-, LRR-, and pyrin domain-containing protein 3 were elevated by LPS exposure, but only IL-1β expression was suppressed by AFN treatment. Both AFN and LPS treatments increased cellular glutathione levels, but attenuation of glutathione synthesis by buthionine sulfoximine (BSO) did not alter expression of Il-1β. Anal. revealed direct NRF2 binding to the Il1b promoter which was enhanced by AFN and inhibited the transcriptional activity of DNA polymerase II. Conclusions: Our data demonstrate that AFN-induced NRF2 activation directly suppresses IL-1β synthesis independent of NFκB and glutathione-mediated antioxidant mechanisms. NRF2 binding to the promoter region of IL1β directly inhibits transcription of the IL1β gene. Collectively, our research suggests that gold compounds elicit NRF2-dependent pulmonary protection by suppressing macrophage-mediated inflammation. And ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) was used in the research process.

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Cancer Drug Resistance | Cas: 34031-32-8 was involved in experiment

Massai, Lara;Cirri, Damiano;Marzo, Tiziano;Messori, Luigi published 《Auranofin and its analogs as prospective agents for the treatment of colorectal cancer》. The research results were published in《Cancer Drug Resistance》 in 2022.Application of 34031-32-8 The article conveys some information:

A review. Today colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. This disease is poorly chemo-sensitive toward the existing medical treatments so that new and more effective therapeutic agents are urgently needed and intensely sought. Platinum drugs, oxaliplatin in particular, were reported to produce some significant benefit in CRC treatment, triggering the general interest of medicinal chemists and oncologists for metal-based compounds as candidate anti-CRC drugs. Within this frame, gold compounds and, specifically, the established antiarthritic drug auranofin with its analogs, form a novel group of promising anticancer agents. Owing to its innovative mechanism of action and its favorable pharmacol. profile, auranofin together with its derivatives are proposed here as novel exptl. agents for CRC treatment, capable of overcoming resistance to platinum drugs. Some encouraging results in this direction have already been obtained. A few recent studies demonstrate that the action of auranofin may be further potentiated through the preparation of suitable pharmaceutical formulations capable of protecting the gold pharmacophore from unselective reactivity or through the design of highly synergic drug combinations. The perspectives of the research in this field are outlined. The experimental procedure involved many compounds, such as ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Proetto, Maria T. et al. published new progress in experiments with the help of cas: 34031-32-8

((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold(cas: 34031-32-8) is a disease-modifying antirheumatic drug (DMARD) and has been used to study the anti-proliferative effects against OVCAR-3 human ovarian carcinoma cells.Safety of ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold

Proetto, Maria T.;Alexander, Kelsey;Melaimi, Mohand;Bertrand, Guy;Gianneschi, Nathan C. published 《Cyclic (Alkyl)(Amino)Carbene (CAAC) Gold(I) Complexes as Chemotherapeutic Agents》 in 2021. The article was appeared in 《Chemistry – A European Journal》. They have made some progress in their research.Safety of ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold The article mentions the following:

Cyclic (Alkyl)(Amino)Carbenes (CAACs) have become forceful ligands for gold due to their ability to form very strong ligand-metal bonds. Inspired by the success of Auranofin and other gold complexes as antitumor agents, we have studied the cytotoxicity of bis- and mono-CAAC-gold complexes on different cancer cell lines: HeLa (cervical cancer), A549 (lung cancer), HT1080 (fibrosarcoma) and Caov-3 (ovarian cancer). Further investigations aimed at elucidating their mechanism of action are described. This includes quantification of affinities for TrxR, evaluation of their bioavailability and determination of associated cell death process. Moreover, Transmission Electron Microscopy (TEM) was used to study morphol. changes upon exposure. Noticeably, a significant reduction in non-specific binding to serum proteins was observed with CAAC complexes when compared to Auranofin. These results confirm the potential of CAAC-gold complexes in biol. environments, which may result in more specific drug-target interactions and decreased side effects. To complete the study, the researchers used ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Journal of Analytical Atomic Spectrometry | Cas: 34031-32-8 was involved in experiment

Lamarche, J.;Bierla, K.;Ouerdane, L.;Szpunar, J.;Ronga, L.;Lobinski, R. published 《Mass spectrometry insights into interactions of selenoprotein P with auranofin and cisplatin》 in 2022. The article was appeared in 《Journal of Analytical Atomic Spectrometry》. They have made some progress in their research.Formula: C20H36AuO9PS The article mentions the following:

The reactivity of selenoprotein P (a serum selenoprotein containing 10 selenocysteine (SeCys), 17 cysteine (Cys) and 14 histidine (His) residues) with two metallodrugs (auranofin and cisplatin) was investigated. The selenoprotein was purified from human serum by sequential affinity chromatog. using immobilized metal (Co2+) affinity chromatog. (IMAC) and heparine affinity, followed by solid-phase extraction preconcentration The purified selenoprotein P was sequenced by nanoLC-MS/MS to reach a complete sequence coverage. It eluted from SEC as two major peaks likely to correspond to the glycosylated and non-glycosylated forms and a minor one, probably a truncated form. Size-exclusion chromatog. with the selective Se (78Se) and metal (197Au or 195Pt) detection by ICP MS showed the co-elution of selenoprotein P forms with Au and with Pt. SEC-ICP MS of the tryptic digest showed a considerable shift of the elution of selenium towards the lower mol. masses while preserving the co-elution of selenium and the metal at some elution times. NanoHPLC – electrospray MS/MS anal. of the post-reaction mixture demonstrated the formation of peptides with the privileged binding to Cys and His residues for cisplatin and SeCys and Cys residues for auranofin. And ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) was used in the research process.

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Cas: 34031-32-8 | Sharma, Nidhipublished an article in 2021

Recommanded Product: 34031-32-8《Repurposing of Auranofin Against Bacterial Infections: An In silico and In vitro Study》 was published in 2021. The authors were Sharma, Nidhi;Singh, Arti;Sharma, Ruchika;Kumar, Anoop, and the article was included in《Current Computer-Aided Drug Design》. The author mentioned the following in the article:

The aim of the study was to find out the role of auranofin as a promising broadspectrum antibacterial agent. In vitro assays (Percentage growth retardation, Bacterial growth kinetics, Biofilm formation assay) and In silico study (Molegro virtual docker (MVD) version 6.0 and Mol. operating environment (MOE) version 2008.10 software). The in vitro assays have shown that auranofin has good antibacterial activity against Gram pos. and Gram neg. bacterial strains. Further, auranofin has shown synergistic activity in combination with ampicillin against S. aureus and B. subtilis whereas in combination with neomycin has just shown additive effect against E. coli, P. aeruginosa and B. pumilus. In vivo results have revealed that auranofin alone and in combination with standard drugs significantly decreased the bioburden in the zebrafish infection model as compared to control. The mol. docking study have shown good interaction of auranofin with penicillin-binding protein (2Y2M), topoisomerase (3TTZ), UDP-3-O-[3-hydroxymyristoyl] N-acetylglucosaminedeacetylase (3UHM), cell adhesion protein (4QRK), β-lactamase (5CTN) and arylsulphatase (1HDH) enzyme as that of reference ligand which indicate the multimodal mechanism of action of auranofin. Finally, MTT assay has shown the non-cytotoxic effect of auranofin. In conclusion, auranofin in combination with existing antibiotics, could be developed as a broad spectrum antibacterial agent; however, further studies are required to confirm its safety and efficacy. This study provides the possibility of the use of auranofin apart from its established therapeutic indication in combination with existing antibiotics to tackle the problem of resistance.((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) were involved in the experimental procedure.

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Cas: 34031-32-8 | Chakraborty, Parichita et al. made new progress in 2021

((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold(cas: 34031-32-8) is an efficient inducer of mitochondrial membrane permeability transition pore in the presence of calcium ions related to its inhibition of mitochondrial thioredoxin reductase.Product Details of 34031-32-8

Chakraborty, Parichita;Oosterhuis, Dorenda;Bonsignore, Riccardo;Casini, Angela;Olinga, Peter;Scheffers, Dirk-Jan published 《An Organogold Compound as Potential Antimicrobial Agent against Drug-Resistant Bacteria: Initial Mechanistic Insights》 in 2021. The article was appeared in 《ChemMedChem》. They have made some progress in their research.Product Details of 34031-32-8 The article mentions the following:

The rise of antimicrobial resistance has necessitated novel strategies to efficiently combat pathogenic bacteria. Metal-based compounds have been proven as a possible alternative to classical organic drugs. Here, we have assessed the antibacterial activity of seven gold complexes of different families. One compound, a cyclometalated Au(III) CN complex, showed activity against Gram-pos. bacteria, including multi-drug resistant clin. strains. The mechanism of action of this compound was studied in Bacillus subtilis. Overall, the studies point towards a complex mode of antibacterial action, which does not include induction of oxidative stress or cell membrane damage. A number of genes related to metal transport and homeostasis were upregulated upon short treatment of the cells with gold compound Toxicity tests conducted on precision-cut mouse tissue slices ex vivo revealed that the organogold compound is poorly toxic to mouse liver and kidney tissues, and may thus, be treated as an antibacterial drug candidate. The experimental procedure involved many compounds, such as ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Tanaka, Katsuki et al. published new experimental results with the assistance of cas: 34031-32-8

Computed Properties of C20H36AuO9PS《Oxidative stress inducers potentiate 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated pre-cardiac edema in larval zebrafish》 was published in 2021. The authors were Tanaka, Katsuki;Adachi, Hikaru;Akasaka, Hironobu;Tamaoki, Junya;Fuse, Yuji;Kobayashi, Makoto;Kitazawa, Takio;Teraoka, Hiroki, and the article was included in《Journal of Veterinary Medical Science》. The author mentioned the following in the article:

We reported the involvement of oxidative stress and prostaglandins including thromboxane and prostacyclin in pre-cardiac edema (early edema) caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). While the involvement of oxidative stress in TCDDinduced toxicity has been frequently reported, the mechanism of its action is still unclear. In the present study, oxidative stress inducers including paraquat, hydrogen peroxide (H₂O₂) and rotenone augmented early edema (edema) induced by a low concentration of TCDD (0.1 ppb) at 55 h post fertilization (hpf), while each of them alone did not cause edema. Edema caused by TCDD plus oxidative stress inducers was almost abolished by antioxidants, an antagonist for thromboxane receptor (ICI-192,605) and an agonist for prostacyclin receptor (beraprost), suggesting that the site of action of these inducers was in the regular signaling pathway after activation of aryl hydrocarbon receptor type 2 (AHR2) by TCDD. Oxidative stress inducers also enhanced edema caused by an agonist for the thromboxane receptor (U46619), and the enhancement was also inhibited by antioxidants. Sulforaphane and auranofin, activators of Nrf2 that is a master regulator of anti-oxidative response, did not affect U46619-evoked edema but almost abolished TCDD-induced edema and potentiation by paraquat in both TCDD- and U46619- induced edema. Taken together, the results suggest that oxidative stress augments pre-cardiac edema caused by TCDD via activation of thromboxane receptor-mediated signaling in developing zebrafish. As paraquat and other oxidative stress inducers used also are environmental pollutants, interaction between dioxin-like compounds and exogenous source of oxidative stress should also be considered. The experimental procedure involved many compounds, such as ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Cas: 34031-32-8 was involved in experiment | Scientific Reports 2022

Ito, Kan;Nishida, Yoshihiro;Hamada, Shunsuke;Shimizu, Koki;Sakai, Tomohisa;Ohkawara, Bisei;Alman, Benjamin A.;Enomoto, Atsushi;Ikuta, Kunihiro;Koike, Hiroshi;Zhang, Jiarui;Ohno, Kinji;Imagama, Shiro published 《Efficacy of auranofin as an inhibitor of desmoid progression》. The research results were published in《Scientific Reports》 in 2022.Formula: C20H36AuO9PS The article conveys some information:

Abstract: Anticancer drugs and mol. targeted therapies are used for refractory desmoid-type fibromatosis (DF), but occasionally cause severe side effects. The purpose of this study was to identify an effective drug with fewer side effects against DF by drug repositioning, and evaluate its efficacy. FDA-approved drugs that inhibit the proliferation of DF cells harboring S45F mutations of CTNNB1 were screened. An identified drug was subjected to the investigation of apoptotic effects on DF cells with anal. of Caspase 3/7 activity. Expression of β-catenin was evaluated with western blot anal., and immunofluorescence staining. Effects of the identified drug on in vivo DF were analyzed using Apc1638N mice. Auranofin was identified as a drug that effectively inhibits the proliferation of DF cells. Auranofin did not affect Caspase 3/7 activity compared to control. The expression level of β-catenin protein was not changed regardless of auranofin concentration Auranofin effectively inhibited the development of tumorous tissues by both oral and i.p. administration, particularly in male mice. Auranofin, an anti-rheumatic drug, was identified to have repositioning effects on DF. Since auranofin has been used for many years as an FDA-approved drug, it could be a promising drug with fewer side effects for DF. To complete the study, the researchers used ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis

Cas: 34031-32-8 was involved in experiment | Comparative Biochemistry and Physiology, Part C: Toxicology & Pharmacology 2021

Recommanded Product: 34031-32-8In 2021, Isei, Michael O.;Stevens, Don;Kamunde, Collins published 《Temperature rise and copper exposure reduce heart mitochondrial reactive oxygen species scavenging capacity》. 《Comparative Biochemistry and Physiology, Part C: Toxicology & Pharmacology》published the findings. The article contains the following contents:

Mitochondria produce and scavenge reactive oxygen species (ROS); however, whether oxidative distress due to exogenous stress arises from excessive production or impaired scavenging remains unclear. We assessed the effect of copper (Cu) and thermal stress on kinetics of ROS (H2O2) consumption in mitochondria isolated from fish heart. Mitochondria were energized with succinate, glutamate-malate or palmitoylcarnitine (PC) and incubated with 1-25μM Cu at 11 (control) and 23°C. We found that H2O2 consumption capacity of heart mitochondria varies with substrate and is additively reduced by temperature rise and Cu. While Cu is a potent inhibitor of H2O2 consumption in mitochondria oxidizing glutamate-malate and succinate, mitochondria oxidizing PC are resistant to the inhibitory effect of the metal. Moreover, the sensitivity of H2O2 consumption pathways to Cu depend on the substrate and are greatly impaired during oxidation of glutamate-malate. Pharmacol. manipulation of mitochondrial antioxidant systems revealed that NADPH-dependent peroxidase systems are the centerpieces of ROS scavenging in heart mitochondria, with the glutathione-dependent pathway being the most prominent while catalase played a minimal role. Surprisingly, Cu is as efficacious in inhibiting thioredoxin-dependent peroxidase pathway as auranofin, a selective inhibitor of thioredoxin reductase. Taken together, our study uncovered unique mechanisms by which Cu alters mitochondrial H2O2 homeostasis including its ability to inhibit specific mitochondrial ROS scavenging pathways on a par with conventional inhibitors. Importantly, because of additive inhibitory effect on mitochondrial ROS removal mechanisms, hearts of organisms jointly exposed to Cu and thermal stress are likely at increased risk of oxidative distress. The experimental procedure involved many compounds, such as ((2S,3R,4S,5R,6R)-3,4,5-Triacetoxy-6-(acetoxymethyl)tetrahydro-2H-pyran-2-thio)(triethylphosphine)gold (cas: 34031-32-8) .

Reference:
Phosphine ligand,
Chiral phosphines in nucleophilic organocatalysis