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The aim of this research was to find an effective drug with fewer side effects against DF by drug repositioning and determine its efficacy. DF cells harboring S45F mutations of CTNNB1 were tested for FDA-approved drugs that stop cell proliferation of DF cells harboring S45F mutations of CTNNB1. Using Apc1638N mice, effects of the metabolized drug on in vivo DF were investigated. Auranofin was identified as a drug that effectively stops cell proliferation of DF cells. Since auranofin has been used for many years as an FDA-approved drug, it could be a promising drug with less side effects on DF, it could be a promising drug with fewer side effects for DF.
Source link: https://doi.org/10.1038/s41598-022-15756-9
Using a murine model of vaginal infection, this research sought to determine in vivo activity of auranofin against N. gonorrhoeae. Infected mice treated with auranofin were seen to have a significant decrease in N. gonorrhoeae recovered from the vain, compared to the vehicle over the course of therapy. In conclusion, auranofin has the potential to be further investigated as a novel, safe anti-gonococcal drug, which may help with the urgent need for new antimicrobial agents for N. gonorrhoeae infection.
Source link: https://doi.org/10.1371/journal.pone.0266764
The effects of Auranofin on protein expression and protein oxidation in A2780 cancer cells were investigated by a protocol based on simultaneous expression proteomics and redox proteomics results. The proteomics results show that the most important cellular changes elicited by AF therapy are thioredoxin reduction, alteration of the cell redox state, impairment of mitochondrial functions, and generation of ER stress.
Source link: https://doi.org/10.1016/j.redox.2022.102294
We hypothesize that auranofin could avert pancreatic duct carcinoma formation by blocking Txnrd1 and HIF-1u03b1. Methods: Human pancreatic duct carcinoma cell lines' sensitivity was determined in vitro based on IC50. A greater number of PDX samples were able to be tested with high accuracy with ex vivo live tissue slice assays of xenografts. In vivo pancreatic ductal adenocarcinoma mouse models using MiaPaCa-2 Luc+ cells were intended to determine the optimal dose and antitumor activity. Results: We found that ten of the 15 tested pancreatic ductal adenocarcinoma cell lines were sensitive to auranofin with IC50s below 5 °Cmol/L. For 13 PDX tissue samples treated with 10 u03bcmol/L auranofin, a growth inhibition of greater than 44% was observed. The optimal dose in the absence of gross solid organ metastasis in the absence of gross solid organ metastasis was 15 mg/kg IP, according to In vivo studies, who were up to 13 weeks post-treatment.
Source link: https://doi.org/10.1016/j.sopen.2019.05.004
Pancreatic cancer accounts for nearly one-quarter of all new cancers worldwide. P-AscH u2212 has been shown to sensitize cancer cells to ionizing radiation in a way that is dependent on the production of H2O2 while simultaneously shielding normal tissue from radiation damage. Au's blocking of the thioredoxin antioxidant system elevates the overall peroxide burden on cancer cells. We have additional evidence confirming the safety of AuU2019 in breast, colon, lung, and ovarian cancer as well as P-AscH, u2212 and ionizing radiation in pancreatic cancer therapy, in favor of recent research establishing Au. u2019's effectiveness in pancreatic cancer therapy. Multiple ways to raise H2 O 2 -dependent toxicity among pancreatic cancer cells can be combined by P-AscH u2212 and Au in the treatment of pancreatic cancer, as well as a promising translatable route by which to improve radiation quality and patient outcomes can be combined.
Source link: https://doi.org/10.3390/antiox11050971
Auranofin, an orally administered chrysotherapeutic agent approved for the treatment of rheumatoid arthritis that is being repurposed for several indications, including bacterial infections. AF-AcCys has an antibacterial activity that is quite similar to that of AF against Staphylococcus aureus, however, it is about 20 times less effective against Staphylococcus epidermidis. AF-AcCys, which is similarly to AF, promotes protein metalation through the [AuPEt 3 ] + fragment, according to a bioinorganic study. In AF-AcCys, we conducted a comparative experimental stability study and a theoretical estimation of bond dissociation energies to shed light on the pharmacological relationships between AF and AF-AcCys, revealing the higher strength of the Au2013S bond in AF-AcCys. The differences and similarities between AF and AF-AcCys are discussed, as well as the challenges and consequences that chemical structure modifications imply.
Source link: https://doi.org/10.3390/molecules27082578
We investigated whether Prima-1Met's activity could be mimicked by auranofin, a thioredoxin reductase inhibitor. We then compared the effectiveness of auranofin and Prima-1Met in 18 myeloma cell lines and ten samples from patients with multiple myeloma or plasma cell leukemia in ten samples from patients with multiple myeloma or plasma cell leukemia. These results showed that auranofin and Prima-1Met had both overcome cell death resistance in myeloma cells due to either p53 deficiency or mitochondrial dysfunction.
Source link: https://doi.org/10.3389/fonc.2019.00128
As microbial resistance to drugs continues to rise at an alarming rate, finding new ways to combat pathogens is of utmost importance. We examine the U. S. Food and Drug Administration's test findings of auranofin, ebselen, and PX-12 as antimicrobial agents targeting the thioredoxin system in this article. We propose that the thioredoxin system may be a useful therapeutic target with broad spectrum antimicrobial activity.
Source link: https://doi.org/10.3389/fmicb.2018.00336
Cellular epithelium apoptosis is the primary pathological cause of radiation-induced intestinal injury. We investigated the effects of auranofin on intestinal epithelial cells' radiosensitivity by analysing this data. The treatment with a mixture of 1 bcM auranofin and 5 Gy ionizing radiation in IEC-6 cells demonstrated clear additive effects on caspase 3 cleavage and apoptotic DNA fragmentation, as shown by the auranofin administration in mice, and radiation-induced intestinal injury in mice. In addition, transfection of IEC-6 cells with a small interfering RNA specific against thioredoxin reductase raised the radiosensitivity of these cells. These results show that auranofin-induced radiosensitization of intestinal epithelial cells is mediated by oxidative stress induced by the deregulation of thioredoxin redox system, and epithelial infection can be a risk factor for acute pelvic cancer disease.
Source link: https://doi.org/10.3389/fphar.2019.00417
Osteoporosis is a degenerative metabolic disorder characterized by an imbalance between osteogenesis and osteoclastogenesis. Consequently, osteoclast maturation can be a novel option for both treating and preventing osteoporosis. In vitro and in vivo, we investigated whether auranofin suppresses osteoclast differentiation. In mouse bone marrow macrophages and Raw264. 7 macrophages, Auranofin was shown to reduce receptor activator of NF-mediated osteoclastogenesis. Both bone mass in ovariectomized mice was significantly improved by oral administration of auranofin.
Source link: https://doi.org/10.1155/2019/3503912
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