Aurothioglucose
(Synonyms: 金硫葡萄糖; Gold thioglucose) 目录号 : GC35431
A TrxR inhibitor
Cas No.:12192-57-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Aurothioglucose is an inhibitor of thioredoxin reductase (TrxR; IC50 = 0.065 ?M for the human placental enzyme).1 It is selective for TrxR over glutathione reductase and glutathione peroxidase (GPX; IC50s = >100 and 80 ?M, respectively). Aurothioglucose (100 ?M) inhibits IL-1β-induced production of IL-6 and IL-8 in isolated human rheumatoid synovial fibroblasts.2 It reduces HIV-1 replication induced by TNF-α in OM10.1 cells latently infected with HIV-1 when used at concentrations of 10 and 25 ?M.3 Aurothioglucose (25 mg/kg) improves survival in a mouse model of acute respiratory distress syndrome (ARDS) induced by LPS and hyperoxia.4 It induces obesity and increases food intake and blood glucose levels in genetically diabetic KK mice.5 Formulations containing aurothioglucose have previously been used in the treatment of rheumatoid arthritis.
1.Gromer, S., Arscott, L.D., Williams, C.H., Jr., et al.Human placenta thioredoxin reductase. Isolation of the selenoenzyme, steady kinetics, and inhibition by therapeutic gold compoundsJ. Biol. Chem.273(32)20096-20101(1998) 2.Yoshida, S., Kato, T., Sakurada, S., et al.Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucoseInt. Immunol.11(2)151-158(1999) 3.Traber, K.E., Okamoto, H., Kurono, C., et al.Anti-rheumatic compound aurothioglucose inhibits tumor necrosis factor-α-induced HIV-1 replication in latently infected OM10.1 and Ach2 cellsInt. Immunol.11(2)143-150(1999) 4.Britt, R.D., Jr., Velten, M., Locy, M.L., et al.The thioredoxin reductase-1 inhibitor aurothioglucose attenuates lung injury and improves survival in a murine model of acute respiratory distress syndromeAntioxid. Redox Signal.20(17)2681-2691(2014) 5.Matsuo, T., and Shino, A.Induction of diabetic alterations by goldthioglucose-obesity in KK,ICR and C57BL miceDiabetologia8(6)391-397(1972)
| Cas No. | 12192-57-3 | SDF | |
| 别名 | 金硫葡萄糖; Gold thioglucose | ||
| Canonical SMILES | O[C@@H]1[C@](O[Au+][SH-]2)([H])C2O[C@H](CO)[C@H]1O | ||
| 分子式 | C6H11AuO5S | 分子量 | 392.18 |
| 溶解度 | Water: 125 mg/mL (318.73 mM); DMSO: 6 mg/mL (15.30 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5498 mL | 12.7492 mL | 25.4985 mL |
| 5 mM | 0.51 mL | 2.5498 mL | 5.0997 mL |
| 10 mM | 0.255 mL | 1.2749 mL | 2.5498 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Effect of Aurothioglucose on glutathione and glutathione-metabolizing and related enzymes in rat liver and kidney
Chem Biol Interact 1987;64(1-2):103-14.PMID:3121194DOI:10.1016/0009-2797(87)90064-0.
The antirheumatic drug Aurothioglucose is an inhibitor of the selenoenzyme GSH peroxidase. During chrysotherapy, the decreased levels of erythrocyte GSH and serum sulfhydryls of rheumatoid arthritis patients are normalized concomitant with clinical efficacy. This investigation examined the in vivo and in vitro effect of gold(I) as Aurothioglucose on enzymes related to the GSH redox cycle or metabolism. The enzymes measured were GSH peroxidase, GSSG reductase, gamma-glutamyl transpeptidase, gamma-glutamylcysteine synthetase, GSH S-transferase, GSH thiotransferase, glucose-6-phosphate dehydrogenase, superoxide dismutase and catalase. Rats were injected with 30 mumol Aurothioglucose/kg body wt. daily for 7 days by intramuscular injection. GSH levels in aurothioglucose-treated rats were 68% higher in erythrocytes (P less than 0.005) and 45% higher in kidney (P less than 0.001) than in control rats. Treatment with Aurothioglucose did not elevate plasma or liver GSH. The enzyme activities that were changed by Aurothioglucose treatment were GSH peroxidase in kidney (41% decreased, P = 0.005) and liver (13% decreased, P less than 0.05), gamma-glutamyl transpeptidase in kidney (15% decreased, P less than 0.05), and catalase in kidney (58% decreased, P less than 0.001). Kidney glucose-6-phosphate dehydrogenase activity was increased 50% (P less than 0.005) and GSH S-transferase was increased 72% (P less than 0.001). In vitro the only liver enzymes inhibited more than 50% by concentrations of less than 50 microM Aurothioglucose were GSH peroxidase (50% inhibited by 25 microM Aurothioglucose) and GSH thiotransferase (50% inhibited by 5 microM Aurothioglucose). Studies of in vitro enzyme inhibition by Aurothioglucose could not be used to predict decreased enzyme activities in vivo. Although decreased activities of two major enzymes that utilize GSH, GSH peroxidase and gamma-glutamyl transpeptidase, coincided with elevated GSH in kidneys of aurothioglucose-treated rats, a direct cause and effect relationship remains speculative.
Aurothioglucose inhibits murine thioredoxin reductase activity in vivo
J Nutr 1999 Jan;129(1):194-8.PMID:9915899DOI:10.1093/jn/129.1.194.
Gold (I)-containing compounds, including Aurothioglucose (ATG), are potent in vitro inhibitors of several selenocysteine-containing enzymes. Gold compounds have also been shown to potentiate the virulence of several viruses in mice, including coxsackievirus, implicated as a possible infectious agent in Keshan disease. One possible mechanism by which gold compounds may be increasing the virulence of viral infections in mice is by acting as a selenium antagonist in vivo and inducing oxidative stress. To investigate the possible role of gold compounds in inducing oxidative stress in mice, we assessed the ability of ATG administered in vivo to inhibit the activity of the selenocysteine-containing enzymes thioredoxin reductase (TR) and glutathione peroxidase (GPX1). Doses as low as 0. 025 mg ATG/g body weight caused significant and prolonged inhibition of TR activity in all tissues examined. No such inhibition of GPX1 activity was seen, indicating differential in vivo sensitivity of the enzymes to inhibition by ATG. In liver and heart, some recovery of TR activity was observed after a 7-d period, but no recovery was observed in pancreas or kidney. Because TR is involved in several important cellular redox functions, its inhibition most likely will affect multiple cellular processes. These results indicate that in vivo administration of ATG results in significant and long-lasting inhibition of TR activity. Such inhibition of TR could lead to increased levels of oxidative stress in vivo, thereby increasing the virulence of several viruses including the coxsackievirus.
Comparison of auranofin and Aurothioglucose in the treatment of rheumatoid arthritis: a single blind study
Clin Rheumatol 1984 Mar;3 Suppl 1:51-6.PMID:6432414DOI:10.1007/BF03342622.
Fifty-two patients with rheumatoid arthritis were studied in a single blind trial comparing Aurothioglucose and auranofin. The duration of the study was 52 weeks. Twenty-six patients, 13 in each treatment group, dropped out during the first year of treatment. The main reason for discontinuing treatment with Aurothioglucose was adverse reactions and, in the auranofin group, lack of efficacy. In those patients who continued therapy the results of treatment were comparable; patients on Aurothioglucose improved slightly more than auranofin treated patients, although the difference was not statistically significant.
Parenteral gold preparations. Efficacy and safety of therapy after switching from Aurothioglucose to aurothiomalate
J Rheumatol 2005 Jun;32(6):1026-30.PMID:15940762doi
Objective: For reasons of insufficient quality of the raw material, Aurothioglucose was withdrawn from the Dutch market at the end of 2001. Aurothiomalate became available as an alternative preparation. We followed a cohort of patients during the first year after switching from Aurothioglucose to aurothiomalate to study efficacy and tolerability. Methods: Patients were observed at baseline and at 3 and 12 months after switching. At each visit, data on adverse drug reactions (ADR), withdrawal, and disease activity were collected. Results: In total 120 patients were included [age 63(SD 15) yrs, 68% female, 93% with rheumatoid arthritis, duration of disease 15 (SD 9) years, 82% IgM rheumatoid factor-positive, with 9 (SD 9, range 0.1-45) yrs of previous Aurothioglucose therapy]. Nineteen patients (16%) reported an ADR taking aurothiomalate not previously experienced with Aurothioglucose, the most frequently reported being pruritus, dermatitis/stomatitis, and chrysiasis/hyperpigmentation. Twenty-nine patients (24%) withdrew from aurothiomalate within 12 months of followup for reasons of inefficacy (14%), ADR (7%), or disease in state of remission (3%). Kaplan-Meier estimates show aurothiomalate survival rates of 78.5% after 12 months. No statistically significant differences between the disease activity indicators during followup visits compared with the baseline visit were detected for the patients continuing aurothiomalate. Conclusion: Within the first 12 months after switching from Aurothioglucose, 24% of patients withdrew from aurothiomalate. Sixteen percent of patients reported novel ADR. For the population continuing to take aurothiomalate no clinically relevant changes in disease activity were recorded after switching.
Aurothioglucose in rheumatoid arthritis. Outcome of treatment in patients intolerant of sodium aurothiomalate
Med J Aust 1984 Sep 15;141(6):349-51.PMID:6438454doi
Forty-three patients in whom treatment with sodium aurothiomalate was discontinued because of adverse reactions that either were relatively severe or recurred on rechallenge received treatment with Aurothioglucose in oily base. Thirty-six of them had rheumatoid arthritis, four had psoriatic arthritis and three had juvenile chronic arthritis. Aurothioglucose therapy was introduced cautiously and increased gradually to a maintenance regimen, usually 5-20 mg/week, administered by intramuscular injection. The clinical response was good in 25 patients (60%), 14 of whom continued to receive Aurothioglucose therapy on a long-term basis. Adverse reactions to Aurothioglucose developed in 17 patients (40%); these were generally mild, and, in all but four patients, were of the same type as those induced by sodium aurothiomalate therapy. Results show that Aurothioglucose in oily base may be successfully administered in a low-dose regimen to selected patients who are intolerant of sodium aurothiomalate.