Cu-GTSM
(Synonyms: CuII(gtsm), copper-GTSM) 目录号 : GC49557A copper-containing compound with diverse biological activities
Cas No.:68341-14-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cu-GTSM is a copper-containing compound and an analog of Cu-ATSM that has diverse biological activities.1,2,3,4 It is active against methicillin-sensitive and -resistant S. aureus clinical isolates (IC50s = 0.3-0.6 µM for all).1 Cu-GTSM inhibits the growth of SK-N-MC neuroepithelioma cells and MRC-5 fibroblasts (IC50s = 0.009 and 0.27 µM, respectively).2 It induces the production of reactive oxygen species (ROS) in SK-N-MC cells when used at a concentration of 5 µM. Cu-GTSM (2.5 mg/kg) reduces tumor burden in the transgenic adenocarcinoma of mouse prostate (TRAMP) model but induces weight loss and renal toxicity in the same model.3 Cu-GTSM-containing positron-emitting copper isotopes have been used in PET imaging applications for copper trafficking in the TASTPM transgenic mouse model of Alzheimer’s disease.4
1.Haeili, M., Moore, C., Davis, C.J.C., et al.Copper complexation screen reveals compounds with potent antibiotic properties against methicillin-resistant Staphylococcus aureusAntimicrob Agents Chemother.58(7)3727-3736(2014) 2.Stefani, C., Al-Eisawi, Z., Jansson, P.J., et al.Identification of differential anti-neoplastic activity of copper bis(thiosemicarbazones) that is mediated by intracellular reactive oxygen species generation and lysosomal membrane permeabilizationJ. Inorg. Biochem.15220-37(2015) 3.Cater, M.A., Pearson, H.B., Wolyniec, K., et al.Increasing intracellular bioavailable copper selectively targets prostate cancer cellsACS Chem. Biol.8(7)1621-1631(2013) 4.Torres, J.B., Andreozzi, E.M., Dunn, J.T., et al.PET imaging of copper trafficking in a mouse model of alzheimer diseaseJ. Nucl. Med.57(1)109-114(2016)
| Cas No. | 68341-14-0 | SDF | Download SDF |
| 别名 | CuII(gtsm), copper-GTSM | ||
| Canonical SMILES | CNC1=N[N]2=CC=[N]3[Cu+2]2([S-]1)[S-]C(NC)=N3 | ||
| 分子式 | C6H10CuN6S2 | 分子量 | 293.9 |
| 溶解度 | DMF: 20 mg/mL,DMSO: 10 mg/mL,Ethanol: Slightly soluble,PBS (pH 7.2): 0.16 mg/mL | 储存条件 | -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 | 3.4025 mL | 17.0126 mL | 34.0252 mL |
| 5 mM | 0.6805 mL | 3.4025 mL | 6.805 mL |
| 10 mM | 0.3403 mL | 1.7013 mL | 3.4025 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。
PET Imaging of Copper Trafficking in a Mouse Model of Alzheimer Disease
J Nucl Med 2016 Jan;57(1):109-14.PMID:26449834DOI:10.2967/jnumed.115.162370.
Alzheimer disease (AD) is a fatal neurodegenerative disorder characterized by progressive neuronal loss and cognitive decline. The lack of reliable and objective diagnostic markers for AD hampers early disease detection and treatment. Growing evidence supports the existence of a dysregulation in brain copper trafficking in AD. The aim of this study was to investigate brain copper trafficking in a transgenic mouse model of AD by PET imaging with (64)Cu, to determine its potential as a diagnostic biomarker of the disorder. Methods: Brain copper trafficking was evaluated in 6- to 8-mo-old TASTPM transgenic mice and age-matched wild-type controls using the (64)Cu bis(thiosemicarbazone) complex (64)Cu-GTSM (glyoxalbis(N(4)-methyl-3-thiosemicarbazonato) copper(II)), which crosses the blood-brain barrier and releases (64)Cu bioreductively into cells. Animals were intravenously injected with (64)Cu-GTSM and imaged at 0-30 min and 24-25 h after injection. The images were analyzed by atlas-based quantification and texture analysis. Regional distribution of (64)Cu in the brain 24 h after injection was also evaluated via ex vivo autoradiography and compared with amyloid-β plaque deposition in TASTPM mice. Results: Compared with controls, in TASTPM mice PET image analysis demonstrated significantly increased (by a factor of ~1.3) brain concentration of (64)Cu at 30 min (P < 0.01) and 24 h (P < 0.05) after injection of the tracer and faster (by a factor of ~5) (64)Cu clearance from the brain (P < 0.01). Atlas-based quantification and texture analysis revealed significant differences in regional brain uptake of (64)Cu and PET image heterogeneity between the 2 groups of mice. Ex vivo autoradiography showed that regional brain distribution of (64)Cu at 24 h after injection did not correlate with amyloid-β plaque distribution in TASTPM mice. Conclusion: The trafficking of (64)Cu in the brain after administration of (64)Cu-GTSM is significantly altered by AD-like pathology in the TASTPM mouse model, suggesting that (64)Cu-GTSM PET imaging warrants clinical evaluation as a diagnostic tool for AD and possibly other neurodegenerative disorders.
Metformin induces an intracellular reductive state that protects oesophageal squamous cell carcinoma cells against cisplatin but not copper-bis(thiosemicarbazones)
BMC Cancer 2014 May 5;14:314.PMID:24886082DOI:10.1186/1471-2407-14-314.
Background: Oesophageal squamous cell carcinoma (OSCC) is a highly aggressive carcinoma with a poor survival rate. One of the most commonly used chemotherapeutic drugs, cisplatin, displays varied and often poor efficacy in vivo. Therefore, alternative, cost-effective and more efficacious treatments are required. Metformin has been previously shown to reduce proliferative rates in various carcinoma cell lines. We report for the first time, the effect of metformin on OSCC cell proliferation and show that it antagonises cisplatin-induced but not copper-bis(thiosemicarbazone)-induced cytotoxicity in OSCC cells. Methods: Cell proliferation and stage of the cell cycle were quantified by trypan blue counts and flow cytometry, respectively. All cytotoxicity measurements were made using the tetrazolium based MTT assay. Metabolic alterations to cells were determined as follows: glycolysis via a lactate dehydrogenase assay, reducing equivalents by MTT reduction and reduced intracellular thiols by monobromobimane-thiol fluorescence, and glutathione depletion using buthionine sulfoximine. Inductively coupled plasma mass spectrometry was used to quantify cisplatin-DNA adduct formation. Results: Metformin was found to reduce cell proliferation significantly in all OSCC cell lines, with an accumulation of cells in G0/G1 phase of the cell cycle. However, metformin significantly protected OSCC cells against cisplatin toxicity. Our results indicate that a major mechanism of metformin-induced cisplatin resistance results from a significant increase in glycolysis, intracellular NAD(P)H levels with a concomitant increase in reduced intracellular thiols, leading to decreased cisplatin-DNA adduct formation. The glutathione synthesis inhibitor buthionine sulfoximine significantly ablated the protective effect of metformin. We subsequently show that the copper-bis(thiosemicarbazones), Cu-ATSM and Cu-GTSM, which are trapped in cells under reducing conditions, cause significant OSCC cytotoxicity, both alone and in combination with metformin. Conclusions: This is the first study showing that metformin can be used to decrease cell proliferation in OSCC cells. However, metformin protects against cisplatin cytotoxicity by inducing a reducing intracellular environment leading to lower cisplatin-DNA adduct formation. As such, we advise that caution be used when administering cisplatin to diabetic patients treated with metformin. Furthermore, we propose a novel combination therapy approach for OSCC that utilises metformin with metformin-compatible cytotoxic agents, such as the copper-bis(thiosemicarbazones), Cu-ATSM and Cu-GTSM.