DC_AC50
目录号 : GC15206
DC_AC50是一种小分子化合物，可抑制铜转运蛋白ATOX-1与CCS，Kd值分别为6.8±1.7µM和8.2±2.7µM。
Cas No.:497061-48-0
Sample solution is provided at 25 µL, 10mM.
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DC_AC50 is a small molecule that inhibits the copper-trafficking proteins ATOX-1 and CCS, with Kd values of 6.8±1.7µM and 8.2±2.7µM, respectively[1]. DC_AC50 is a self-fluorescing compound with excitations at 290nm and 355nm, and emission at 494nm[1]. DC_AC50 can block the copper transport interface of the two major copper chaperones ATOX-1 and CCS to increase intracellular copper levels and lead to enhanced oxidative stress in the cells[2]. DC_AC50 has been widely used to enhance intracellular reactive oxygen species (ROS) levels and inhibit tumor cell growth[3].
In vitro, DC_AC50 treatment for 72 hours significantly inhibited the viability of Abrams and D17 cells with IC50 values of 9.88µM and 12.57µM, respectively[4]. Treatment with 25μM DC_AC50 for 7 days can effectively inhibit the proliferation of BRAF-mutated melanoma cells and weaken the activation of the MAPK pathway[5]. Treatment with 10μM DC_AC50 for 24 hours significantly inhibited the growth of HepG2 cells, while promoting the accumulation of ROS and cell apoptosis[6]. 20µM of DC_AC50 pretreatment for 24 hours significantly inhibited the production of ROS and the M1 polarization of mouse macrophages induced by CuCl2[7].
In vivo, DC_AC50 treatment via intraperitoneal injection at a dose of 50mg/kg/day for 5 weeks inhibited tumor growth and suppressed angiogenesis in mice of MDA-MB-468 xenograft model[8]. Intraperitoneal injection of 20mg/kg/day dose of DC_AC50 for 21 consecutive days markedly reduced tumor growth in the xenograft mouse model of A549 cells, and suppressed the expression of ATOX1 in the tumors[9].
References:
[1] Wang J, Luo C, Shan C, et al. Inhibition of human copper trafficking by a small molecule significantly attenuates cancer cell proliferation[J]. Nature chemistry, 2015, 7(12): 968-979.
[2] Karginova O, Weekley C, Raoul A, et al. Selective inhibition of copper metabolism as a novel approach to treat triple-negative breast cancer[J]. Cancer Research, 2017, 77(13_Supplement): 3552-3552.
[3] Li W Y, Kan J L, Wan J J, et al. A reactive oxygen species-responsive covalent organic framework for tumor combination therapy[J]. Chemical Communications, 2023, 59(36): 5423-5426.
[4] Inkol J M, Poon A C, Mutsaers A J. Inhibition of copper chaperones sensitizes human and canine osteosarcoma cells to carboplatin chemotherapy[J]. Veterinary and comparative oncology, 2020, 18(4): 559-569.
[5] Kim Y J, Bond G J, Tsang T, et al. Copper chaperone ATOX1 is required for MAPK signaling and growth in BRAF mutation-positive melanoma[J]. Metallomics, 2019, 11(8): 1430-1440.
[6] Ouyang Q, Jia S, Zhu Q, et al. ATOX1 Promotes Hepatocellular Carcinoma Carcinogenesis via Activation of the c-Myb/PI3K/AKT Signaling Pathway[J]. Journal of Clinical and Translational Hepatology, 2025, 13(8): 630.
[7] Chen M X, Chen Y, Fu R, et al. Atox1 regulates macrophage polarization in intestinal inflammation via ROS-NLRP3 inflammasome pathway[J]. Journal of Translational Medicine, 2024, 22(1): 497.
[8] Karginova O, Weekley C M, Raoul A, et al. Inhibition of copper transport induces apoptosis in triple-negative breast cancer cells and suppresses tumor angiogenesis[J]. Molecular cancer therapeutics, 2019, 18(5): 873-885.
[9] Qin X, Wang P, Liang H, et al. Curcumin suppresses copper accumulation in non-small cell lung cancer by binding ATOX1[J]. BMC Pharmacology and Toxicology, 2024, 25(1): 54.
DC_AC50是一种小分子化合物，可抑制铜转运蛋白ATOX-1与CCS，Kd值分别为6.8±1.7µM和8.2±2.7µM[1]。DC_AC50具有自发荧光特性，激发波长为290nm和355nm，发射波长为494nm[1]。DC_AC50通过阻断ATOX-1和CCS的铜转运界面，提高细胞内铜水平并增强氧化应激[2]。DC_AC50已广泛应用于提升细胞内活性氧水平及抑制肿瘤细胞生长[3]。
在体外，DC_AC50处理72小时能显著抑制Abrams和D17细胞活力，IC50值分别为9.88µM和12.57µM[4]。使用25µM的DC_AC50处理BRAF突变型黑色素瘤细胞7天，可有效抑制细胞增殖并减弱MAPK通路活化[5]。用10µM的DC_AC50处理HepG2细胞24小时，能显著抑制细胞生长并促进活性氧积累与细胞凋亡[6]。以20µM的DC_AC50预处理小鼠巨噬细胞24小时，可显著抑制氯化铜诱导的ROS生成及M1型极化[7]。
在体内，每日腹腔注射50mg/kg/day剂量的DC_AC50连续5周，能抑制MDA-MB-468移植瘤小鼠的肿瘤生长与血管发生[8]。连续21天每日腹腔注射20mg/kg/day剂量的DC_AC50，可显著抑制A549细胞异种移植瘤小鼠模型的肿瘤生长，并降低肿瘤组织中ATOX1蛋白表达[9]。
| Cell experiment [1]: | |
Cell lines | Abrams cells |
Preparation Method | Abrams cells were cultured in Dulbecco's Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 100U/ml penicillin/streptomycin. Cells were cultured in a humidified incubator with 5% CO2 at 37°C. Cells were seeded in 96-well plates at a density of 2×103 cells/well and incubated for 16 hours. Each cell line was treated with increasing concentrations of DC_AC50 (0.1, 1, 10, and 100µM) for 72 hours. Cells were then fixed with 4% paraformaldehyde for 10min, rinsed with water, and then fixed with 0.5% crystal violet in 20% methanol. The dye was dried overnight, then eluted with 10% acetic acid, and the absorbance was read at 590nm. |
Reaction Conditions | 0.1, 1, 10, and 100µM; 72h |
Applications | DC_AC50 treatment significantly inhibited the viability of Abrams cells in a dose-dependent manner. |
| Animal experiment [2]: | |
Animal models | Female Foxn1nu/nu mice |
Preparation Method | Eight-week-old female Foxn1nu/nu mice were anesthetized by inhalation of 2% vaporized isoflurane, and 4×106 MDA-MB-468 cells (100μl) were injected unilaterally into the fourth inguinal mammary gland at the base of the nipple. Seven days after cell implantation, mice were randomly and blindly assigned to treatment groups (6-8 mice per group) and given an intraperitoneal injection of either DC_AC50 or DMSO (vehicle control) at a dose of 50mg/kg/day. Mice were monitored twice weekly for tumor growth and body weight. The tumor was measured using a caliper, and the tumor volume was calculated using equation 1/2(length×width2). The entire experiment was continued for 5 weeks after DC_AC50 administration. |
Dosage form | 50mg/kg/day for 5 weeks; i.p. |
Applications | DC_AC50 treatment inhibited tumor growth in mice with the MDA-MB-468 xenograft model. |
References: | |
| Cas No. | 497061-48-0 | SDF | |
| 化学名 | 3-amino-N-(2-bromo-4,6-difluorophenyl)-6,7-dihydro-5H-cyclopenta[b]thieno[3,2-e]pyridine-2-carboxamide | ||
| Canonical SMILES | NC1=C(C(NC2=C(C=C(F)C=C2Br)F)=O)SC3=NC4=C(CCC4)C=C31 | ||
| 分子式 | C17H12BrF2N3OS | 分子量 | 424.26 |
| 溶解度 | DMSO: 10 mg/ml | 储存条件 | Store at -20°C |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.357 mL | 11.7852 mL | 23.5705 mL |
| 5 mM | 471.4 μL | 2.357 mL | 4.7141 mL |
| 10 mM | 235.7 μL | 1.1785 mL | 2.357 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
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