Ammonium tetrathiomolybdate(VI)
目录号 : GC67669Ammonium tetrathiomolybdate(VI)是一种由铵阳离子和四硫代钼酸根(VI)阴离子组成的无机化合物，常用于心脑血管等疾病的代谢研究及作为重金属解毒的螯合剂。
Cas No.:15060-55-6
Sample solution is provided at 25 µL, 10mM.
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Ammonium tetrathiomolybdate(VI) is an inorganic compound composed of ammonium cations and tetrathiomolybdate(VI) anions. Ammonium tetrathiomolybdate(VI) is commonly used in metabolic research of cardiovascular and cerebrovascular diseases and as a chelating agent for heavy metal detoxification[1]. The chemical formula of Ammonium tetrathiomolybdate(VI) is (NH₄)₂MoS₄. Ammonium tetrathiomolybdate(VI) is highly soluble in water and serves as a source of molybdenum in biological systems. Ammonium tetrathiomolybdate(VI) is particularly valuable in the study of molybdenum-dependent enzymes such as sulfite oxidase and xanthine oxidase[2]. The thiolate ligands in this compound enable Ammonium tetrathiomolybdate(VI) to act as a chelator, binding to heavy metals like copper and iron.The neuroprotective effects of Ammonium tetrathiomolybdate (VI) are receiving extensive attention in cerebral ischemia research[3]. Additionally, Ammonium tetrathiomolybdate(VI) copper chelation complexes exhibit antibacterial properties[4].
In vitro, AC16 cardiomyocytes were treated with Ammonium tetrathiomolybdate(VI) (20μM). Pre-treatment with Ammonium tetrathiomolybdate(VI) significantly increased cell viability, indicating Ammonium tetrathiomolybdate(VI) protective effect against copper-induced cytotoxicity[5]. In HeLa cells, treatment with Ammonium tetrathiomolybdate(VI) (20μM) failed to affect the increase in LC3-II levels induced by ML-SA5 (1μM) and could not reverse the autophagy-inhibiting effect of ML-SA5[6].
In vivo, a rat model of focal cerebral ischemia-reperfusion (tMCAO, ischemia for 90 minutes) was established. Ammonium tetrathiomolybdate(VI) (10mg/kg) was administered intravenously immediately before reperfusion, followed by continuous intravenous infusion at 10mg/kg/h for 60 minutes. This treatment improved the motor coordination and spontaneous movement duration of tMCAO mice and reduced the infarct area[7]. In a model of endometriosis induced by autologous uterine tissue transplantation in TNFR1⁻/⁻ female C57BL/6 mice, oral administration of Ammonium tetrathiomolybdate(VI) (0.3mg) for 1 month resulted in the chelation of copper ions, downregulation of estradiol levels and angiogenesis-related genes, inhibition of cell proliferation, and induction of oxidative stress. These effects collectively slowed the progression of endometriosis in TNFR1⁻/⁻ mice[8].
References:
[1] Zhang M, Qiu H, Mao L, et al. Ammonium tetrathiomolybdate triggers autophagy-dependent NRF2 activation in vascular endothelial cells. Cell Death Dis. 2022 Aug 25;13(8):733.
[2] Langlois DK, Querubin JR, Schall WD, et al. Ammonium tetrathiomolybdate treatment of copper-associated hepatopathy in dogs. J Vet Intern Med. 2019 May;33(3):1336-1343.
[3] Mendonça BP, Cardoso JDS, Michels M, et al. Neuroprotective effects of ammonium tetrathiomolybdate, a slow-release sulfide donor, in a rodent model of regional stroke. Intensive Care Med Exp. 2020 Apr 9;8(1):13.
[4] Zhang L, Tsai IC, Ni Z, et al. Copper Chelation Therapy Attenuates Periodontitis Inflammation through the Cuproptosis/Autophagy/Lysosome Axis. Int J Mol Sci. 2024 May 28;25(11):5890.
[5] Huo S, Wang Q, Shi W, et al. ATF3/SPI1/SLC31A1 Signaling Promotes Cuproptosis Induced by Advanced Glycosylation End Products in Diabetic Myocardial Injury. Int J Mol Sci. 2023 Jan 14;24(2):1667.
[6] Qi J, Xing Y, Liu Y, et al. MCOLN1/TRPML1 finely controls oncogenic autophagy in cancer by mediating zinc influx. Autophagy. 2021 Dec;17(12):4401-4422.
[7] Dyson A, Dal-Pizzol F, Ammonium tetrathiomolybdate following ischemia/reperfusion injury: Chemistry, pharmacology, and impact of a new class of sulfide donor in preclinical injury models. PLoS Med. 2017 Jul 5;14(7):e1002310.
[8] Conforti RA, Delsouc MB, Zabala AS, et al. The copper chelator ammonium tetrathiomolybdate inhibits the progression of experimental endometriosis in TNFR1-deficient mice. Sci Rep. 2023 Jun 26;13(1):10354.
Ammonium tetrathiomolybdate(VI)是一种由铵阳离子和四硫代钼酸根(VI)阴离子组成的无机化合物，常用于心脑血管等疾病的代谢研究及作为重金属解毒的螯合剂[1]。Ammonium tetrathiomolybdate(VI)的化学式为(NH₄)₂MoS₄，易溶于水，作为生物系统中钼的来源，在研究亚硫酸盐氧化酶和黄嘌呤氧化酶等钼依赖酶时具有重要价值[2]。Ammonium tetrathiomolybdate(VI)的硫醇盐配体使其能够作为螯合剂，与铜、铁等重金属结合。在脑缺血研究中，Ammonium tetrathiomolybdate(VI)的神经保护作用正受到广泛关注[3]，同时Ammonium tetrathiomolybdate与铜的螯合化合物具有杀菌作用[4]。
在体外，Ammonium tetrathiomolybdate(VI) (20μM)处理AC16心肌细胞，Ammonium tetrathiomolybdate(VI)的预处理能够显著提高细胞的存活率，且Ammonium tetrathiomolybdate(VI)对铜诱导的细胞毒性具有保护作用[5]。Ammonium tetrathiomolybdate(VI) (20μM)处理HeLa细胞，Ammonium tetrathiomolybdate(VI)未能影响由ML-SA5（1μM）诱导的LC3-II水平增加，且无法逆转ML-SA5的自噬抑制作用[6]。
在体内，建立大鼠局灶性脑缺血再灌注模型（tMCAO，缺血90分钟），在再灌注前立即通过静脉注射 Ammonium tetrathiomolybdate(VI)（10mg/kg），随后持续静脉输注10mg/kg/h维持60分钟，Ammonium tetrathiomolybdate(VI)可提升tMCAO小鼠的运动协调能力和自发运动活动时间，并降低脑梗死面积[7]。取自体子宫组织移植诱导子宫内膜异位症模型的TNFR1⁻/⁻雌性C57BL/6小鼠口服Ammonium tetrathiomolybdate(VI)（0.3mg），连续1个月。Ammonium tetrathiomolybdate(VI)可通过螯合铜离子，下调雌二醇水平及血管生成相关基因，抑制细胞增殖并诱导氧化应激，从而减缓TNFR1⁻/⁻小鼠子宫内膜异位症的进展[8]。
| Cell experiment [1]: | |
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Cell lines |
AC16 cardiomyocytes |
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Preparation Method |
AC16 cardiomyocytes were seeded into 96-well plates with 5 × 103 cells per well and cultured for 24 hours. The cells were then treated with different concentrations (0, 10, 20, 50, and 100μM) of Ammonium tetrathiomolybdate(VI). Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay after 48 hours of treatment. |
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Reaction Conditions |
0, 10, 20, 50, and 100μM; 48 hours |
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Applications |
Ammonium tetrathiomolybdate(VI) improved the cell viability of AC16 cardiomyocytes treated with copper ionophores and copper ions, Ammonium tetrathiomolybdate(VI) protective effect against copper-induced cytotoxicity |
| Animal experiment [2]: | |
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Animal models |
TNFR1⁻/⁻ female C57BL/6 mice |
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Preparation Method |
Female TNFR1⁻/⁻ C57BL/6 mice (2 months old) were used to induce endometriosis by autologous uterine tissue transplantation to the intestinal mesentery. From the 15th postoperative day, the mice received oral administration of 0.3mg Ammonium tetrathiomolybdate(VI) daily until sacrifice at 1 month post-induction. |
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Dosage form |
0.3mg/mouse daily for 2 weeks; oral gavage |
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Applications |
Ammonium tetrathiomolybdate(VI) reduced copper and estradiol levels in peritoneal fluid, decreased endometriotic lesion volume and weight, inhibited cell proliferation (PCNA-positive cells), reduced blood vessel density, and downregulated angiogenic genes (Vegfa, Fgf2, Pdgfb). |
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References: |
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| Cas No. | 15060-55-6 | SDF | Download SDF |
| 分子式 | H8MoN2S4 | 分子量 | 260.27 |
| 溶解度 | DMSO : 5 mg/mL (19.21 mM; Need ultrasonic) | 储存条件 | 4°C, protect from light |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.8422 mL | 19.2108 mL | 38.4216 mL |
| 5 mM | 0.7684 mL | 3.8422 mL | 7.6843 mL |
| 10 mM | 0.3842 mL | 1.9211 mL | 3.8422 mL |
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2.
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