Antimycin A1
(Synonyms: 抗黴素A1) 目录号 : GC42818An active component of the antimycin A antibiotic complex
Cas No.:642-15-9
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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- SDS (Safety Data Sheet)
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Antimycin A, an antibiotic produced by Streptomyces species that demonstrates antifungal, insecticidal, nematocidal, and piscicidal properties, is a mixture of Antimycins A1, A2, A3, and A4. [1] It blocks mitochondrial respiration and can deplete cellular levels of ATP via inhibition of complex III of the mitochondrial electron transport chain (ETC). Antimycin A prevents the transfer of electrons between the b-cytochromes and ubiquinone at the Q(inner) site of complex III. This results in the stabilization of the ubisemiquinone radical at the Q(outer) site of complex III, leading to increased production of superoxide. [2][3] Antimycin A is widely used in research to shunt electron flow through the ETC in order to study the chemical details of oxygen respiration. Additionally, antimycin A has been shown to inhibit Bcl-2 and Bcl-xL proteins, inducing apoptosis.[3][4][5]
Reference:
[1]. Seipke, R.F., and Hutchings, M.I. The regulation and biosynthesis of antimycins. Beilstein J.Org.Chem. 9, 2556-2563 (2013).
[2]. Muller, F., Crofts, A.R., and Kramer, D.M. Multiple Q-cycle bypass reactions at the Qo site of the cytochrome bc1 complex. Biochemistry 41(25), 7866-7874 (2002).
[3]. Muller, F.L., Roberts, A.G., Bowman, M.K., et al. Architecture of the Qo site of the cytochrome bc1 complex probed by superoxide production. Biochem. 42(21), 6493-6499 (2003).
[4]. Azmi, A.S., and Mohammad, R.M. Non-peptidic small molecule inhibitors against Bcl-2 for cancer therapy. J.Cell Physiol. 218(1), 13-21 (2009).
[5]. Marton, A., Mihalik, R., Bratincsak, A., et al. Apoptotic cell death induced by inhibitors of energy conservation--Bcl-2 inhibits apoptosis downstream of a fall of ATP level. Eur. J. Biochem. 250(2), 467-475 (1997).
| Cas No. | 642-15-9 | SDF | |
| 别名 | 抗黴素A1 | ||
| 化学名 | 2(or 3)-methyl-butanoic acid, (2R,3S,6S,7R,8R)-3-[[3-(formylamino)-2-hydroxybenzoyl]amino]-8-hexyl-2,6-dimethyl-4,9-dioxo-1,5-dioxonan-7-yl ester | ||
| Canonical SMILES | CC(C)CC(O[C@H]([C@H]1CCCCCC)[C@H](C)OC([C@@H](NC(C2=CC=CC(NC([H])=O)=C2O)=O)[C@@H](C)OC1=O)=O)=O | ||
| 分子式 | C28H40N2O9 | 分子量 | 548.6 |
| 溶解度 | Soluble in ethanol, methanol, DMSO, DMF | 储存条件 | Store at -20°C, protect from light |
| 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 | 1.8228 mL | 9.1141 mL | 18.2282 mL |
| 5 mM | 0.3646 mL | 1.8228 mL | 3.6456 mL |
| 10 mM | 0.1823 mL | 0.9114 mL | 1.8228 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。
Inhibition of angiogenesis and HIF-1alpha activity by Antimycin A1
Biol Pharm Bull 2006 Jul;29(7):1344-8.PMID:16819166DOI:10.1248/bpb.29.1344.
We identified Antimycin A1 as an inhibitor of the hypoxia-response element (HRE) from screening using a reporter under the control of HRE under hypoxic conditions. Antimycin A1 was effective at 20 pg/ml in inhibiting the reporter activity. The expression of vascular endothelial growth factor (VEGF) mRNA during hypoxia was also inhibited by Antimycin A1. Angiogenesis induced by implantation of mouse sarcoma-180 cells was significantly inhibited by non-toxic doses of Antimycin A1. Hypoxia inducible factor (HIF)-1alpha protein levels were significantly decreased by Antimycin A1, but its mRNA level was not affected. Antimycin A1 is known to be an inhibitor of mitochondrial electron transport system, and depletion of mitochondria abolished antimycin A1-effect, at least in part. Inhibitors of proteasome or protein synthesis did not affect the decrease in HIF-1alpha level induced by Antimycin A1. These results indicate that Antimycin A1 inhibited angiogenesis through decrease in VEGF production caused by inhibition of HIF-1alpha activation.
Simple isolation of Antimycin A1 and some of its toxicological properties
Appl Microbiol 1969 Jan;17(1):102-5.PMID:5774751DOI:10.1128/am.17.1.102-105.1969.
An unidentified actinomycete, RTI 246, was found to produce antimycin A(1) in high yield on a high protein cereal medium. The antibiotic compound was extracted from the cells and isolated in pure form by crystallization. It was identified by ultraviolet, infrared, nuclear magnetic resonance, and mass spectroscopy and by alkaline hydrolysis to antimycic acid and a neutral lactone. The intravenous LD(50) was 1.0 mg/kg in white mice, whereas the intraperitoneal LD(50) was 1.50 +/- 0.19 mg/kg. Animals receiving an intraperitoneal injection displayed an incoordination of the hind limbs and impaired reflexes before showing signs of respiratory distress. These findings indicated that antimycin A(1) possesses a neurotoxic property separate from its well-documented property as a respiratory poison.
Ginkgo extract EGb 761(®) shields from slowly accumulating neurodegenerative-like changes in a newly developed cell culture model induced by the combined action of low doses of Antimycin A1 and 2-deoxy-D-glucose
J Neural Transm (Vienna) 2011 Aug;118(8):1247-54.PMID:21479515DOI:10.1007/s00702-011-0637-2.
Different cell culture models were already used to analyze the molecular base of the neuroprotective activities of the Ginkgo biloba extract EGb 761(®) after a single or short-term application. In these previous studies cells were severely injured with agents that promptly induce fatal cellular damage, like vast oxidative stress or mitochondrial dysfunction, and the protective effects of EGb 761(®) on such acute damage were evaluated. Our present study aimed to test EGb 761(®) action in cell cultures, where cellular functions are only moderately impaired by a longer lasting, but relatively modest oxidative stress, reduction of mitochondrial function and reduced intracellular energy levels, thereby causing only slow occurence of cellular damage over a time period of 2 weeks. To this end we used neuroblastoma cells (SK-N-MC) that were treated with low doses of a combination of Antimycin A1 and 2-deoxy-D: -glucose. Addition of EGb 761(®) to the culture medium efficiently shielded the cells from progressing injury by reduced ATP-levels, oxidized redox state, lipid peroxidation damage and oxidative damage of mitochondrial DNA. As a result the cells were protected from apoptotic death that was observed in cultures without EGb 761(®) after 2 weeks of damage occurence. This cell culture system characterizing moderate cellular stress will be applied in future studies to further investigate the mode of action of single EGb 761(®) compounds.