AEM1
目录号 : GC42743
An inhibitor of Nrf2-induced gene expression
Cas No.:1030123-90-0
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
Cancer cell survival appears partly dependent on antioxidative enzymes, whose expression is regulated by the Keap1-Nrf2 pathway, to quench potentially toxic reactive oxygen species generated by their metastatic transformation. AEM1 is an inhibitor of Nrf2-induced gene transcription at the antioxidant response element in cells at 1 to 10 µM. It sensitizes lung carcinoma A549 cells to chemotherapeutic agents and inhibits the growth of A549 cells in vitro and in vivo in animals. The effectiveness of AEM1 against cancer cells is restricted to those harboring mutations that render Nrf2 constitutively active.
| Cas No. | 1030123-90-0 | SDF | |
| Canonical SMILES | FC(C=C1)=CC=C1C2=CSC3=C2C(NCC4=CC=C(OCO5)C5=C4)=NC=N3 | ||
| 分子式 | C20H14FN3O2S | 分子量 | 379.4 |
| 溶解度 | DMF: 30 mg/mL,DMF:PBS (pH 7.2) (1:4): 0.2 mg/mL,DMSO: 20 mg/mL,Ethanol: 0.25 mg/mL | 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 | 2.6357 mL | 13.1787 mL | 26.3574 mL |
| 5 mM | 0.5271 mL | 2.6357 mL | 5.2715 mL |
| 10 mM | 0.2636 mL | 1.3179 mL | 2.6357 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。
Defects in root development and gravity response in the AEM1 mutant of rice are associated with reduced auxin efflux
J Plant Physiol 2005 Jun;162(6):678-85.PMID:16008090DOI:10.1016/j.jplph.2004.09.012.
The phytohormone auxin is involved in the regulation of a variety of developmental processes. In this report, we describe how the processes of lateral root and root hair formations and root gravity response in rice are controlled by auxin. We use a rice mutant AEM1 (auxin efflux mutant) because the mutant is defective in these characters. The AEM1 line was originally isolated as a short lateral root mutant, but we found that the mutant has a defect in auxin efflux in roots. The acropetal and basipetal indole-3-acetic acid (IAA) transports were reduced in AEM1 roots compared to wild type (WT). Furthermore, gravitropic bending as well as efflux of radioactive IAA was impaired in the mutant roots. We also propose a unique distribution of endogenous IAA in AEM1 roots. An immunoassay revealed a 4-fold-endogenous IAA content in the AEM1 roots compared to WT, and the application of IAA to the shoot of WT seedlings mimicked the short lateral root phenotype of AEM1, suggesting that the high content of IAA in AEM1 roots impaired the elongation of lateral roots. However, the high level of IAA in AEM1 roots contradicts the auxin requirement for root hair formation in the epidermis of mutant roots. Since the reduced development in root hairs of AEM1 roots was rescued by exogenous auxin, the auxin level in the epidermis is likely to be sub-optimum in AEM1 roots. This discrepancy can be solved by the ideas that IAA level is higher in the stele and lower in the epidermis of AEM1 roots compared to WT and that the unique distribution of IAA in AEM1 roots is induced by the defect in auxin efflux. All these results suggest that AEM1 may encode a component of auxin efflux carrier in rice and that the defects in lateral roots, root hair formation and root gravity response in AEM1 mutant are due to the altered auxin efflux in roots.
A Small Molecule Inhibits Deregulated NRF2 Transcriptional Activity in Cancer
ACS Chem Biol 2015 Oct 16;10(10):2193-8.PMID:26270491DOI:10.1021/acschembio.5b00448.
NRF2 serves as the master regulator of oxidative stress resistance in mammalian cells. Although NRF2 activation decreases tumorigenic events in normal cells, accumulating evidence suggests that cancers have broadly selected for NRF2-activating mutations to promote anabolic growth and chemoresistance. Small molecules which inhibit NRF2 activity may therefore offer promise as an alternative anticancer treatment in NRF2 dependent cancers. We have used a high throughput screen to identify small molecules which decrease NRF2 transcriptional activity at antioxidant response element sites. One such molecule, termed AEM1, is capable of broadly decreasing the expression of NRF2 controlled genes, sensitizing A549 cells to various chemotherapeutic agents, and inhibiting the growth of A549 cells in vitro and in vivo. Profiling of multiple cell lines for their responsiveness to AEM1 revealed that AEM1's activities are restricted to cell lines harboring mutations which render NRF2 constitutively active.
A novel sirtuin 2 (SIRT2) inhibitor with p53-dependent pro-apoptotic activity in non-small cell lung cancer
J Biol Chem 2014 Feb 21;289(8):5208-16.PMID:24379401DOI:10.1074/jbc.M113.487736.
Sirtuin 2 (SIRT2) is an NAD(+)-dependent protein deacetylase whose targets include histone H4 lysine 16, p53, and α-tubulin. Because deacetylation of p53 regulates its effect on apoptosis, pharmacological inhibition of SIRT2-dependent p53 deacetylation is of great therapeutic interest for the treatment of cancer. Here, we have identified two structurally related compounds, AEM1 and AEM2, which are selective inhibitors of SIRT2 (IC50 values of 18.5 and 3.8 μM, respectively), but show only weak effects on other sirtuins such as SIRT1, SIRT3, and yeast Sir2. Interestingly, both compounds sensitized non-small cell lung cancer cell lines toward the induction of apoptosis by the DNA-damaging agent etoposide. Importantly, this sensitization was dependent on the presence of functional p53, thus establishing a link between SIRT2 inhibition by these compounds and p53 activation. Further, treatment with AEM1 and AEM2 led to elevated levels of p53 acetylation and to increased expression of CDKN1A, which encodes the cell cycle regulator p21(WAF1), as well as the pro-apoptotic genes PUMA and NOXA, three transcriptional targets of p53. Altogether, our data suggest that inhibition of SIRT2 by these compounds causes increased activation of p53 by decreasing SIRT2-dependent p53 deacetylation. These compounds thus provide a good opportunity for lead optimization and drug development to target p53-proficient cancers.
Adsorption and anticorrosive behavior of aromatic epoxy monomers on carbon steel corrosion in acidic solution: computational studies and sustained experimental studies
RSC Adv 2019 May 14;9(26):14782-14796.PMID:35516296DOI:10.1039/c9ra01672d.
Herein, the synthesis, characterization and corrosion inhibition effectiveness of two aromatic epoxy monomers (AEMs) namely, 2-(oxiran-2-yl-methoxy)-N,N-bis(oxiran-2-yl-methyl)aniline (AEM1) and N,N-bis(oxiran-2-ylmethyl)-2-((oxiran-2-ylmethyl) thio)aniline (AEM2), in carbon steel corrosive dissolution in 1 M HCl solution is investigated using computational and experimental techniques. AEM1 and AEM2 were characterized using FT-IR, 1H NMR and 13C NMR spectroscopy techniques. Electrochemical results demonstrated that AEMs act as reasonably good corrosion inhibitors for carbon steel in 1 M HCl medium and their effectiveness followed the sequence: AEM2 (95.4%) > AEM1 (94.3%). A PDP study showed that AEMs act as mixed-type inhibitors with slight anodic predominance. Adsorption of the AEMs obeyed the Langmuir isotherm model. Interactions between AEMs and the metallic surface was further studied using DFT and MD simulations that give several computational parameters such as I, A, E HOMO, E LUMO, ΔE, δ, χ, ρ, σ, η, ΔN and E ads. The experimental and computational results were in good agreement and well complimented each other.
Microbial metabolism studies of the antimalarial drug arteether
Pharm Res 1990 Feb;7(2):199-203.PMID:2308900DOI:10.1023/a:1015845306124.
Microbial metabolism studies of the antimalarial drug arteether (1) have shown that arteether is metabolized by a number of microorganisms. Large-scale fermentation with Aspergillus niger (ATCC 10549) and Nocardia corallina (ATCC 19070) have resulted in the isolation of four microbial metabolites which have been characterized using two-dimensional nuclear magnetic resonance (2D-NMR) techniques. These metabolites have been identified as "AEM1" (2), 3 alpha-hydroxydeoxyarteether (3), 3 alpha-hydroxydeoxydihydroartemisinin (4), and deoxydihydroartemisinin (5).