CAY10464
目录号 : GC43159
A potent, selective aryl hydrocarbon receptor antagonist
Cas No.:688348-37-0
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
The aryl hydrocarbon receptor (AhR) is a ligand-dependent intracellular transcription factor whose ligands include some of the most infamous xenobiotics, including dioxin (TCDD, 2,3,7,8-tetrachlorodibenzoparadioxin), benzo[a]pyrene, and numerous polyaromatic hydrocarbons from soot particles and coal tar. CAY10464 is a potent and selective AhR antagonist, with a Ki of 1.4 nM when tested in rabbit liver cytosol preparations. It is inactive as an estrogen receptor ligands even at 100 µM.
| Cas No. | 688348-37-0 | SDF | |
| Canonical SMILES | COc1ccc(cc1)\C=C/c1cc(Cl)cc(Cl)c1 | ||
| 分子式 | C15H12Cl2O | 分子量 | 279.2 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS (pH 7.2)(1:1): .5 mg/ml,Ethanol: 10 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 | 3.5817 mL | 17.9083 mL | 35.8166 mL |
| 5 mM | 0.7163 mL | 3.5817 mL | 7.1633 mL |
| 10 mM | 0.3582 mL | 1.7908 mL | 3.5817 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。
Resveratrol Analogs with Antioxidant Activity Inhibit Intestinal Epithelial Cancer Caco-2 Cell Growth by Modulating Arachidonic Acid Cascade
J Agric Food Chem 2019 Jan 23;67(3):819-828.PMID:30575383DOI:10.1021/acs.jafc.8b05982.
trans-Resveratrol has beneficial effects on colorectal cancer, through its antioxidant capacity, and its roles in regulating eicosanoid synthesis. This study determines how changes in resveratrol structure affected its biological activities. Our results showed that trans- and cis-resveratrol and hydroxylated analogs (piceatannol) (10-25 μM) displayed similar antioxidant activities (2-3 fold higher than trolox) and inhibit eicosanoid synthesis and Caco-2 growth (76.5 ± 2.7%, 48.2 ± 3.1% and 41.1 ± 2.3%, p ≤ 0.05). These effects can be related with an increase of the percentage of cells in the S phase (156.3 ± 5.6, 91.2 ± 3.3 and 64.1 ± 2.8, p ≤ 0.05) as a consequence of the impairment of the cells in G0/G1. Furthermore, we observed that these molecules induce apoptosis at 100 μM (48.2 ± 6.6%, p ≤ 0.05; 4.3 ± 2.5% and 21.2 ± 3.3%, p ≤ 0.05). These actions were related with changes of the mitochondrial membrane potential involved in the intrinsic pathway of apoptosis. However, methoxylated (pterostilbene, pinostilbene, trans-trimethoxy-resveratrol, and CAY10616) (0.1-10 μM) and halogenated (PDM11, CAY10464, PDM2, and CAY465) (1-10 μM) stilbenes inhibited Caco-2 cell growth, with a higher potency than resveratrol (50% inhibition at 0.1-1 μM) but without effects on oxidative stress and arachidonic acid cascade. Thus, our results show that the antioxidant effect of hydroxyl stilbenes is related to eicosanoid synthesis regulation and the basic stilbene structure of two benzene rings bonded through a central ethylene, is responsible for its effects on Caco-2 cell growth/DNA synthesis/cell cycle independently of redox state/eicosanoid synthesis modulation.
Inhibition of apolipoprotein A-I gene by the aryl hydrocarbon receptor: a potential mechanism for smoking-associated hypoalphalipoproteinemia
Life Sci 2012 Jul 26;91(1-2):64-9.PMID:22727790DOI:10.1016/j.lfs.2012.06.002.
Aims: Smokers have lower plasma concentrations of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apo A-I) compared with nonsmokers. To determine the molecular basis of this observation, the effect of activation of the aryl hydrocarbon receptor (AhR) on apo A-I gene expression was examined. Main methods: HepG2 cells were treated with AhR receptor agonists benzo(a)pyrene (BaP) and CAY10465, and AhR receptor antagonist CAY10464 and apo A-I protein, mRNA levels and promoter activity were measured. The effect of nicotine on apo A-I protein secretion was also tested. Using a series or apo A-I gene promoter deletion constructs, a xenobiotic response element (XRE) was identified. Key findings: Treatment of HepG2 cells with the AhR receptor agonists BaP and CAY10465, inhibited apo A-I protein synthesis while nicotine, which does not bind AhR had no effect. Benzo(a)pyrene treatment also suppressed apo A-I mRNA and gene promoter activity. Treatment of HepG2 cells with the AhR receptor antagonist CAY10464 reversed the suppressive effect of BaP on apo A-I gene expression. A putative xenobiotic response element (XRE) was identified between nucleotides -325 and -186 (relative to the transcriptional start site, +1). Significance: These results suggest that the cigarette smoking related environmental contaminant BaP promotes hypoalphalipoproteinemia in part through activation of the hepatic AhR.