Powder: -20°C for 3 years | In solvent: -80°C for 1 year
AZ876 是高亲和力的 LXR 激动剂。它在人的 (h)LXRα 和 hLXRβ 比 GW3965 要分别强 25 和 2.5 倍。
规格 | 价格/CNY | 货期 | 数量 | |
---|---|---|---|---|
1 mg | ¥ 397 | 现货 | ||
5 mg | ¥ 843 | 现货 | ||
10 mg | ¥ 1,240 | 现货 | ||
50 mg | ¥ 1,995 | 现货 | ||
100 mg | ¥ 3,775 | 现货 |
产品描述 | AZ876 is a potent, highly selective LXR agonist with Ki/EC50 of 7/6 nM and 11/73 nM for hLXRα and hLXRβ respectively. |
靶点活性 | LXR:6 nM (EC50, cell free) |
体外活性 | AZ876 suppressed up-regulation of hypertrophy- and fibrosis-related genes and further inhibited prohypertrophic and profibrotic TGFβ-Smad2/3 signaling. In cardiomyocytes, phenylephrine-stimulated cellular hypertrophy was significantly decreased in AZ876-treated cells. In cardiac fibroblasts, AZ876 prevented TGFβ- and angiotensin II-induced fibroblast collagen synthesis, and inhibited up-regulation of the myofibroblastic marker, α-smooth muscle actin [2]. |
体内活性 | Low-dose AZ876 had no effect on plasma or liver lipids, whereas high-dose AZ876 increased plasma triglycerides and reduced cholesterol compared with controls. Low-dose AZ876 reduced lesion area; and high-dose AZ876 strongly decreased lesion area, lesion number, and severity. In either dose, AZ876 did not affect lesion composition [1]. Cardiac hypertrophy was induced in C57Bl6/J mice via transverse aortic constriction (TAC) for 6 weeks. During this period, mice received chow supplemented or not with AZ876 (20?μmol/kg/day). In murine hearts, LXRα protein expression was up-regulated ~7-fold in response to TAC. LXR activation with AZ876 attenuated this increase, and significantly reduced TAC-induced increases in heart weight, myocardial fibrosis, and cardiac dysfunction without affecting blood pressure [2]. |
激酶实验 | Binding vectors for His-tagged protein production were prepared by inserting the ligand-binding domain cDNA of human LXRα (amino acids 205–447) in pET28 and the ligand-binding domain cDNA of LXRβ (amino acids 216–461) in pET24D. Proteins were expressed in Escherichia coli and purified on Ni+ columns. Binding assays using LXRα and LXRβ protein were run by adding reagents to Wallac Isoplate 1450–514. Briefly, each 96 plate well contained assay buffer (20 mM Tris pH 7.5, 80 mM NaCl, 2 mM dithiothreitol, 0.125% Chaps and 10% glycerol), 0.1 mg SPA beads (polylysine-coated yttrium silicate beads), LXRα (0.5 μg) or LXRβ (0.25 μg), 30 nM 3H-ligand (specific activity of 473 Kbq/nmol) and test compound in a 10-point dose-response dilution. The assay mixture was shaken gently for 2 h on a plate shaker after which the beads were allowed to settle for 1 hour before counting. Transactivation vectors were prepared by inserting the ligand-binding domain cDNA sequences of human or mouse LXRα and LXRβ in frame with the yeast Gal4 transcription factor DNA binding domain and the nuclear localization signal from the T-antigen of polyomavirus in the eucaryotic expression vector pSG5. The ligand-binding domain cDNA of human LXRα and LXRβ was the same as mentioned previously. The mouse sequence corresponded to amino acids 203–445 for LXRα and amino acids 201–446 for LXRβ. The vectors were co-transfected with a pGL3 luciferase reporter plasmid containing a minimal SV40 promoter and five copies of the UAS Gal4 recognition site into U2/OS osteosarcoma cells. Ligands were added as 10-point dose-response curves and then luciferase activity was measured after 48 h [1]. |
动物实验 | Cardiac hypertrophy was induced in male C57Bl6/J mice via transverse aortic constriction (TAC) for 6 weeks. During this period, sham and TAC-operated mice were randomized to receive either regular chow (control) or chow supplemented with AZ876 (20 μmol/kg/day). Cardiac function was assessed with echocardiography and invasive haemodynamics. In vitro studies were performed in isolated neonatal rat ventricular myocytes (NRVMs) and adult rat cardiac fibroblasts. Leucine and proline tracer assays were used to measure protein and collagen synthesis, respectively [2]. |
分子量 | 439.57 |
分子式 | C24H29N3O3S |
CAS No. | 898800-26-5 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
DMSO: 55 mg/mL (125.12 mM)
可选溶剂 | 浓度 体积 质量 | 1 mg | 5 mg | 10 mg | 25 mg |
DMSO | 1 mM | 2.275 mL | 11.3748 mL | 22.7495 mL | 56.8738 mL |
5 mM | 0.455 mL | 2.275 mL | 4.5499 mL | 11.3748 mL | |
10 mM | 0.2275 mL | 1.1375 mL | 2.275 mL | 5.6874 mL | |
20 mM | 0.1137 mL | 0.5687 mL | 1.1375 mL | 2.8437 mL | |
50 mM | 0.0455 mL | 0.2275 mL | 0.455 mL | 1.1375 mL | |
100 mM | 0.0227 mL | 0.1137 mL | 0.2275 mL | 0.5687 mL |
对于不同动物的给药剂量换算,您也可以参考 更多...
请在以下方框中输入您的动物实验信息后点击计算,可以得到母液配置方法和体内配方的制备方法: 比如您的给药剂量是10 mg/kg,每只动物体重20 g,给药体积100 μL,一共给药动物10 只,您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。
母液配置方法:2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL), 如您需要配置的浓度超过该产品的溶解度,请先与我们联系。
体内配方的制备方法:取 50 μL DMSO 主液,加入 300 μL PEG300, 混匀澄清,再加 50 μL Tween 80,混匀澄清,再加 600 μL ddH2O, 混匀澄清。
您可能有的问题的答案可以在抑制剂处理说明中找到,包括如何准备库存溶液,如何存储产品,以及基于细胞的分析和动物实验需要特别注意的问题。
AZ876 898800-26-5 Metabolism Liver X Receptor AZ-876 Liver X receptor LXR AZ 876 Inhibitor inhibit inhibitor