Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Rofecoxib (MK 966) 是可口服的 COX-2特异性抑制剂,具有抗炎、解热和镇痛特性以及潜在的抗肿瘤特性。在人骨肉瘤细胞和中国仓鼠卵巢细胞中,对人 COX-2 的 IC50值分别为 26 和 18 nM。
规格 | 价格/CNY | 货期 | 数量 | |
---|---|---|---|---|
50 mg | ¥ 311 | 现货 | ||
100 mg | ¥ 410 | 现货 | ||
200 mg | ¥ 565 | 现货 | ||
1 mL * 10 mM (in DMSO) | ¥ 459 | 现货 |
产品描述 | Rofecoxib (MK 966) binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in an inhibition of the conversion of arachidonic acid to prostaglandins. Rofecoxib is a synthetic, nonsteroidal derivative of phenyl-furanone with anti-inflammatory, antipyretic and analgesic properties and potential antineoplastic properties. COX-related metabolic pathways may represent key regulators of cell proliferation and neo-angiogenesis. Some epithelial tumor cell types overexpress pro-angiogenic COX-2. |
靶点活性 | COX-2:18 nM |
体外活性 | Rofecoxib inhibits the COX-2-dependent production of PGE2 in human osteosarcoma cells with an IC50 of 26 nM. Rofecoxib is a time-dependent inhibitor of purified human recombinant COX-2 with an IC50 of 0.34 μM. Rofecoxib causes inhibition of purified human COX-1 in a non-time-dependent manner. In a human whole blood assay, Rofecoxib selectively inhibits lipopolysaccharide-induced, COX-2-derived PGE2 synthesis with an IC50 value of 0.53 μM compared with an IC50 value of 18.8 μM for the inhibition of COX-1-derived thromboxane B2 synthesis after blood coagulation. [1] Rofecoxib moderately inhibits phenacetin O-deethylation with an IC50 of 23 μM. And a 30-minute preincubation with microsomes and NADPH considerably increases the inhibitory effect of Rofecoxib with an IC50 of 4.2 μM. Inactivation of CYP1A2 by rofecoxib requires NADPH, and is characterized by a K i of 4.8 μM. [2] |
体内活性 | Rofecoxib potently inhibits carrageenan-induced paw edema, carrageenan-induced paw hyperalgesia, lipopolysaccharide-induced pyresis with IC50 of 1.5 mg/kg, 1.0 mg/kg and 0.24 mg/kg, respectively. Rofecoxib also blocks adjuvant-induced arthritis with an IC50 of 0.74 mg/kg/day. Rofecoxib also has a protective effect on adjuvant-induced destruction of cartilage and bone structures in rats. [1] Oral administration of rofecoxib decreases portal pressure in rats that are treated with CCl4 for 8 weeks. In addition, rofecoxib administration reduces the number of activated HSCs and to downregulate hepatic protein levels of three detected types of collagen, laminin, VEGF and CTGF in CCl4-treated rats. [3] |
激酶实验 | In vitro biochemical and pharmacological assaysinhibition studies with recombinant human COX-1 and COX-2: Microsomal preparations of recombinant human COX-1 and COX-2 are prepared from a vaccinia virus-COS-7 cell expression system. Recombinant human COX-1 and COX-2 are expressed in baculovirus-Sf9 cells, and enzymes are purified. Enzymatic activity is monitored continuously by either a fluorescence assay measuring the appearance of the oxidized form of the reducing agent cosubstrate homovanillic acid or by oxygen consumption. The HPLC assay for the assessment of inhibition of purified COX-1 by Rofecoxib with 0.1 μM arachidonic acid substrate concentration, the determination of the stoichiometry of the complex between COX-2 and Rofecoxib, the dissociation rate constant of the enzyme-inhibitor complex by recovery of enzymatic activity, and the recovery of intact Rofecoxib from that complex are all performed as described previously. The solvent system for the HPLC analysis of Rofecoxib is 15:85 MeOH/aqueous potassium phosphate (1 g/liter), with elution by a linear gradient of 15 to 75% MeOH over 25 minutes with detection at 275 nm on a Novapak C18 column. |
细胞实验 | The human osteosarcoma cell line has been shown to selectively express COX-2 by reverse transcription-polymerase chain reaction and immunoblot analysis, whereas undifferentiated human lymphoma U937 cells selectively express COX-1. The production of PGE2 by these cells after arachidonic acid challenge is used as an index of cellular COX-2 and COX-1 activity, respectively. Rofecoxib is preincubated for 5 to 15 minutes with the cells under serum-free conditions [Hanks' balanced salt solution (HBSS)] before a 10-minutes stimulation with 10 μM arachidonic acid and measurement of PGE2 production. COX activity in each cell line is defined as the difference in PGE2 concentrations in samples incubated in the presence or absence of arachidonic acid.(Only for Reference) |
别名 | MK 966, 罗非昔布, 罗非考昔, MK-0966 |
分子量 | 314.36 |
分子式 | C17H14O4S |
CAS No. | 162011-90-7 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
DMSO: 59 mg/mL (187.7 mM)
Ethanol: < 1 mg/mL (insoluble or slightly soluble)
H2O: < 1 mg/mL (insoluble or slightly soluble)
可选溶剂 | 浓度 体积 质量 | 1 mg | 5 mg | 10 mg | 25 mg |
DMSO | 1 mM | 3.1811 mL | 15.9053 mL | 31.8107 mL | 79.5267 mL |
5 mM | 0.6362 mL | 3.1811 mL | 6.3621 mL | 15.9053 mL | |
10 mM | 0.3181 mL | 1.5905 mL | 3.1811 mL | 7.9527 mL | |
20 mM | 0.1591 mL | 0.7953 mL | 1.5905 mL | 3.9763 mL | |
50 mM | 0.0636 mL | 0.3181 mL | 0.6362 mL | 1.5905 mL | |
100 mM | 0.0318 mL | 0.1591 mL | 0.3181 mL | 0.7953 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。
Rofecoxib 162011-90-7 Immunology/Inflammation Neuroscience COX inhibit MK 966 MK 0966 Cyclooxygenase MK0966 罗非昔布 Inhibitor MK966 罗非考昔 MK-0966 MK-966 inhibitor