Atorvastatin Calcium
mRNA synthesis
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Inhibitor Cocktails
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
HMG-CoA还原酶是甲羟戊酸途径的关键酶,合成胆固醇。HMG-CoA是限速酶,在降低血液中胆固醇的浓度方面发挥着重要作用。HMG-CoA还原酶位于内质网,含八个跨膜结构域。HMG-CoA还原酶抑制剂可以诱导肝脏低密度脂蛋白(LDL)受体表达,从而促进血浆LDL分解代谢以及降低血浆胆固醇浓度(动脉粥样硬化的重要决定因素之一)。HMG-CoA还原酶在胆固醇合成中起着重要作用。HMG-CoA是降胆固醇药物的唯一靶点。此外,HMG-CoA还原酶在各种生理过程中同样起着重要作用。HMG-CoA还原酶活性与生殖细胞迁移缺陷相关。抑制HMG-CoA还原酶活性可以导致脑出血[1]。
Atorvastatin是一种HMG-CoA还原酶抑制剂,其IC50值为154 nM。Atorvastatin可以有效治疗某些血脂异常和高胆固醇血症[1]。给予40 mg的Atorvastatin,于40天后,降低了40%的总胆固醇[1]。Atorvastatin还可以用于治疗具有正常胆固醇水平的冠心病或中风患者[2]。在接受血液成分单采术患者中,Atorvastatin通过诱导LDL受体表达来减少低密度脂蛋白。
Atorvastatin被CYP3A4(细胞色素P450 3A4)代谢为几种具有重要疗效的代谢产物[3]。
参考文献:
[1]. van Dam M, Zwart M, de Beer F, Smelt AH, Prins MH, Trip MD, Havekes LM, Lansberg PJ, Kastelein JJ: Long term efficacy and safety of atorvastatin in the treatment of severe type III and combined dyslipidaemia. Heart 2002, 88(3):234-238.
[2]. Sever PS, Dahlof B, Poulter NR, Wedel H, Beevers G, Caulfield M, Collins R, Kjeldsen SE, Kristinsson A, McInnes GT et al: Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003, 361(9364):1149-1158.
[3]. Lennernas H: Clinical pharmacokinetics of atorvastatin. Clin Pharmacokinet 2003, 42(13):1141-1160.
Physical Appearance | A solid |
Storage | Store at -20°C |
M.Wt | 1155.34 |
Cas No. | 134523-03-8 |
Formula | 2(C33H34FN2O5)·Ca |
Solubility | ≥57.75 mg/mL in DMSO; insoluble in H2O; ≥2.94 mg/mL in EtOH with gentle warming and ultrasonic |
Chemical Name | calcium;(3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoate |
SDF | Download SDF |
Canonical SMILES | CC(C)C1=C(C(=C(N1CCC(CC(CC(=O)[O-])O)O)C2=CC=C(C=C2)F)C3=CC=CC=C3)C(=O)NC4=CC=CC=C4.CC(C)C1=C(C(=C(N1CCC(CC(CC(=O)[O-])O)O)C2=CC=C(C=C2)F)C3=CC=CC=C3)C(=O)NC4=CC=CC=C4.[Ca+2] |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。 |
细胞实验 [1]: | |
细胞系 |
单核细胞和VSMC |
制备方法 |
在DMSO中的溶解度大于57.8 mg/mL。若配制更高浓度的溶液,一般步骤如下:请将试管置于37 °C加热10分钟和/或将其置于超声波浴中震荡一段时间。原液于-20 °C可放置数月。 |
反应条件 |
0.1或1 μM |
实验结果 |
在单核细胞和VSMC中,Atorvastatin Calcium (0.1 μM) 显著抑制由Ang II和TNF-α诱导的NF-κB活化。此外,Atorvastatin Calcium (1 μM) 也下调Ang II和TNF-α诱导的MCP-1和IP-10表达。 |
动物实验 [2]: | |
动物模型 |
后肢缺血小鼠 |
给药剂量 |
2或8 mg/kg/day;口服给药;持续4周 |
实验结果 |
在后肢缺血小鼠中,Atorvastatin Calcium 在8 mg/kg的剂量下显著恢复血流量。此外,8 mg/kg Atorvastatin Calcium治疗组的缺血/正常灌注比例也有所增加。缺血肌肉组织分析结果表明,Atorvastatin Calcium显著增加毛细血管数量。同时,Atorvastatin Calcium上调上述组织中的CXCR4表达。 |
注意事项 |
请于室内测试所有化合物的溶解度。虽然化合物的实际溶解度可能与其理论值略有不同,但仍处于实验系统误差的允许范围内。 |
References: [1]. Ortego M, Bustos C, Hernández-Presa MA, Tuón J, Díaz C, Hernández G, Egido J. Atorvastatin reduces NF-kappaB activation and chemokine expression in vascular smooth muscle cells and mononuclear cells. Atherosclerosis. 1999 Dec;147(2):253-61. [2]. Chiang KH, Cheng WL, Shih CM, Lin YW, Tsao NW, Kao YT, Lin CT, Wu SC, Huang CY, Lin FY. Statins, HMG-CoA Reductase Inhibitors, Improve Neovascularization by Increasing the Expression Density of CXCR4 in Endothelial Progenitor Cells. PLoS One. 2015 Aug 26;10(8):e0136405. |
质量控制和MSDS
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