Atorvastatin

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Atorvastatin

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:

134523-00-5

包装与价格：

包装	价格(元)
50mg	电议
500mg	电议

产品介绍

化学性质

Storage	Store at -20°C
M.Wt	558.64
Cas No.	134523-00-5
Formula	C₃₃H₃₅FN₂O₅
Solubility	≥104.9 mg/mL in DMSO; insoluble in EtOH; insoluble in H2O
Chemical Name	(3R,5R)-7-(2-(4-fluorophenyl)-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)-1H-pyrrol-1-yl)-3,5-dihydroxyheptanoic acid
Canonical SMILES	CC(C)C1=C(C(NC2=CC=CC=C2)=O)C(C3=CC=CC=C3)=C(C4=CC=C(F)C=C4)N1CC[C@@H](O)C[C@@H](O)CC(O)=O
运输条件	蓝冰运输或根据您的需求运输。
一般建议	为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。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。

资料参考

Atorvastatin is an orally active HMG-CoA reductase inhibitor, with the ability to effectively decrease blood lipids via the mevalonate pathway. Apart from the primary function of lowering plasma cholesterol levels, Atorvastatin also shows beneficial effects on the cardiovascular system, predominantly via inhibition of small GTPases (e.g. Ras and Rho). These G proteins are extensively involved in the mechanism of diverse cardiovascular pathologies, and inhibition of Ras/Rho underlies many of the cholesterol-independent effects of Atorvastatin on the vascular wall. In addition, Atorvastatin has been shown to inhibit abdominal aortic aneurysm formation by inhibiting the endoplasmic reticulum stress signal pathway.

References:

1. Nawrocki JW, Weiss SR, Davidson MH, et al. Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG-CoA reductase inhibitor. Arteriosclerosis, Thrombosis, and Vascular Biology, 1995, 15(5): 678-682.

2. Turner NA, Midgley L, O'Regan DJ, et al. Comparison of the efficacies of five different statins on inhibition of human saphenous vein smooth muscle cell proliferation and invasion. Journal of Cardiovascular Pharmacology, 2007, 50(4): 458-461.

3. Li Y, Lu G, Sun D, et al. Inhibition of endoplasmic reticulum stress signaling pathway: A new mechanism of statins to suppress the development of abdominal aortic aneurysm. PLoS One, 2017, 12(4): e0174821.

试验操作

Cell experiment:[2]
Cell lines	Human saphenous vein smooth muscle cells
Reaction Conditions	Incubated for 4 days
Applications	Atorvastatin inhibited the proliferation and invasion activities of human saphenous vein smooth muscle cells, with IC50 values of 0.39 μM and 2.39 μM, respectively
Animal experiment:[3]
Animal models	Angiotensin Ⅱ (Ang Ⅱ)-induced Apolipoprotein E-deficient (ApoE^–/–) mice
Dosage form	20 ~ 30 mg/kg Once daily by oral route for 28 days
Applications	In the Ang Ⅱ-inducedApoE^–/–mice, Atorvastatin treatment significantly reduced endoplasmic reticulum stress signaling proteins, the number of apoptotic cells, as well as the activation of Caspase12 and Bax. Furthermore, Atorvastatin also remarkably inhibited a variety of proinflammatory cytokines such as IL-6, IL-8 and IL-1β.
Note	The technical data provided above is for reference only.
	References: 1. Nawrocki JW, Weiss SR, Davidson MH, et al. Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG-CoA reductase inhibitor. Arteriosclerosis, Thrombosis, and Vascular Biology, 1995, 15(5): 678-682. 2. Turner NA, Midgley L, O'Regan DJ, et al. Comparison of the efficacies of five different statins on inhibition of human saphenous vein smooth muscle cell proliferation and invasion. Journal of Cardiovascular Pharmacology, 2007, 50(4): 458-461. 3. Li Y, Lu G, Sun D, et al. Inhibition of endoplasmic reticulum stress signaling pathway: A new mechanism of statins to suppress the development of abdominal aortic aneurysm. PLoS One, 2017, 12(4): e0174821.