CAS NO: | 134523-00-5 |
包装 | 价格(元) |
50mg | 电议 |
500mg | 电议 |
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。 |
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.
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. |