atorvastatin
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.
| 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 |
| SDF | Download SDF |
| 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 |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| Cell experiment:[2] | |
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Cell lines |
Human saphenous vein smooth muscle cells |
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Reaction Conditions |
Incubated for 4 days |
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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] | |
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Animal models |
Angiotensin Ⅱ (Ang Ⅱ)-induced Apolipoprotein E-deficient (ApoE−/−) mice |
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Dosage form |
20 ~ 30 mg/kg Once daily by oral route for 28 days |
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Applications |
In the Ang Ⅱ-induced ApoE−/− 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. |
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Note |
The technical data provided above is for reference only. |
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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. |
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Quality Control & MSDS
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Chemical structure
