Atorvastatin hemicalcium trihydrate

Modify Date: 2025-08-25 10:10:11

Atorvastatin hemicalcium trihydrate Structure
Atorvastatin hemicalcium trihydrate structure
Common Name Atorvastatin hemicalcium trihydrate
CAS Number 344920-08-7 Molecular Weight 632.73
Density N/A Boiling Point N/A
Molecular Formula C33H35FN2O5.1/2Ca.3H2O Melting Point N/A
MSDS N/A Flash Point N/A

 Use of Atorvastatin hemicalcium trihydrate


Atorvastatin hemicalcium trihydrate is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin hemicalcium trihydrate inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 μM and 2.39 μM, respectively[1][2][3].

 Names

Name Atorvastatin hemicalcium trihydrate

 Atorvastatin hemicalcium trihydrate Biological Activity

Description Atorvastatin hemicalcium trihydrate is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin hemicalcium trihydrate inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 μM and 2.39 μM, respectively[1][2][3].
Related Catalog
In Vitro Atorvastatin hemicalcium trihydrate treatment decreases apoptosis of myocardial cells by down-regulating GRP78, caspase-12 and CHOP expression in myocardial cells after myocardial infarction, and the endoplasmic reticulum (ER) stress is activated in response to heart failure and angiotensin II (Ang II) stimulation[4].
In Vivo Atorvastatin (20-30 mg/kg; oral gavage; once a day; for 28 days; ApoE−/− mice) hemicalcium trihydrate treatment significantly reduces endoplasmic reticulum (ER) stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β are all remarkably inhibited after Atorvastatin treatment[5]. Animal Model: Forty 8-week-old ApoE−/− mice induced with angiotensin II (Ang II)[5] Dosage: 20 mg/kg, 30 mg/kg Administration: Oral gavage; once a day; for 28 days Result: Significantly reduced ER stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE−/− mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β were all remarkably inhibited.
References

[1]. Santodomingo-Garzón T, et al. Atorvastatin inhibits inflammatory hypernociception. Br J Pharmacol. 2006 Sep;149(1):14-22.

[2]. Turner NA, et al. Comparison of the efficacies of five different statins on inhibition of human saphenous vein smooth muscle cell proliferation and invasion. J Cardiovasc Pharmacol. 2007 Oct;50(4):458-61.

[3]. Nawrocki, J.W., et al., Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG-CoA reductase inhibitor. Arterioscler Thromb Vasc Biol, 1995. 15(5): p. 678-82.

[4]. Song XJ, et al. Atorvastatin inhibits myocardial cell apoptosis in a rat model with post-myocardial infarction heart failure by downregulating ER stress response. Int J Med Sci. 2011;8(7):564-72.

[5]. Li Y, 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 Apr 3;12(4):e0174821.

 Chemical & Physical Properties

Molecular Formula C33H35FN2O5.1/2Ca.3H2O
Molecular Weight 632.73
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