Atorvastatin hemicalcium salt

CAS号

134523-03-8

分子式

C33H34FN2O5·1/2Ca

主要靶点

Ferroptosis|HMG-CoA Reductase|Autophagy

仅限科研使用

Cat No : CM00666

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Synonyms

Ferroptosis|HMGCoA Reductase|HMG-CoA reductase|HMGCR|HMGCoAReductase|CI 981|CI981|CI-981|Autophagy|Atorvastatin hemicalcium|Atorvastatin hemicalcium salt|Atorvastatin Calcium|Atorvastatin|Lipitor|Sortis|阿托伐他汀钙



产品信息

CAS号 134523-03-8
分子式 C33H34FN2O5·1/2Ca
主要靶点 Ferroptosis|HMG-CoA Reductase|Autophagy
主要通路 凋亡|代谢|自噬
分子量 577.67
纯度 99.89%, 此纯度可做参考,具体纯度与批次有关系,可咨询客服
储存条件 Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
别名 Ferroptosis|HMGCoA Reductase|HMG-CoA reductase|HMGCR|HMGCoAReductase|CI 981|CI981|CI-981|Autophagy|Atorvastatin hemicalcium|Atorvastatin hemicalcium salt|Atorvastatin Calcium|Atorvastatin|Lipitor|Sortis|阿托伐他汀钙

靶点活性

HMG-CoA reductase:8 nM

体内活性

方法:为研究对动脉粥样硬化的作用,将 Atorvastatin hemicalcium salt (10 mg/kg) 灌胃给药给易损动脉粥样硬化斑块小鼠模型,每天一次,持续八周。 结果:Atorvastatin 在该剂量下没有降低血浆总胆固醇水平或影响斑块进展。然而,与对照组相比,Atorvastatin 治疗组的易损斑块数量显著减少。Atorvastatin 可以改善小鼠的斑块稳定性,而与血浆胆固醇水平无关。[3]

体外活性

方法:胃癌干细胞 MKN45 用 Atorvastatin hemicalcium salt (0.39-25 μM) 处理 7 天,通过 CellTiter-Glo luminescent assay 检测细胞增殖。 结果:Atorvastatin 以 2.1 μM 的 IC50 值剂量依赖性地抑制 MKN45 细胞的增殖。[1] 方法:HUVECs 细胞用 Atorvastatin hemicalcium salt (0.7-35 μM) 处理 24 h,通过 Western Blot 检测靶点蛋白表达水平。 结果:35 μM Atorvastatin 治疗后,凋亡标志物 cleaved caspase-3 和 cleaved PARP-1 的蛋白表达水平在 HUVECs 中显著上调。[2]

溶解度

DMSO:50 mg/mL (43.28 mM)

细胞实验

Briefly, SV-SMC from 5 different patients are seeded into 24-well cell culture plates at a density of 1×104?cells per well in full growth medium. Cells are incubated overnight and then quiesced in serum free medium for 3 days before transfer to full growth medium (10% FCS) containing 5 different statins (simvastatin, atorvastatin, fluvastatin, lovastatin, and pravastatin)at a range of concentrations. All statins are tested on cells from each individual patient. Medium and drugs are replaced after 2 days, and viable cell numbers are determined in triplicate wells after 4 days using Trypan Blue and a hemocytometer. The increase in cell number is calculated by subtracting the starting cell number (day 0) from the final cell number (day 4). Data are then normalized to control values (no statin) to correct for differences in proliferation rates between cells from different patients.

参考文献

1.Choi YS, et al. Atorvastatin inhibits the proliferation of MKN45-derived gastric cancer stem cells in a mevalonate pathway-independent manner. Korean J Physiol Pharmacol. 2022 Sep 1;26(5):367-375.
2.Zhao WB, et al. Effects of various doses of atorvastatin on vascular endothelial cell apoptosis and autophagy in vitro. Mol Med Rep. 2019 Mar;19(3):1919-1925.
3.Nie P, et al. Atorvastatin improves plaque stability in ApoE-knockout mice by regulating chemokines and chemokine receptors. PLoS One. 2014 May 9;9(5):e97009.
4.Aviram M, et al. Atherosclerosis, 1998, 138(2), 271-280.
5.Rajamannan NM, et al. Circulation, 2002, 105(22), 2660-2665.
6.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.

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