PZ0190
阿伐麦布
≥98% (HPLC)
别名:
CI-1011; PD 148515; [[2,4,6-三(1-甲基乙基)苯基]乙酰基]-, 2,6-双(1-甲基乙基)苯基酯]氨基磺酸
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关于此项目
经验公式（希尔记法）:
C29H43NO4S
化学文摘社编号:
分子量:
501.72
UNSPSC Code:
12352200
PubChem Substance ID:
MDL number:
NACRES:
NA.28
产品名称
阿伐麦布, ≥98% (HPLC)
InChI
1S/C29H43NO4S/c1-17(2)22-14-25(20(7)8)27(26(15-22)21(9)10)16-28(31)30-35(32,33)34-29-23(18(3)4)12-11-13-24(29)19(5)6/h11-15,17-21H,16H2,1-10H3,(H,30,31)
SMILES string
CC(C)c1cc(C(C)C)c(CC(=O)NS(=O)(=O)Oc2c(cccc2C(C)C)C(C)C)c(c1)C(C)C
InChI key
PTQXTEKSNBVPQJ-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to tan
solubility
DMSO: ≥40 mg/mL
relevant disease(s)
Alzheimer′s disease; cardiovascular diseases
storage temp.
room temp
Quality Level
Application
阿伐麦布已被用作Huh7.5.1细胞中酰基辅酶A：胆固醇酰基转移酶（ACAT）的抑制剂，以测试其与直接作用抗病毒药物（DAA）的组合效果，以及其对适应酸中毒的癌细胞中脂质滴积累的影响。它可以用作ACAT的抑制剂来评估克氏锥虫中胆固醇的酯化。
Biochem/physiol Actions
阿伐麦布（CI-1011）是一种口服生物可利用的Acyl-CoA:胆固醇O-酰基转移酶（ACAT）抑制剂
阿伐麦布（CI-1011）是一种口服生物可利用的Acyl-CoA:胆固醇O-酰基转移酶（ACAT）抑制剂。它最初作为一种抗惊厥药物被开发，并且被证明能够显著降低血浆总甘油三酯和VLDL-胆固醇，但后来的临床试验令人失望。ACAT也被作为阿尔茨海默病的潜在治疗靶点进行了研究。最近已经研究了阿伐麦布通过限制可扩散淀粉样蛋白-β（Abeta）的产生和增加清除来削弱淀粉样蛋白病变的作用。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
[Acyl-coenzyme A: cholesterol acyltransferase (ACAT)].
Akira Miyazaki et al.
Nihon rinsho. Japanese journal of clinical medicine, 62 Suppl 12, 89-91 (2005-01-22)
Miria Gomes Pereira et al.
PloS one, 10(6), e0128949-e0128949 (2015-06-13)
Trypanosoma cruzi epimastigotes store high amounts of cholesterol and cholesteryl esters in reservosomes. These unique organelles are responsible for cellular digestion by providing substrates for homeostasis and parasite differentiation. Here we demonstrate that under nutritional lipid stress, epimastigotes preferentially mobilized
John R Burnett et al.
Biochimica et biophysica acta, 1738(1-3), 10-18 (2006-01-24)
Previously, we have shown, in vivo, that the acyl coenzyme A: cholesterol acyltransferase (ACAT) inhibitor avasimibe decreases hepatic apolipoprotein (apo) B secretion into plasma. To test the hypothesis that avasimibe modulates postprandial triglyceride-rich lipoprotein (TRL) metabolism in vivo, an oral
Jean-Claude Tardif et al.
The American journal of cardiology, 98(1), 23-27 (2006-06-21)
We assessed vascular changes during atherosclerosis regression. Compensatory enlargement of coronary arteries accommodates plaque burden during atherosclerosis development. Lipid-lowering therapy has altered the natural history of coronary atherosclerosis, but the arterial changes that occur during disease regression need to be
Yves Rival et al.
DNA and cell biology, 23(5), 283-292 (2004-06-01)
It is now recognized that atherosclerosis complications are related to the unstable character of the plaque rather than its volume. Vulnerable plaques often contain a large lipid core, a reduced content of smooth muscle cells, and accumulation of inflammatory cells.
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