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文件

M2537

米法斯丁

Name: 米法斯丁
Brand: SIGMA

≥98% (HPLC), powder or crystals

别名:

ML-236B, 康帕丁

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About This Item

经验公式（希尔记法）:

C₂₃H₃₄O₅

CAS号:

73573-88-3

分子量:

390.51

Beilstein:

1269441

MDL编号:

MFCD05662341

UNSPSC代码:

12352200

PubChem化学物质编号:

24278540

NACRES:

NA.77

质量水平

200

检测方案

≥98% (HPLC)

形式

powder or crystals

颜色

white to light yellow

mp

151 °C

溶解性

ethanol: 25-26 mg/mL, clear, colorless

抗生素抗菌谱

neoplastics

作用机制

enzyme | inhibits

创始人

Daiichi-Sankyo

储存温度

2-8°C

SMILES字符串

[H][C@]12[C@H](CCC=C1C=C[C@H](C)[C@@H]2CC[C@@H]3C[C@@H](O)CC(=O)O3)OC(=O)[C@@H](C)CC

InChI

1S/C23H34O5/c1-4-14(2)23(26)28-20-7-5-6-16-9-8-15(3)19(22(16)20)11-10-18-12-17(24)13-21(25)27-18/h6,8-9,14-15,17-20,22,24H,4-5,7,10-13H2,1-3H3/t14-,15-,17+,18+,19-,20-,22-/m0/s1

InChI key

AJLFOPYRIVGYMJ-INTXDZFKSA-N

基因信息

human ... HMGCL(3155) , HMGCR(3156)
rat ... Hmgcr(25675)

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一般描述

化学结构：他汀

美伐他汀(Mevastatin)是一种聚酮，属于他汀类化合物。结构中含有一个羟基-六氢萘环。

应用

美伐他汀已用于：

通过细胞毒性检测分析其对慢性淋巴细胞白血病(CLL)细胞的影响
分析其作为异戊二烯化抑制剂，对K-Ras转染人胚胎肾细胞(HEK)的影响
研究其作为他汀类药物，对人乳腺癌细胞和胶质母细胞瘤的体外抗癌作用

生化/生理作用

美伐他汀是一种参与胆固醇合成的主要酶——3-羟基3-甲戊二酰辅酶A还原酶（HMG-CoA还原酶）的选择性抑制剂，可用作降胆固醇药。美伐他汀来源于各种真菌。美伐他汀可作为抗骨吸收剂，对骨质疏松症有治疗作用。可通过诱发破骨细胞凋亡抑制骨吸收。美伐他汀也参与蛋白质（如Ras）异戊二烯化的抑制。可通过抑制转录因子Rho的四异戊二烯化，提高内皮一氧化氮合酶(eNOS)mRNA和蛋白质水平。

特点和优势

该化合物由第一三共制药开发。要浏览其他制药公司开发的化合物列表批准的药物/候选药物的列表，点击这里。

包装

无底玻璃瓶。内含物装在插入的融合锥内。

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)

分析证书(COA)

输入产品批号来搜索分析证书(COA) 。批号可以在产品标签上"批“ （Lot或Batch）字后找到。

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The bisphosphonate incadronate (YM175) causes apoptosis of human myeloma cells in vitro by inhibiting the mevalonate pathway.

C M Shipman et al.

Cancer research, 58(23), 5294-5297 (1998-12-16)

It has recently been suggested that bisphosphonates may have direct antitumor effects in vivo, in addition to their therapeutic antiresorptive properties. Bisphosphonates can inhibit proliferation and cause apoptosis in human myeloma cells in vitro. In macrophages, bisphosphonate-induced apoptosis was recently

Compactin suppresses bone resorption by inhibiting the fusion of prefusion osteoclasts and disrupting the actin ring in osteoclasts.

J T Woo et al.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 15(4), 650-662 (2000-04-26)

Compactin (mevastatin), which inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and thus biosynthesis of cholesterol and the prenylation of proteins, inhibits osteoclastic bone resorption. Although it has been suggested that compactin inhibits bone resorption by inducing apoptosis of osteoclasts, the pathway by

Nitrogen-containing bisphosphonates inhibit the mevalonate pathway and prevent post-translational prenylation of GTP-binding proteins, including Ras.

S P Luckman et al.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 13(4), 581-589 (1998-04-29)

Bisphosphonates are currently the most important class of antiresorptive drugs used for the treatment of metabolic bone diseases. Although the molecular targets of bisphosphonates have not been identified, these compounds inhibit bone resorption by mechanisms that can lead to osteoclast

Compactin-a review.

R Chakravarti et al.

Applied microbiology and biotechnology, 64(5), 618-624 (2004-03-23)

Compactin, a hypocholesterolemic molecule, is a competitive inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase, which is a regulatory enzyme for cholesterol biosynthesis. The structural similarity and high affinity of the acid form of compactin and HMG, the natural substrate of enzyme, results

The association of statins plus LDL receptor-targeted liposome-encapsulated doxorubicin increases in vitro drug delivery across blood-brain barrier cells.

Ml Pinzón-Daza et al.

British journal of pharmacology, 167(7), 1431-1447 (2012-07-14)

The passage of drugs across the blood-brain barrier (BBB) limits the efficacy of chemotherapy in brain tumours. For instance, the anticancer drug doxorubicin, which is effective against glioblastoma in vitro, has poor efficacy in vivo, because it is extruded by

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