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Merck
CN
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文件

安全信息

SML0612

Sigma-Aldrich

Perifosine

≥98% (HPLC)

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别名:
4-[[Hydroxy(octadecyloxy)phosphinyl]oxy]-1,1-dimethyl-piperidinium inner salt, KRX-0401, Octadecyl-(1,1-dimethyl-4-piperidylio) phosphate
经验公式(希尔记法):
C25H52NO4P
分子量:
461.66
UNSPSC代码:
12352200
NACRES:
NA.77

质量水平

检测方案

≥98% (HPLC)

形式

powder

颜色

white to beige

溶解性

H2O: 10 mg/mL, clear

运输

wet ice

储存温度

−20°C

InChI

1S/C25H52NO4P/c1-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-24-29-31(27,28)30-25-20-22-26(2,3)23-21-25/h25H,4-24H2,1-3H3

InChI key

SZFPYBIJACMNJV-UHFFFAOYSA-N

应用

Perifosine has been used as an alkyl phospholipid AKT inhibitor.

生化/生理作用

Perifosine (KRX-0401) is a selective bioavailable alkylphospholipid inhibitor of protein kinase B/Akt (PKB/Akt) with anti-proliferative activity. Perifosine acts on cell membranes, selectively targeting proliferating cells, inducing growth arrest and apoptosis.
Perifosine (octadecyl-(1,1-dimethyl-4-piperidylio)) is an antitumor compound. It acts at lipid rafts and stops lysosomal accumulation and mTORC1 (mammalian target of rapamycin complex 1) signaling. This drug exhibits significant antiproliferative activity in vitro and in vivo in various human cancer model systems.

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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Perifosine, a novel alkylphospholipid, inhibits protein kinase B activation.
Kondapaka SB, et al.
Molecular Cancer Therapeutics, 2(11), 1093-1103 (2003)
TUFT1 interacts with RABGAP1 and regulates mTORC1 signaling.
Kawasaki N, et al.
Cell discovery, 4(1), 1-1 (2018)
Natsumi Kawasaki et al.
Cell discovery, 4, 1-1 (2018-02-10)
The mammalian target of rapamycin (mTOR) pathway is commonly activated in human cancers. The activity of mTOR complex 1 (mTORC1) signaling is supported by the intracellular positioning of cellular compartments and vesicle trafficking, regulated by Rab GTPases. Here we showed
José M Bravo-San Pedro et al.
Cell metabolism, 30(4), 754-767 (2019-08-20)
Autophagy facilitates the adaptation to nutritional stress. Here, we show that short-term starvation of cultured cells or mice caused the autophagy-dependent cellular release of acyl-CoA-binding protein (ACBP, also known as diazepam-binding inhibitor, DBI) and consequent ACBP-mediated feedback inhibition of autophagy.

实验方案

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