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经验公式(希尔记法):
C17H18O2
化学文摘社编号:
分子量:
254.32
UNSPSC Code:
51111800
NACRES:
NA.77
MDL number:
产品名称
PaPE-1, ≥98% (HPLC)
InChI
1S/C17H18O2/c1-10-7-14(8-11(2)17(10)19)12-3-5-15-13(9-12)4-6-16(15)18/h3,5,7-9,16,18-19H,4,6H2,1-2H3/t16-/m0/s1
InChI key
UCXWFKNKSWDWCD-INIZCTEOSA-N
SMILES string
O[C@H]1CCC2=C1C=CC(C3=CC(C)=C(O)C(C)=C3)=C2
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 25 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
PaPE-1 is a "Pathway Preferential Estrogen" that activates the extranuclear signaling pathway without activating the nuclear signaling pathway. PaPE-1 bound 50,000-fold less well to ERα and Erβ estrogen receptors. PaPE-1 activated extranuclear-initiated ER-regulated genes, but showed essentially no activation of nuclear-initiated estrogen receptor (ER) gene targets such as the progesterone receptor. Unlike estradiol (E2), PaPE-1 did not stimulate proliferation of MCF-7 breast cancer cells. Like estradiol, PaPE-1 strongly activated MAPK and mTOR pathway. Instead, it showed preferential estrogen-like activity in non-reproductive (metabolic and vascular) tissues, reducing body weight gain and fat accumulation in ovariectomized mice and accelerating repair of endothelial damage in the vascualture.
PaPE-1 is a "Pathway Preferential Estrogen" that activates the extranuclear signaling pathway without activating the nuclear signaling pathway.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2
存储类别
11 - Combustible Solids
wgk
WGK 3
Zeynep Madak-Erdogan et al.
Science signaling, 9(429), ra53-ra53 (2016-05-26)
There is great medical need for estrogens with favorable pharmacological profiles that support desirable activities for menopausal women, such as metabolic and vascular protection, but that lack stimulatory activities on the breast and uterus. We report the development of structurally
Laura Marroqui et al.
Chemosphere, 265, 129051-129051 (2020-12-01)
Bisphenol-S (BPS) and Bisphenol-F (BPF) are current Bisphenol-A (BPA) substitutes. Here we used pancreatic β-cells from wild type (WT) and estrogen receptor β (ERβ) knockout (BERKO) mice to investigate the effects of BPS and BPF on insulin secretion, and the
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