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Merck

SML3414

Sigma-Aldrich

GW627368X

≥98% (HPLC)

别名:

2-(4-(4,9-Diethoxy-1-oxo-1H-benzo[f]isoindol-2(3H)-yl)phenyl)-N-(phenylsulfonyl)acetamide, 4-(4,9-Diethoxy-1,3-dihydro-1-oxo-2H-benz[f]isoindol-2-yl)-N-(phenylsulfonyl)benzeneacetamide, GW 627368, GW 627368X, GW-627368, GW-627368X, GW627368

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About This Item

经验公式(希尔记法):
C30H28N2O6S
分子量:
544.62
MDL號碼:
分類程式碼代碼:
12352200

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

O=C(CC1=CC=C(C=C1)N(C2=O)CC3=C2C(OCC)=C4C=CC=CC4=C3OCC)NS(=O)(C5=CC=CC=C5)=O

InChI

1S/C30H28N2O6S/c1-3-37-28-23-12-8-9-13-24(23)29(38-4-2)27-25(28)19-32(30(27)34)21-16-14-20(15-17-21)18-26(33)31-39(35,36)22-10-6-5-7-11-22/h5-17H,3-4,18-19H2,1-2H3,(H,31,33)

InChI 密鑰

XREWXJVMYAXCJV-UHFFFAOYSA-N

生化/生理作用

GW627368X is a potent and selective prostaglandin E2 receptor EP4 antagonist with additional affinity for thromboxane A2 receptor (pKi = 7.0/EP4, 6.8/TP, <5.3/DP, EP1, EP2, EP3, FP & IP) that effectively reduces basal (non-detectable at 0.1 nM with COX inhibition or pIC50 = 6.3 without) and PGE2-stimulated cAMP (pKb = 7.9) in human EP4-expressing HEK293 cells. GW627368X inhibits EP4-, but not EP2-, induced tissue relaxation (pKb = 9.2; precontracted piglet & rabbit saphenous vein), but not TP agonist U46619-elevated tissue tone (pKb <5) ex vivo, and blocks PGE2-enhanced HBV virus replication in mice in vivo (1 mg/kg/day i.p.) by preventing CD8 + T-cell impairment by PGE2

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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J F Hiken et al.
Oncogene, 36(16), 2319-2327 (2016-11-22)
Approximately 75% of breast cancers express estrogen receptor α (ERα) and depend on estrogen signals for continued growth. Aromatase inhibitors (AIs) prevent estrogen production and inhibit ER signaling, resulting in decreased cancer recurrence and mortality. Advanced tumors treated with AIs
Tomomi Ohmura et al.
Molecular biology of the cell, 28(12), 1622-1635 (2017-04-22)
The role of prostaglandin A2 (PGA2) in modulation of vascular endothelial function is unknown. We investigated effects of PGA2 on pulmonary endothelial cell (EC) permeability and inflammatory activation and identified a receptor mediating these effects. PGA2 enhanced the EC barrier

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