所有图片(1)
别名:
(2R)-N-\ [(1S)-2,2-二甲基-1-\ [（甲氨基）羰基]-丙基]-2-\ [(1S)-1-\ [甲酰（羟基）氨基] 乙基]-5-苯基戊酰胺, GI4023
经验公式（希尔记法）:
C21H33N3O4
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质量水平
检测方案
≥98% (HPLC)
形式
powder
颜色
white to beige
溶解性
DMSO: 15 mg/mL, clear
储存温度
2-8°C
SMILES字符串
ON(C=O)[C@@H](C)[C@@H](CCCC1=CC=CC=C1)C(N[C@@H](C(C)(C)C)C(NC)=O)=O
InChI
1S/C21H33N3O4/c1-15(24(28)14-25)17(13-9-12-16-10-7-6-8-11-16)19(26)23-18(20(27)22-5)21(2,3)4/h6-8,10-11,14-15,17-18,28H,9,12-13H2,1-5H3,(H,22,27)(H,23,26)/t15-,17+,18+/m0/s1
InChI key
GHVMTHKJUAOZJP-CGTJXYLNSA-N
应用
GI254023X 已被用于抑制 ADAM10（ADAM 金属肽酶结构域 10）。
生化/生理作用
GI254023X 是一种强效、选择性 ADAM10 金属蛋白酶抑制剂，对 α-分泌酶 ADAM10 的选择性是 ADAM17 (TACE) 的 100 倍。在使用重组 TACE 和 ADAM10 胞外域的研究中，GI254023X 的 IC50 ADAM10 为 5.3 nM，TACE 为 541 nM。
GI254023X 是一种强效选择性 ADAM10 金属蛋白酶抑制剂。
GI254023X 阻断 ADAM10（ADAM 金属肽酶域 10）的活性，并降低上皮细胞和内皮细胞中人类白细胞抗原 (HLA) 介导的细胞毒性和细胞外 E-cadherin 的裂解。
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
ADAM10 cell surface expression but not activity is critical for Staphylococcus aureus α-hemolysin-mediated activation of the NLRP3 inflammasome in human monocytes.
Ezekwe E A D, et al.
Toxins, 8(4), 95-95 (2016)
Kazuhiro Aoki et al.
Developmental cell, 43(3), 305-317 (2017-11-08)
The biophysical framework of collective cell migration has been extensively investigated in recent years; however, it remains elusive how chemical inputs from neighboring cells are integrated to coordinate the collective movement. Here, we provide evidence that propagation waves of extracellular
Laura S Christian et al.
Cell reports, 35(6), 109118-109118 (2021-05-13)
As a critical machinery for rapid pathogen removal, resident memory T cells (TRMs) are locally generated after the initial encounter. However, their development accompanying tumorigenesis remains elusive. Using a murine breast cancer model, we show that TRMs develop in the tumor
Joshua A Kulas et al.
American journal of physiology. Endocrinology and metabolism, 316(1), E106-E120 (2018-11-14)
The amyloid precursor protein (APP) is a type I transmembrane glycoprotein widely studied for its role as the source of β-amyloid peptide, accumulation of which is causal in at least some cases of Alzheimer's disease (AD). APP is expressed ubiquitously
Paul M Jordan et al.
Cell reports, 33(2), 108247-108247 (2020-10-15)
Underlying mechanisms of how infectious inflammation is resolved by the host are incompletely understood. One hallmark of inflammation resolution is the activation of specialized pro-resolving mediators (SPMs) that enhance bacterial clearance and promote tissue repair. Here, we reveal α-hemolysin (Hla)
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