SML0789
GI254023X
≥98% (HPLC), powder, ADAM10 metalloproteinase inhibitor
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
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关于此项目
经验公式（希尔记法）:
C21H33N3O4
化学文摘社编号:
分子量:
391.50
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77
产品名称
GI254023X, ≥98% (HPLC)
质量水平
方案
≥98% (HPLC)
表单
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。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
The Mouse-specific Splice Variant mRAGE_v4 Encodes a Membrane-bound RAGE that is Resistant to Shedding and does not Contribute to the Production of Soluble RAGE.
Di Maggio S, et al.
PLoS ONE, 11(9), e0153832-e0153832 (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
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)
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
Jian Li et al.
Pain medicine (Malden, Mass.), 18(9), 1752-1766 (2017-02-09)
Increasing evidence suggests the potential involvement of metalloproteinase family proteins in the pathogenesis of neuropathic pain, although the underlying mechanisms remain elusive. Using the spinal nerve ligation model, we investigated whether ADAM10 proteins participate in pain regulation. By implementing invitro
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