SML3880
CST626
≥98% (HPLC)
别名:
(2S,4S)-1-((S)-2-Cyclohexyl-2-((S)-2-(methylamino)-propanamido)acetyl)-4-(3-((5-(((S)-1-((2S,4R)-4-hydroxy-2-(((S)-1-(4-(4-methylthiazol-5-yl)phenyl)ethyl)carbamoyl)pyrrolidin-1-yl)-3,3-dimethyl-1-oxobutan-2-yl)amino)-5-oxopentyl)oxy)phenoxy)-N-((R)-1,2,3,4-tetrahydronaphthalen-1-yl)pyrrolidine-2-carboxamide, IAP-VHL hetero-PROTAC 9
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所有图片(1)
About This Item
经验公式（希尔记法）:
C61H82N8O9S
分子量:
1103.42
UNSPSC代码:
12352200
生化/生理作用
BIR domain-targeting degrader of inhibitor of apoptosis proteins (IAPs) cIAP1/2 and XIAP.
CST626 is a degrader of cellular inhibitor of apoptosis (IAP) proteins (cIAP1/cIAP2/XIAP DC50 post 16h = 2.4/6.2/0.7 nM with >99% degradation observed post 3h treatment at 100 nM; MM1S cells) that effectively reduces the viability of hematological cancer cultures, including MM (IC50 post 96h = 8.5 nM/NCI-H929, 1.14µM/JJN3, 2.54 µM/RPMI-8826), AML (IC50 post 96h = 2.1 nM/MOLM13, 420 nM/K562, 1.17 µM/HEL) and DLBCL (IC50 post 96h = 1.6 nM/SUDHL6, 460 nM/DB, 1.69 µM/SUDHL4). CST626 is composed of a von Hippel-Lindau (VHL) ligand VH032 derivative linked to a monovalent Smac (DIABLO) AVPI motif-based IAP BIR domain-targeting ligand.
CST626 is a degrader of cellular inhibitor of apoptosis (IAP) proteins (cIAP1/cIAP2/XIAP DC50 post 16h = 2.4/6.2/0.7 nM with >99% degradation observed post 3h treatment at 100 nM; MM1S cells) that effectively reduces the viability of hematological cancer cultures, including MM (IC50 post 96h = 8.5 nM/NCI-H929, 1.14µM/JJN3, 2.54 µM/RPMI-8826), AML (IC50 post 96h = 2.1 nM/MOLM13, 420 nM/K562, 1.17 µM/HEL) and DLBCL (IC50 post 96h = 1.6 nM/SUDHL6, 460 nM/DB, 1.69 µM/SUDHL4). CST626 is composed of a von Hippel-Lindau (VHL) ligand VH032 derivative linked to a monovalent Smac (DIABLO) AVPI motif-based IAP BIR domain-targeting ligand.
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Yuen Lam Dora Ng et al.
Journal of medicinal chemistry, 66(7), 4703-4733 (2023-03-31)
Proteolysis targeting chimeras (PROTACs) represent a new pharmacological modality to inactivate disease-causing proteins. PROTACs operate via recruiting E3 ubiquitin ligases, which enable the transfer of ubiquitin tags onto their target proteins, leading to proteasomal degradation. However, several E3 ligases are
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