D5794
二酰甘油激酶抑制剂II
solid
别名:
3-[2-[4-(双(4-氟苯基)亚甲基)-1-哌啶基]乙基]-2,3-二氢-2-硫代-4(1H)-喹唑啉酮, R59949
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关于此项目
经验公式（希尔记法）:
C28H25F2N3OS
化学文摘社编号:
分子量:
489.58
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
41106300
MDL number:
产品名称
二酰甘油激酶抑制剂II, solid
InChI
1S/C28H25F2N3OS/c29-22-9-5-19(6-10-22)26(20-7-11-23(30)12-8-20)21-13-15-32(16-14-21)17-18-33-27(34)24-3-1-2-4-25(24)31-28(33)35/h1-12H,13-18H2,(H,31,35)
SMILES string
Fc1ccc(cc1)\C(=C2\CCN(CCN3C(=S)Nc4ccccc4C3=O)CC2)c5ccc(F)cc5
InChI key
ZCNBZFRECRPCKU-UHFFFAOYSA-N
biological source
synthetic (organic)
assay
≥97% (HPLC)
form
solid
color
pale yellow
mp
228-230 °C
solubility
0.1 M HCl: slightly soluble
0.1 M NaOH: slightly soluble
DMSO: soluble
H2O: insoluble
ethanol: soluble
ethyl acetate: soluble
storage temp.
−20°C
Quality Level
相关类别
Application
甘油二酯激酶抑制剂II可用于确定嵌合抗原受体 (CAR) 改造的细胞毒性T细胞的肿瘤诱导抑制。它还用于诱导T细胞急性淋巴细胞白血病中的pAkt和PKR样细胞外信号调节激酶 (pErk) 信号。
Biochem/physiol Actions
二酰基甘油激酶抑制剂。抑制红细胞膜中[38P]1-油酰基-2-乙酰甘油基-3-磷酸（OAPA）的形成：IC50 = 3.3 μM。
Features and Benefits
这种化合物是激酶磷酸酶生物学研究的特色产品。点击此处发现更多特色激酶磷酸酶生物产品。在sigma.com/discover-bsm可了解更多关于生物活性小分子的其他研究领域。
存储类别
11 - Combustible Solids
wgk
WGK 3
ppe
dust mask type N95 (US), Eyeshields, Gloves
T Kurz et al.
Cardiovascular research, 42(1), 48-56 (1999-08-06)
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Liquan Yang et al.
Molecular pharmacology, 78(1), 105-113 (2010-04-01)
We demonstrated recently that opioid-induced activation of phospholipase D2 (PLD2) enhances mu- (MOPr) and delta-opioid receptor endocytosis/recycling and thus reduces the development of opioid receptor desensitization and tolerance. However, the mechanistic basis for the PLD2-mediated induction of opioid receptor endocytosis
R W Erickson et al.
The Journal of biological chemistry, 274(32), 22243-22250 (1999-07-31)
The superoxide-generating neutrophil NADPH oxidase can be activated in cell-free reconstitution systems by several agonists, most notably arachidonic acid and the detergent sodium dodecyl sulfate. In this study, we show that both phosphatidic acids and diacylglycerols can serve separately as
X Du et al.
The Biochemical journal, 357(Pt 1), 275-282 (2001-06-21)
We have previously shown that unsaturated fatty acids amplify platelet-derived-growth-factor (PDGF)-induced protein kinase C (PKC) activation in vascular smooth-muscle cells (VSMCs). Diacylglycerol-induced PKC activation is normally terminated by diacylglycerol kinases (DGKs). We thus hypothesized that fatty acids act by inhibiting
Marylana Saadeh et al.
PloS one, 7(1), e30200-e30200 (2012-01-25)
Chronic exposure (24-72 hrs) of pancreatic islets to elevated glucose and fatty acid leads to glucolipoxicity characterized by basal insulin hypersecretion and impaired glucose-stimulated insulin secretion (GSIS). Our aim was to determine the mechanism for basal hypersecretion of insulin. We
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