SML2358
D-NMAPPD
≥98% (HPLC)
同義詞:
(1R, 2R)-N-myristoylamino-4′-nitro-phenylpropandiol-1, 3, (1R,2R)-B13, B13, N-[(1R,2R)-2-Hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]tetradecanamide, [R-(R*,R*)]-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrophenyl)ethyl]-tetradecanamide
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About This Item
推薦產品
化驗
≥98% (HPLC)
形狀
powder
光學活性
[α]/D -28 to -34, c = 0.1 in chloroform-d
顏色
white to beige
溶解度
DMSO: 2 mg/mL, clear
儲存溫度
2-8°C
SMILES 字串
[N+](=O)([O-])c1ccc(cc1)[C@@H](O)[C@H](NC(=O)CCCCCCCCCCCCC)CO
InChI
1S/C23H38N2O5/c1-2-3-4-5-6-7-8-9-10-11-12-13-22(27)24-21(18-26)23(28)19-14-16-20(17-15-19)25(29)30/h14-17,21,23,26,28H,2-13,18H2,1H3,(H,24,27)/t21-,23-/m1/s1
InChI 密鑰
XUSDVLHKNBOGJY-FYYLOGMGSA-N
生化/生理作用
D-NMAPPD (B13), a myristoyl-CoA analog, is a cell penetrant inhibitor of N-myristoyltransferases that suppressed FRS2α (fibroblast growth factor receptor substrate 2) myristoylation. D-NMAPPD inhibits wild-type FGFRs and drug-resistant mutants (FGFRsDRM) oncogenic signaling in cancer cells. D-NMAPPD potently inhibits growth of xenograft tumors in mice. D-NMAPPD is a potent inhibitor of ceramidase that elevates endogenous ceramide levels and suppress growth of cancer cells.
cell penetrant inhibitor of N-myristoyltransferases that suppressed FRS2α myristoylation; potent inhibitor of ceramidase that elevates endogenous ceramide levels.
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
Mototeru Yamane et al.
Biochemistry and biophysics reports, 11, 174-181 (2017-09-29)
In this study, we showed that the dual addition of glucosyl ceramide synthase and ceramidase inhibitors to A549 cell culture led to the possibility of ceramide channel formation via endogenous palmitoyl-ceramide accumulation with an increase in cholesterol contents in the
Qianjin Li et al.
The Journal of biological chemistry, 293(17), 6434-6448 (2018-03-16)
Fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling facilitates tumor initiation and progression. Although currently approved inhibitors of FGFR kinase have shown therapeutic benefit in clinical trials, overexpression or mutations of FGFRs eventually confer drug resistance and thereby abrogate the desired
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