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Z-Ile-Leu-aldehyde_161710-10-7_DataSheet_MedChemExpress

Z-Ile-Leu-aldehyde_161710-10-7_DataSheet_MedChemExpress

Product Name:

Z-Ile-Leu-aldehyde CAS No.:

161710-10-7Cat. No.:

HY-12465MWt:

362.46Formula:

C20H30N2O4Purity :>98%

Solubility:Mechanisms:Biological Activity:

References:

Caution: Not fully tested. For research purposes only

Medchemexpress LLC

https://www.sodocs.net/doc/0016771997.html,

[1]. Schwarzer R, et al. Notch pathway inhibition controls myeloma bone disease in the murine MOPC315.BM

model. Blood Cancer J. 2014 Jun 13;4:e217.[2]. Schwarzer R, et al. Notch is an essential upstream regulator of NF-κB and is relevant for survival of

Hodgkin and Reed-Sternberg cells. Leukemia. 2012 Apr;26(4):806-13.[3]. Okuhashi Y, et al. Gamma-secretase inhibitors induce erythroid differentiation in erythroid leukemia cell

lines. Anticancer Res. 2010 Oct;30(10):4071-4. Z-Ile-Leu-aldehyde(Z-IL-CHO; GSI-XII) is a potent gamma-Secretase inhibitor; Notch signaling inhibitor.

IC50 value:

Target: gamma-Secretase inhibitor in vitro: GSI-XII induces apoptosis of murine MOPC315.BM myeloma cells with high Notch activity. GSI XII impairs murine osteoclast differentiation of receptor activator of NF-κB ligand (RANKL)-stimulated RAW264.7cells in vitro [1]. Notch-signaling inhibition in HRS cells by the γ-secretase inhibitor (GSI) XII results in decreased alternative p52/RelB NF-κB signaling, interfering with processing of the NF-κB2 gene product p100 into its active form p52 [2]. GSI treatment induced morphologic erythroid differentiation and promoted hemoglobin production. GSI treatment suppressed short-term growth and colony formation, while treatment

with GSI-XXI promoted the growth of AA cells [3].in vivo: In the murine MOPC315.BM myeloma...

Pathways:Neuronal Signaling; Target:γ-secretase

Pathways:Wnt/Hedgehog/Notch; Target:Notch Product Data Sheet

DMSO

11 D e e r P a r k D r i v e , S u i t e 102D M o n m o u t h J u n c t i o n , N J 08852,U S A

E m a i l : i n f o @m e d c h e m e x p r e s s .c o m W e b : w w w .m e d c h e m e x p r e s s .c o m

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