Z-Ile-Leu-aldehyde

Modify Date: 2024-01-17 16:56:33

Z-Ile-Leu-aldehyde structure	Common Name	Z-Ile-Leu-aldehyde
	CAS Number	161710-10-7	Molecular Weight	362.46300
	Density	N/A	Boiling Point	N/A
	Molecular Formula	C₂₀H₃₀N₂O₄	Melting Point	N/A
	MSDS	N/A	Flash Point	N/A

Use of Z-Ile-Leu-aldehyde

Z-Ile-Leu-aldehyde(Z-IL-CHO; GSI-XII) is a potent gamma-Secretase inhibitor; Notch signaling inhibitor.IC50 value:Target: gamma-Secretase inhibitorin 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 RAW264.7 cells 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 model GSI XII has potent anti-MM activity and reduces osteolytic lesions as evidenced by diminished myeloma-specific monoclonal immunoglobulin (Ig)-A serum levels and quantitative assessment of bone structure changes via high-resolution microcomputed tomography scans [1].

Name	Z-Ile-Leu-aldehyde
Synonym	More Synonyms

Description	Z-Ile-Leu-aldehyde(Z-IL-CHO; GSI-XII) is a potent gamma-Secretase inhibitor; Notch signaling inhibitor.IC50 value:Target: gamma-Secretase inhibitorin 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 RAW264.7 cells 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 model GSI XII has potent anti-MM activity and reduces osteolytic lesions as evidenced by diminished myeloma-specific monoclonal immunoglobulin (Ig)-A serum levels and quantitative assessment of bone structure changes via high-resolution microcomputed tomography scans [1].
Related Catalog	Signaling Pathways >> Neuronal Signaling >> γ-secretase Signaling Pathways >> Stem Cell/Wnt >> γ-secretase Signaling Pathways >> Stem Cell/Wnt >> Notch Research Areas >> Cancer
References	[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.

Description

Related Catalog

Signaling Pathways >> Neuronal Signaling >> γ-secretase

Signaling Pathways >> Stem Cell/Wnt >> γ-secretase

Signaling Pathways >> Stem Cell/Wnt >> Notch

Research Areas >> Cancer

References

[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.