ChemicalBook--->CAS DataBase List--->1239875-86-5

1239875-86-5

1239875-86-5 Structure

1239875-86-5 Structure
IdentificationBack Directory
[Name]

SGI 7079
[CAS]

1239875-86-5
[Synonyms]

CS-2333
SGI 7079
SGI-7079 /SGI7079
SGI-7079;SGI 7079;SGI7079
3-[2-[[3-Fluoro-4-(4-methyl-1-piperazinyl)phenyl]amino]-5-methyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl]benzeneacetonitrile
2-(3-(2-((3-Fluoro-4-(4-methylpiperazin-1-yl)phenyl)amino)-5-methyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl)phenyl)acetonitrile
Benzeneacetonitrile, 3-[2-[[3-fluoro-4-(4-methyl-1-piperazinyl)phenyl]amino]-5-methyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl]-
[Molecular Formula]

C26H26FN7
[MDL Number]

MFCD28963942
[MOL File]

1239875-86-5.mol
[Molecular Weight]

455.53
Chemical PropertiesBack Directory
[storage temp. ]

Store at -20°C
[solubility ]

DMF: 30 mg/ml; DMSO: 30 mg/ml; DMSO:PBS(pH 7.2) (1:3): 0.25 mg/ml
[form ]

A crystalline solid
[color ]

Light yellow to yellow
Safety DataBack Directory
[Symbol(GHS) ]

GHS hazard pictograms
GHS07
[Signal word ]

Warning
[Hazard statements ]

H302-H315-H319-H335
[Precautionary statements ]

P261-P264-P270-P271-P280-P301+P312-P330-P302+P352-P321-P304+P340-P305+P351+P338-P332+P313-P362+P364-P337+P313-P403+P233-P405-P501
Hazard InformationBack Directory
[Description]

SGI-7079 is an inhibitor of the receptor tyrosine kinase Axl. It inhibits proliferation of inflammatory breast cancer cells (IC50s = 0.43 and 0.15 μM for SUM149 and KPL-4 cells, respectively), decreases invasion, and halts the cell cycle in the G1 phase. SGI-7079 synergistically increases the potency of erlotinib on EGFR inhibition. In a mouse xenograft model of non-small cell lung cancer, SGI-7079 dose-dependently inhibits tumor growth, an effect that is greater when used in combination with erlotinib.
[Uses]

3-[2-[[3-Fluoro-4-(4-methyl-1-piperazinyl)phenyl]amino]-5-methyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl]benzeneacetonitrile is an anticancer agent and a selective Axl inhibitor.
[IC 50]

Axl
[References]

[1] XIAOPING WANG. TIG1 promotes the development and progression of inflammatory breast cancer through activation of Axl kinase.[J]. Cancer research, 2013, 73 21: 6516-6525. DOI: 10.1158/0008-5472.can-13-0967
[2] LAUREN AVERETT BYERS. An epithelial-mesenchymal transition gene signature predicts resistance to EGFR and PI3K inhibitors and identifies Axl as a therapeutic target for overcoming EGFR inhibitor resistance.[J]. Clinical Cancer Research, 2013: 279-290. DOI: 10.1158/1078-0432.ccr-12-1558
Spectrum DetailBack Directory
[Spectrum Detail]

SGI 7079(1239875-86-5)1HNMR
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