2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Biological activity
Description
Target:
Axl
In Vivo
SGI-7079 inhibits tumor growth in a dose dependent manner, and at the maximum dose, inhibited tumor growth by 67%, compared to control. The combined inhibition of Axl (SGI-7079) plus EGFR (Erlotinib) is significantly more effective than either drug alone. Notably, SGI-7079 + Erlotinib (25/100 mg/kg) reduced the tumor growth by 82%. Axl blockade by SGI-7079 inhibits the growth of mesenchymal NSCLC xenograft tumors. [2]
In Vitro
SGI-7079 treatment inhibits the phosphorylation of Axl at Tyr 702 upon Gas6 stimulation in SUM149 cells. The growth of SUM149 and KPL-4 in soft agar, one of the hallmark characteristics of cellular transformation and uncontrolled cell growth, is also significantly inhibited by SGI-7079 treatment. SGI-7079 treatment also significantly decreases the migration and invasion of SUM149 cells and the invasion of KPL-4 cells. Taken together, Axl inhibitor SGI-7079 significantly inhibits the proliferation, migration, and invasion of IBC cells, suggesting that Axl may be a promising therapeutic target in patients with IBC. [1]
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Wang X, et al. TIG1 promotes the development and progression of inflammatory breast cancer through activation of Axl kinase. Cancer Res. 2013 Nov 1;73(21):6516-25.
[2]. Byers LA, et al. 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. Clin Cancer Res. 2013 Jan 1;19(1):279-90.
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