Size : | Price | Quantity | |
---|---|---|---|
10 mg | $40.00 | ||
50 mg | $110.00 |
Axitinib (319460-85-0) is a potent inhibitor of VEGFR-2, -3, and -1, IC50 = 0.2, 0.1-0.3, and 1.2 nM respectively1 displaying minimal activity against a panel of ~100 protein kinases. Inhibits angiogenesis and vascular permeability.2 Also inhibits BCR-ABL1 (T315I) with high potency, Ki = 149 pM for autophosphorylated ABL1 (T315I).3 Inhibits proliferation of Ba/F3 cells expressing BCR-ABL1 (T315I). Clinically useful anticancer agent.4 Axitinib downregulated STAT3 expression leading to a significant decrease in immunosuppressive myeloid-derived suppressor cells.5 It increased CD8+ T cells, reduced myeloid-derived suppressor cells, and suppressed the expressions of proinflammatory cytokines in B116F1 melanoma cells.6
References/Citations:
1) Hu-Lowe et al. (2008), Nonclinical antiangiogenesis and antitumor activities of axitinib (AG-013736), an oral, potent and selective inhibitor of vascular endothelial growth factor receptor tyrosine kinases 1,2,3; Cancer Res., 14 7272
2) Ma and Waxman (2008), Modulation of the antitumor activity of metronomic cyclophosphamide by the angiogenesis inhibitor axitinib; Mol. Cancer Ther., 7 79
3) Pemovska et al. (2015), Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation; Nature, 519 102
4) Rixe et al. (2007), Axitinib treatment in patients with cytokine-refractory metastatic renal-cell cancer; a phase II study; Lancet Oncol., 8 975
5) Yuan et al. (2014), Axitinib augments antitumor activity in renal cell carcinoma via STAT3-dependent reversal of myeloid-derived suppressor cell accumulation; Biomed.Pharmacother. 68 751
6) Zhang et al. (2014), Axitinib, a selective inhibitor of vascular endothelial growth factor receptor, exerts an anticancer effect in melanoma through promoting antitumor immunity; Anticancer Drugs 25 204
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Axitinib (319460-85-0) is a potent inhibitor of VEGFR-2, -3, and -1, IC50 = 0.2, 0.1-0.3, and 1.2 nM respectively1 displaying minimal activity against a panel of ~100 protein kinases. Inhibits angiogenesis and vascular permeability.2 Also inhibits BCR-ABL1 (T315I) with high potency, Ki = 149 pM for autophosphorylated ABL1 (T315I).3 Inhibits proliferation of Ba/F3 cells expressing BCR-ABL1 (T315I). Clinically useful anticancer agent.4 Axitinib downregulated STAT3 expression leading to a significant decrease in immunosuppressive myeloid-derived suppressor cells.5 It increased CD8+ T cells, reduced myeloid-derived suppressor cells, and suppressed the expressions of proinflammatory cytokines in B116F1 melanoma cells.6
References/Citations:
1) Hu-Lowe et al. (2008), Nonclinical antiangiogenesis and antitumor activities of axitinib (AG-013736), an oral, potent and selective inhibitor of vascular endothelial growth factor receptor tyrosine kinases 1,2,3; Cancer Res., 14 7272
2) Ma and Waxman (2008), Modulation of the antitumor activity of metronomic cyclophosphamide by the angiogenesis inhibitor axitinib; Mol. Cancer Ther., 7 79
3) Pemovska et al. (2015), Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation; Nature, 519 102
4) Rixe et al. (2007), Axitinib treatment in patients with cytokine-refractory metastatic renal-cell cancer; a phase II study; Lancet Oncol., 8 975
5) Yuan et al. (2014), Axitinib augments antitumor activity in renal cell carcinoma via STAT3-dependent reversal of myeloid-derived suppressor cell accumulation; Biomed.Pharmacother. 68 751
6) Zhang et al. (2014), Axitinib, a selective inhibitor of vascular endothelial growth factor receptor, exerts an anticancer effect in melanoma through promoting antitumor immunity; Anticancer Drugs 25 204
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