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AKB-6899, a prolyl hydroxylase domain 3 (PHD3) inhibitor, is a selective HIF-2α stabilizer. AKB-6899 also increases soluble form of the VEGF receptor (sVEGFR-1) production from GM-CSF-treated macrophages, and has antitumor and antiangiogenic effects[1].

AKB-6899 (10 μM; 24 hours) increases the leves of HIF-2α protein, with no corresponding increase in HIF-1α. AKB-6899 also increases soluble form of the VEGF receptor (sVEGFR-1) production from GM-CSF-treated macrophages, with no effect on HIF-1α accumulation or VEGF production[1].

AKB-6899 (17.5 mg/kg; i.p.; 3 times per week; for 16 days) treatment significantly reduces tumor growth in a murine melanoma model[1].

[1]. Julie M Roda, et al. Stabilization of HIF-2α induces sVEGFR-1 production from tumor-associated macrophages and decreases tumor growth in a murine melanoma model. J Immunol. 2012 Sep 15;189(6):3168-77..

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