| Name | AKB-6899 |
| Description | AKB-6899 is an inhibitor of prolyl hydroxylase domain 3 (PHD3) and increases the soluble form of the VEGF receptor (sVEGFR-1) production from GM-CSF-treated macrophages. AKB-6899 leads to stabilization of HIF-2α which induces sVEGFR-1 production from tumor-associated macrophages and decreases tumor growth. |
| In vitro | In murine bone marrow-derived macrophages, AKB-6899 (10 μM; 24 hours) increases the levels of HIF-2α protein, with no corresponding increase in HIF-1α. AKB-6899 shows no effect on HIF-1α accumulation or VEGF production[1]. |
| In vivo | In C57BL/6 mice injected with B16F10 murine melanoma cells, AKB-6899 (17.5 mg/kg; i.p.) significantly reduces tumor growth[1]. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | 10% DMSO+40% PEG300+5% Tween 80+45% Saline : 3.3 mg/mL (11.37 mM), Sonication is recommended. DMSO : 95 mg/mL (327.3 mM), Sonication is recommended.
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| Keywords | VEGFR1 | sVEGFR-1 | PHD3 | Inhibitor | inhibit | Hypoxia-inducible factors | HIFs | HIFProlylHydroxylase | HIF-PH | HIF-2α | HIF/HIFProlylHydroxylase | HIF/HIF Prolyl-Hydroxylase | HIF/HIF ProlylHydroxylase | HIF Prolyl-Hydroxylase | HIF ProlylHydroxylase | HIF | antitumor | antiangiogenic | AKB-6899 | AKB 6899 |
| Inhibitors Related | Ribociclib | Deferoxamine Mesylate | Dapagliflozin | Sorafenib | Chlorogenic Acid | Glucosamine | Hydroxycitric acid tripotassium hydrate | Nintedanib esylate | Glucosamine hydrochloride | Chloramphenicol | Lenvatinib | Pazopanib |
| Related Compound Libraries | Anti-Lung Cancer Compound Library | Glycolysis Compound Library | Anti-Pancreatic Cancer Compound Library | Bioactive Compound Library | Membrane Protein-targeted Compound Library | HIF-1 Signaling Pathway Compound Library | Kinase Inhibitor Library | Tyrosine Kinase Inhibitor Library | Inhibitor Library | Anti-Prostate Cancer Compound Library | Bioactive Compounds Library Max | Anti-Cancer Compound Library |