Deferoxamine (C09-1126-461)

Deferoxamine (Deferoxamine B) is an iron chelator (binds to Fe(III) and many other metal cations), is widely used to reduce iron accumulation and deposition in tissues. Deferoxamine upregulates HIF-1α levels with good antioxidant activity. Deferoxamine also shows anti-proliferative activity, can induce apoptosis and autophagy in cancer cells. Deferoxamine can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19.In VitroDeferoxamine (1 mM; 16 h or 4 weeks) improves HIF-1α function under hypoxic and hyperglycemic conditions and decreases ROS in MEFs cells. Deferoxamine (100 µM; 24 h) increases InsR expression and activity and also induces an increase in p-Akt/total Akt/PKB levels. Deferoxamine (5, 10, 25, 50, 100 µM; 7 or 9 days) inhibits the proliferation of tumor-associated MSCs and bone marrow MSCs. Deferoxamine (5, 10, 25, 50, 100 µM; 7 days) induces apoptosis of MSCs. Deferoxamine (10 µM ; 3 days) influencs the expression of adhesion proteins on MSCs. Deferoxamine (100 µM; 24 h) induces autophagy mediated by the level of HIF-1α in SH-SY5Y cells . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: MEFs cells Concentration: 1 mM Incubation Time: 16 h (hypoxia condition); 4 weeks (hyperglycemic conditions) Result: Significantly attenuated the hyperglycemia-associated increase in ROS levels under hypoxic high glucose conditions. Notably increased normoxic HIF transactivation in MEFs under both high glucose and normal glucose conditions. Western Blot AnalysisCell Line: HepG2 cells Concentration: 100 µM Incubation Time: 24 h Result: Showed a twofold increase of InsR mRNA levels in cells. Increased by twofold InsR binding activity at the half-maximal concentration of 1.1 nM. Cell Proliferation AssayCell Line: TAMSCs and BMMSCs (all isolated from Male C57BL/6J mice (8 week-old; EG-7 induced tumor model)) Concentration: 5, 10, 25, 50, 100 µM Incubation Time: 7 days (TAMSCs); 9 days (BMMSCs). Result: Inhibited the growth of TAMSCs and BMMSCs, and most cells are died at day 7 or 9 when exposed to 50 and 100 µM dose. Apoptosis AnalysisCell Line: TAMSCs, BMMSCs Concentration: 5, 10, 25, 50, 100 µM Incubation Time: 7 days Result: Exhibited proapoptotic effect on TAMSCs and BMMSCs cells. Western Blot AnalysisCell Line: TAMSCs, BMMSCs Concentration: 10 µM Incubation Time: 3 days Result: Remarkably decreased VCAM-1 expression in both TAMSCs and BMMSCs. Cell Autophagy Assay Cell Line: SH-SY5Y cells Concentration: 100 µM Incubation Time: 24 h Result: Increased the ratio of LC3-II/I, an indicator of autophagy, which effects were blocked when autophagy-related gene Beclin 1 was suppressed by Beclin 1 siRNA transfection. Caused a time and dose-dependent increase of HIF-1a, accompanied by the induction of autophagy.In VivoDeferoxamine (560.68 mg/per; drip-on; once daily for 21 days) enhances wound healing and increases neovascularization in aged or diabetic mice . Deferoxamine (200 mg/kg; i.p.; daily for 2 weeks) results in HIF-1α stabilization and increases glucose uptake, hepatic InsR expression, and signaling in vivo. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Aged (21-month-old) and diabetic (12-week-old) C57BL/6J mice (excisional wound model) . Dosage: 560.68 mg/per (10 uL of 1 mM) Administration: Drip-on; once daily for 21 days. Result: Displayed significantly accelerated healing and increased neovascularization in both aged and diabetic mice model. Animal Model: Male Sprague-Dawley rats (180-200 g). Dosage: 200 mg/kg Administration: Intraperitoneal injection; daily for 2 weeks. Result: Significantly increased hepatic HIF-1α protein levels, InsR protein levels, as well as Akt/PKB and activated Akt/PKB were significantly higher in the liver.Form:Solid. Specifications and Purity: ≥98.0%. Molecular Formula: C25H48N6O8. Molecular Weight: 560.7. PubChem CID: 2973. Isomeric SMILES: CC(=O)N(CCCCCNC(=O)CCC(=O)N(CCCCCNC(=O)CCC(=O)N(CCCCCN)O)O)O.