MedChemExpress LLC (MCE)

MedChemExpress - Model Deferoxamine - 70-51-9

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[1][2][3][4][5].

Deferoxamine

MCE China：Deferoxamine

Brand：MedChemExpress (MCE)

Cat. No.HY-B1625

CAS：70-51-9

Synonyms：Deferoxamine B; Deferriferrioxamine B; Deferrioxamine

Purity：99.20%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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 Vitro：Deferoxamine (1 mM; 16 h or 4 weeks) improves HIF-1α function under hypoxic and hyperglycemic conditions and decreases ROS in MEFs cells[1]. Deferoxamine (100 μM; 24 h) increases InsR expression and activity and also induces an increase in p-Akt/total Akt/PKB levels[2]. Deferoxamine (5, 10, 25, 50, 100 μM; 7 or 9 days) inhibits the proliferation of tumor-associated MSCs and bone marrow MSCs[3]. Deferoxamine (5, 10, 25, 50, 100 μM; 7 days) induces apoptosis of MSCs[3]. Deferoxamine (10 μM ; 3 days) influencs the expression of adhesion proteins on MSCs[3]. Deferoxamine (100 μM; 24 h) induces autophagy mediated by the level of HIF-1α in SH-SY5Y cells[4].

In Vivo：Deferoxamine (560.68 mg/per; drip-on; once daily for 21 days) enhances wound healing and increases neovascularization in aged or diabetic mice[1]. 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[2].

References：

[1]. Duscher D, et al. Comparison of the Hydroxylase Inhibitor Dimethyloxalylglycine and the Iron Chelator Deferoxamine in Diabetic and Aged Wound Healing. Plast Reconstr Surg. 2017 Mar;139(3):695e-706e. [Content Brief]

[2]. Dongiovanni P, et al. Iron depletion by deferoxamine up-regulates glucose uptake and insulin signaling in hepatoma cells and in rat liver. Am J Pathol. 2008 Mar;172(3):738-47. [Content Brief]

[3]. Wang G, et al. In vitro assessment of deferoxamine on mesenchymal stromal cells from tumor and bone marrow. Environ Toxicol Pharmacol. 2017 Jan;49:58-64. [Content Brief]

[4]. Wu Y, et al. Neuroprotection of deferoxamine on rotenone-induced injury via accumulation of HIF-1 alpha and induction of autophagy in SH-SY5Y cells. Neurochem Int. 2010 Oct;57(3):198-205. [Content Brief]

[5]. Bellotti D, et al. Deferoxamine B: A Natural, Excellent and Versatile Metal Chelator. Molecules. 2021 May 28;26(11):3255. [Content Brief]

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