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MedChemExpressModel Deferoxamine mesylate - 138-14-7

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Deferoxamine mesylate (Deferoxamine B mesylate) 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 mesylate upregulates HIF-1α levels with good antioxidant activity. Deferoxamine mesylate also shows anti-proliferative activity, can induce apoptosis and autophagy in cancer cells. Deferoxamine mesylate can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19[1][2][3][4][5].
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Deferoxamine mesylate

MCE China:Deferoxamine mesylate

Brand:MedChemExpress (MCE)

Cat. No.HY-B0988

CAS:138-14-7

Synonyms:Desferrioxamine B mesylate; DFOM

Purity:99.94%

Storage:4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

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

Description:Deferoxamine mesylate (Deferoxamine B mesylate) 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 mesylate upregulates HIF-1α levels with good antioxidant activity. Deferoxamine mesylate also shows anti-proliferative activity, can induce apoptosis and autophagy in cancer cells. Deferoxamine mesylate can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19.

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

In Vivo:Deferoxamine mesylate (6.57 μg/per; drip-on; once daily for 21 days) enhances wound healing and increases neovascularization in aged or diabetic mice[1]. Deferoxamine mesylate (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].

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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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