Deferoxamine mesylate is an iron chelator that binds free iron in a stable complex, preventing it from engaging in chemical reactions.
CAS Number: 138-14-7
Molecular Weight: 656.79
Desferrioxamine B mesylate
Chemical Name: O=C(N(CCCCCN)O)CCC(NCCCCCN(C(CCC(NCCCCCN(C(C)=O)O)=O)=O)O)=O.CS(=O)(O)=O
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Solubility: H2O : 125 mg/mL (190.32 mM; Need ultrasonic)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥360 days if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
Deferoxamine treatment significantly increases HIF-1α binding under all culture conditions, including hypoxic and high-glucose. The mechanism of deferoxamine is through improving HIF-1α biological function through scavenging oxygen free radicals. Deferoxamine (5 μM) has significant effect on the tumor-associated stromal cells cellular multiplication, and cells die at day 7 after exposure to 50 μM and 100 μM deferoxamine. Deferoxamine (5 μM-100 μM) inhibits the proliferation of BMMSCs, and induces apoptosis of MSCs in a dose-dependent manner. Deferoxamine influences the expression of adhesion proteins on MSCs. Deferoxamine (30, 60, 120 μM) shows lower expression of HIF-1α in a concentration dependent way in AdMSCs.
Deferoxamine (100 mg/kg, i.p.) lowers the mortality rate of subarachnoid hemorrhage (SAH) rat. Deferoxamine (100 mg/kg, i.p.) attenuates Evan’s blue extravasation in cortex, ameliorates the tight junction detachment and preserves the integrity of the base membrane examined in electron microscope at day 3 after SAH. Deferoxamine attenuates degradation of BBB proteins after SAH and significantly reduces ferritin expression at day 3 in the cortex, and improves neurologic behavior and cognitive deficits after experimental. Ten µL of 1 mM deferoxamine-treated wounds display significantly accelerated healing from day 7 onward and heal significantly faster than control-treated wounds in diabetic mice. Deferoxamine-treated wounds and dimethyloxalylglycine-treated wounds heal significantly faster than control-treated wounds in aged mice. In deferoxamine (10 mg/mL)-treated TG mice, there is a decrease in both soluble and insoluble Aβ40 and Aβ42. Both pGSK3β and β-catenin are significantly increased by approximately 50% in the deferoxamine-treated mice.
- Li Y, et al. Effects of deferoxamine on blood-brain barrier disruption after subarachnoid hemorrhage. PLoS One. 2017 Mar 1;12(3):e0172784
- 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
- 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
Products are for research use only. Not for human use.
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