Deferoxamine mesylate

Deferoxamine mesylate is an iron chelator that binds free iron in a stable complex, preventing it from engaging in chemical reactions.

Product information

CAS Number: 138-14-7

Molecular Weight: 656.79

Formula: C26H52N6O11S

Synonym:

Desferrioxamine B mesylate

DFOM

Chemical Name: O=C(N(CCCCCN)O)CCC(NCCCCCN(C(CCC(NCCCCCN(C(C)=O)O)=O)=O)O)=O.CS(=O)(O)=O

Smiles: CC(=O)N(O)CCCCCNC(=O)CCC(=O)N(O)CCCCCNC(=O)CCC(=O)N(O)CCCCCN.CS(O)(=O)=O

InChiKey: IDDIJAWJANBQLJ-UHFFFAOYSA-N

InChi: InChI=1S/C25H48N6O8.CH4O3S/c1-21(32)29(37)18-9-3-6-16-27-22(33)12-14-25(36)31(39)20-10-4-7-17-28-23(34)11-13-24(35)30(38)19-8-2-5-15-26;1-5(2,3)4/h37-39H,2-20,26H2,1H3,(H,27,33)(H,28,34);1H3,(H,2,3,4)

Technical Data

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

In Vitro:

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.

In Vivo:

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.

References:

1. Li Y, et al. Effects of deferoxamine on blood-brain barrier disruption after subarachnoid hemorrhage. PLoS One. 2017 Mar 1;12(3):e0172784
2. 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
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

Products are for research use only. Not for human use.