Deferoxamine mesylate 是一种铁螯合剂，可将游离铁结合成稳定的复合物。它也是一种铁死亡抑制剂。

Deferoxamine is an iron-chelating agent that binds free iron in a stable complex. It also is an inhibitor of ferroptosis.

Deferoxamine (DFO) had growth-arresting and apoptosis-inducing effect on TAMSCs and bone marrow MSCs (BMMSCs). DFO also influenced the expression pattern of adhesion molecule VCAM-1 on both TAMSCs and BMMSCs [1]. LLC-PK(1) cells were exposed to hypoxia, stimulated with desferrioxamine (Deferoxamine). Although all stimuli elicited HIF-1alpha stabilization with differences in the time-dependent accumulation pattern, significant variations appeared with regard to signaling [2]. No significant differences could be seen between AdMSC seeded collagen-GAG that was exposed to 1% O2 and 120?μM DFO. Cells exposed to 30 or 60?μM of DFO showed lower expression of HIF-1α [3].

The rats were treated with deferoxamine (DFX) or vehicle (100mg/kg) for a maximum of 7 days. In SAH rat, the peak time of brain edema and BBB impairment in the cortex was at day 3 after SAH. SAH resulted in a significant increase in ferritin expression in the cortex. The ferritin positive cells were colocalized with endothelial cells, pericytes, astrocytes, microglia, and neurons [4]. Mice were treated 3x/week with 0.24 C intranasal (IN) DFO for 18 weeks from 36 to 54 weeks of age. IN DFO treatment significantly decreased loss of both reference and working memory in the Morris and radial arm water mazes, and also decreased soluble Aβ40 and Aβ42 in cortex and hippocampus. Further, IN DFO decreased activity of GSK3β, and led to decreases in oxidative stress [5].

After cells were seeded onto the collagen-GAG discs and allowed to adhere for 3?hours, they were placed into a hypoxic incubator with 1% O2 or incubated under standard cell culture conditions with deferoxamine mesylate (DFO) added to final concentrations of 30, 60, or 120?μM. Scaffolds seeded with AdMSCs cultured under standard conditions were used as a control [3].

The animals were divided into 4 groups: sham, SAH, SAH+vehicle and SAH+DFX (100mg/kg) group. DFX was administered intraperitoneally 2 and 6 hours after hemorrhage followed by every 12 hours for a maximum of 7 days. The same time course and dosage of saline were administered in the SAH+vehicle group. Afterward, rats underwent behavioral testing and were euthanized at day 1, 3, 7 and 28 for brain water content calculation, immunohistochemistry or western blot assays. The study was performed in three parts. Part 1 measured the brain water content, Evan's blue extravasation, and ultrastructural abnormalities at day 1, 3 and 7 after SAH to evaluate the time-dependent changes in brain edema and BBB disruption (n = 4 per time point and group). Part 2 investigated the role of iron in SAH-induced BBB disruption at day 1, 3 and 7 by brain water content (n = 4, per time point and group), Evan's blue extravasation (n = 4, per time point and group), transmission electron microscopy (n = 4, per time point and group), immunohistochemistry (n = 4, per time point and group) and western blot analysis (n = 3, per time point and group). Part 3 compared the acute (n = 61, per group at day 1; n = 42, per group at day 3; n = 23, per group at day 7) and long term (n = 4, per group at day 28) neurological function after SAH in each group to determine the effect of iron chelation on SAH-induced neurologic impairment [4].

138-14-7

C26H52N6O11S

656.79

去铁铵;Desferrioxamine B mesylate;desferrioxamine B;甲磺酸去铁胺;DFOM

DMSO:152.3 mM
Powder: -20°C for 3 years
In solvent: -80°C for 2 years