Deferoxamine Mesylate (DFOM) is an iron chelator and ferroptosis inhibitor. Deferoxamine Mesylate binds free iron into a stable complex and reduces iron accumulation. Deferoxamine Mesylate up-regulates HIF-1α levels and induces apoptosis.

方法：人宫颈癌细胞 HeLa 用 Deferoxamine Mesylate (3-100 μM) 处理 72 h，使用 Incucyte HD imaging system 检测细胞数目。
结果：Deferoxamine Mesylate 以浓度依赖的方式抑制细胞生长，在100 μM 下观察到显著的生长抑制。[1]
方法：人结直肠癌细胞 HT29 和 HCT116 用 Deferoxamine Mesylate (50-200 μM) 处理 48 h，使用 Western Blot 方法检测靶点蛋白表达水平。
结果：Deferoxamine Mesylate 以剂量依赖性方式诱导 HIF-1α 的显著表达。[2]
方法：人乳腺癌细胞 MDA-MB-231 和 MCF-7 用 Deferoxamine Mesylate (200 μM) 处理 24 h，使用 Flow Cytometry 方法检测细胞凋亡情况。
结果：Deferoxamine Mesylate 处理后，与未处理的细胞相比，MDA-MB-231 细胞的凋亡率没有变化，而 MCF-7 细胞的凋亡显著增加。[3]

方法：为研究 Deferoxamine Mesylate 是否能减轻实验小鼠的炎症和动脉粥样硬化，将 Deferoxamine Mesylate (100 mg/kg) 腹腔注射给载脂蛋白 E 缺陷 (apoE-/-) 小鼠，每天一次，持续十周。
结果：Deferoxamine Mesylate 使主动脉动脉粥样硬化病变的发展减少 26%。Deferoxamine Mesylate 还降低了血清 MCP-1 水平以及主动脉和心脏中促炎和巨噬细胞标志物的基因表达，同时增加了心脏和肝脏中转铁蛋白受体的蛋白质表达。相反，Deferoxamine Mesylate 治疗对血清胆固醇和甘油三酯水平没有影响。[4]
方法：为研究 Deferoxamine Mesylate 对 ob/ob 小鼠附睾脂肪组织中脂肪细胞功能障碍的影响，将 Deferoxamine Mesylate (100 mg/kg) 腹腔注射给 ob/ob 小鼠，每天一次，持续十五天。
结果：Deferoxamine Mesylate 通过减少活性氧和炎症标志物的分泌，通过增加抗氧化酶、HIF-1α 和 HIF-1α 靶向蛋白的水平，以及通过改变脂肪细胞铁、葡萄糖和脂质相关代谢蛋白，显著改善了脂肪组织生物学的重要参数。同时，Deferoxamine Mesylate 治疗后，肥大的脂肪细胞体积缩小，胰岛素信号通路相关蛋白也被激活。[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].