甲磺酸去铁胺作用机制 - Medchemexpress - MCE中国

1、Product Data SheetDeferoxamine mesylateCat. No.: HY-B0988CAS No.: 138-14-7分式: CHNOS分量: 656.79作靶点: Autophagy; Amyloid-; Mitophagy; Ferroptosis作通路: Autophagy; Neuronal Signaling; Apoptosis储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性数据体外实验 H2O : 33 mg/mL (50.24 mM)* means s

2、oluble, but saturation unknown.SolventMass1 mg 5 mg 10 mgConcentration制备储备液1 mM 1.5226 mL 7.6128 mL 15.2256 mL5 mM 0.3045 mL 1.5226 mL 3.0451 mL10 mM 0.1523 mL 0.7613 mL 1.5226 mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存式和期限：-80C, 6 months; -20C, 1 month。-80C 储存时，请在 6 个内使，-20C 储存时

3、，请在 1 个内使。BIOLOGICAL ACTIVITY物活性 Deferoxamine mesylate种铁螯合剂，可将游离铁与稳定的复合物结合，防其发化学反应。体外研究 Deferoxamine treatment significantly increases HIF-1 binding under all culture conditions, including hypoxic andhigh-glucose. The mechanism of deferoxamine is through improving HIF-1 biological function through s

4、cavengingoxygen free radicals1. Deferoxamine (5 M) has significant effect on the tumor-associated stromal cells cellularmultiplication, and cells die at day 7 after exposure to 50 M and 100 M deferoxamine. Deferoxamine (5 M-100 M) inhibits the proliferation of BMMSCs, and induces apoptosis of MSCs i

5、n a dose-dependent manner. Deferoxamineinfluences the expression of adhesion proteins on MSCs3. Deferoxamine (30, 60, 120 M) shows lower expression ofHIF-1 in a concentration dependent way in AdMSCs4.体内研究Deferoxamine (100 mg/kg, i.p.) lowers the mortality rate of subarachnoid hemorrhage (SAH) rat. D

6、eferoxamine (100Page 1 of 2 www.MedChemEmg/kg, i.p.) attenuates Evans blue extravasation in cortex, ameliorates the tight junction detachment and preservesthe integrity of the base membrane examined in electron microscope at day 3 after SAH. Deferoxamine attenuatesdegradation of BBB proteins after S

7、AH and significantly reduces ferritin expression at day 3 in the cortex, andimproves neurologic behavior and cognitive deficits after experimental1. Ten L of 1 mM deferoxamine-treatedwounds display significantly accelerated healing from day 7 onward and heal significantly faster than control-treated

8、wounds in diabetic mice. Deferoxamine-treated wounds and dimethyloxalylglycine-treated wounds heal significantlyfaster than control-treated wounds in aged mice2. In deferoxamine (10 mg/mL)-treated TG mice, there is a decreasein both soluble and insoluble A40 and A42. Both pGSK3 and -catenin are sign

9、ificantly increased byapproximately 50% in the deferoxamine-treated mice5.PROTOCOLCell Assay 3 Harvested murine tumor and bone marrow-derived MSCs are exposed to varying doses of deferoxamine. Cellviability is assessed by trypan blue exclusion assay. The viable cells are more than 98% before enrolle

10、d forexperiments. A total of 1.5105 TAMSCs/well or 3105 BMMSCs/well are seeded in 6-well plates. Then MSCs areexposed to 5, 10, 25, 50, and 100 M deferoxamine on the following day. After 7 days, the number of TAMSCs iscounted. To assess the cytotoxicity of deferoxamine to primary bone marrow MSCs, 2

11、106 bone marrow cells/wellare seeded in 24-well plates. After 9 days, the number of survival cells is counted. To assess the cell cycle, TAMSCs arestained with propidium iodide, and cell cycle distribution is analyzed by flow cytometry.MCE has not independently confirmed the accuracy of these method

12、s. They are for reference only.Animal Mice are divided into three treatment groups of 17 each: (1) TG mice given IN Deferoxamine (TG-DFO), (2) TG miceAdministration 5 given IN phosphate buffered saline (TG-PBS), and (3) WT mice given IN PBS (WT-PBS). At 30 weeks of age, mice areacclimated to handlin

13、g and then treated intranasally every monday, wednesday, and friday, starting at 36 weeks ofage. Mice are dosed for 18 weeks, until behavior tests at 54 weeks. Dosing continues during the 4 weeks of behaviorto measure both chronic and acute effects. After behavior mice are dosed a final time, and 24

14、 h later euthanized andtissues collected for biochemical analyses. These include soluble and insoluble amyloid as measured by ELISA andIHC, quantification of proteins with Western blot and oxidative markers.MCE has not independently confirmed the accuracy of these methods. They are for reference onl

15、y.户使本产品发表的科研献 ACS Appl Mater Interfaces. 2018 Feb 21;10(7):6180-6189. Theranostics. 2020; 10(11): 51075119. Redox Biol. 2020 Jan;29:101402. J Med Chem. 2019 Oct 10;62(19):8760-8772. Cell Death Dis. 2019 Oct 7;10(10):755.See more customer validations on HYPERLINK www.MedChemE www.MedChemEREFERENCES1.

16、 Li Y, et al. Effects of deferoxamine on blood-brain barrier disruption after subarachnoid hemorrhage. PLoS One. 2017 Mar 1;12(3):e01727842. Duscher D, et al. Comparison of the Hydroxylase Inhibitor Dimethyloxalylglycine and the Iron Chelator Deferoxamine in Diabetic and Aged WoundHealing. Plast Rec

17、onstr Surg. 2017 Mar;139(3):695e-706ePage 2 of 3 www.MedChemE3. Wang G, et al. In vitro assessment of deferoxamine on mesenchymal stromal cells from tumor and bone marrow. Environ Toxicol Pharmacol. 2017Jan;49:58-644. Wahl EA, et al. VEGF released by deferoxamine preconditioned mesenchymal stem cells seeded on collagen-GAG substrates enhancesneovascularization. Sci Rep. 2016 Nov 10;6:368795. Fine JM, et al. Intranasal deferoxamine engages multiple pathways to decrease memory loss in the APP/PS1 model of amyloid ac