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Deferoxamine mesylate
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Deferoxamine mesylate图片
CAS NO:138-14-7
包装与价格:
包装价格(元)
10 mM * 1 mL in Water电议
100mg电议
500mg电议
1 g电议
5 g电议

产品名称
甲磺酸去铁胺
Desferrioxamine B mesylate
DFOM
产品介绍
Deferoxamine mesylate (Deferoxamine B mesylate) 是一种铁螯合剂 (结合 Fe(III) 和许多其他金属阳离子),被广泛用于减少铁在组织中的积累和沉积。Deferoxamine mesylate 可上调HIF-1α水平,具有较好的抗氧化活性,还能抗增殖和诱导癌细胞凋亡。Deferoxamine mesylate 可用于糖尿病、神经退行性疾病以及抗癌和抗 COVID-19 的研究。
生物活性

Deferoxamine mesylate (Deferoxamine B mesylate) is an iron chelator (binds to Fe(III) and many other metal cations), is widely used to reduce iron accumulation and deposition in tissues. Deferoxamine mesylate upregulatesHIF-1αlevels with good antioxidant activity. Deferoxamine mesylate also shows anti-proliferative activity, can induceapoptosisandautophagyincancercells. Deferoxamine mesylate can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19[1][2][3][4][5].

体外研究
(In Vitro)

Deferoxamine mesylate (1 mM; 16 h or 4 weeks) improves HIF-1α function under hypoxic and hyperglycemic conditions and decreases ROS in MEFs cells[1].
Deferoxamine mesylate (100 μM; 24 h) increases InsR expression and activity and also induces an increase in p-Akt/total Akt/PKB levels[2].
Deferoxamine mesylate (5, 10, 25, 50, 100 μM; 7 or 9 days) inhibits the proliferation of tumor-associated MSCs and bone marrow MSCs[3].
Deferoxamine mesylate (5, 10, 25, 50, 100 μM; 7 days) induces apoptosis of MSCs[3].
Deferoxamine mesylate (10 μM ; 3 days) influencs the expression of adhesion proteins on MSCs[3].
Deferoxamine mesylate (100 μM; 24 h) induces autophagy mediated by the level of HIF-1α in SH-SY5Y cells[4].

Western Blot Analysis[1]

Cell Line:MEFs cells
Concentration:1 mM
Incubation Time:16 h (hypoxia condition); 4 weeks (hyperglycemic conditions)
Result:Significantly attenuated the hyperglycemia-associated increase in ROS levels under hypoxic high glucose conditions.
Notably increased normoxic HIF transactivation in MEFs under both high glucose and normal glucose conditions.

Western Blot Analysis[2]

Cell Line:HepG2 cells
Concentration:100 μM
Incubation Time:24 h
Result:Showed a twofold increase of InsR mRNA levels in cells.
Increased by twofold InsR binding activity at the half-maximal concentration of 1.1 nM.

Cell Proliferation Assay[3]

Cell Line:TAMSCs and BMMSCs (all isolated from Male C57BL/6J mice (8 week-old; EG-7 induced tumor model))
Concentration:5, 10, 25, 50, 100 μM
Incubation Time:7 days (TAMSCs); 9 days (BMMSCs)
Result:Inhibited the growth of TAMSCs and BMMSCs, and most cells are died at day 7 or 9 when exposed to 50 and 100 μM dose.

Apoptosis Analysis[3]

Cell Line:TAMSCs, BMMSCs
Concentration:5, 10, 25, 50, 100 μM
Incubation Time:7 days
Result:Exhibited proapoptotic effect on TAMSCs and BMMSCs cells.

Western Blot Analysis[3]

Cell Line:TAMSCs, BMMSCs
Concentration:10 μM
Incubation Time:3 days
Result:Remarkably decreased VCAM-1 expression in both TAMSCs and BMMSCs.

Cell Autophagy Assay[4]

Cell Line:SH-SY5Y cells
Concentration:100 μM
Incubation Time:24 h
Result:Increased the ratio of LC3-II/I, an indicator of autophagy, which effects were blocked when autophagy-related geneBeclin 1was suppressed byBeclin 1siRNA transfection.
Caused a time and dose-dependent increase of HIF-1a, accompanied by the induction of autophagy.
体内研究
(In Vivo)

Deferoxamine mesylate (560.68 mg/per; drip-on; once daily for 21 days) enhances wound healing and increases neovascularization in aged or diabetic mice[1].
Deferoxamine mesylate (200 mg/kg; i.p.; daily for 2 weeks) results in HIF-1α stabilization and increases glucose uptake, hepatic InsR expression, and signaling in vivo[2].

Animal Model:Aged (21-month-old) and diabetic (12-week-old) C57BL/6J mice (excisional wound model)[1].
Dosage:560.68 mg/per (10 uL of 1 mM)
Administration:Drip-on; once daily for 21 days.
Result:Displayed significantly accelerated healing and increased neovascularization in both aged and diabetic mice model.
Animal Model:Male Sprague-Dawley rats (180-200 g)[2].
Dosage:200 mg/kg
Administration:Intraperitoneal injection; daily for 2 weeks.
Result:Significantly increased hepatic HIF-1α protein levels, InsR protein levels, as well as Akt/PKB and activated Akt/PKB were significantly higher in the liver.
Clinical Trial
分子量

656.79

性状

Solid

Formula

C26H52N6O11S

CAS 号

138-14-7

中文名称

甲磺酸去铁胺;去铁胺甲磺酸酯;甲磺酸去铁敏;甲磺酸除铁灵

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

溶解性数据
In Vitro: 

H2O : 250 mg/mL(380.64 mM;Need ultrasonic)

配制储备液
浓度溶剂体积质量1 mg5 mg10 mg
1 mM1.5226 mL7.6128 mL15.2256 mL
5 mM0.3045 mL1.5226 mL3.0451 mL
10 mM0.1523 mL0.7613 mL1.5226 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;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80℃, 6 months; -20℃, 1 month (sealed storage, away from moisture)。-80℃ 储存时,请在 6 个月内使用,-20℃ 储存时,请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液,再依次添加助溶剂:

——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

  • 1.

    请依序添加每种溶剂: PBS

    Solubility: 5.56 mg/mL (8.47 mM); Clear solution; Need ultrasonic

*以上所有助溶剂都可在本网站选购。