Deferoxamine 去铁胺; Deferoxamine B; Deferriferrioxamine B; Deferrioxamine|cas:70-51-9|西域试剂

Deferoxamine 去铁胺; Deferoxamine B; Deferriferrioxamine B; Deferrioxamine,98.0%

产品编号：Bellancom-B1625| CAS NO：70-51-9| 分子式：C₂₅H₄₈N₆O₈| 分子量：560.68

去铁胺（去铁胺B）是一种铁螯合剂（与Fe（III）和许多其他金属阳离子结合），广泛用于减少组织中的铁积累和沉积。去铁胺通过良好的抗氧化活性上调HIF-1α水平。去铁胺还具有抗增殖活性，可诱导癌细胞凋亡和自噬。去铁胺可用于糖尿病、神经退行性疾病以及抗癌和抗新冠肺炎[5]的研究。

本网站销售的所有产品仅用于工业应用或者科学研究等非医疗目的,不可用于人类或动物的临床诊断或者治疗,非药用,非食用，

货号	包装	价格	库存与货期	购买量	操作
Bellancom-B1625		￥7700.00	杭州北京（现货）
Bellancom-B1625		￥12500.00	杭州北京（现货）

增值税发票√顺丰快递√订货电话：18601927057

Deferoxamine 去铁胺; Deferoxamine B; Deferriferrioxamine B; Deferrioxamine

产品介绍

Deferoxamine (Deferoxamine B) 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 具有较好的抗氧化活性，可上调 HIF-1α 水平。Deferoxamine 还具有抗增殖活性，能诱导癌细胞凋亡和自噬。Deferoxamine 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 (Deferoxamine B) 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 upregulates HIF-1α levels with good antioxidant activity. Deferoxamine also shows anti-proliferative activity, can induce apoptosis and autophagy in cancer cells. Deferoxamine can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19^[4]^[5].

体外研究

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

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis

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

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

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

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

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 gene Beclin 1 was suppressed by Beclin 1 siRNA transfection. Caused a time and dose-dependent increase of HIF-1a, accompanied by the induction of autophagy.

体内研究
(In Vivo)

Deferoxamine (560.68 mg/per; drip-on; once daily for 21 days) enhances wound healing and increases neovascularization in aged or diabetic mice.
Deferoxamine (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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Aged (21-month-old) and diabetic (12-week-old) C57BL/6J mice (excisional wound model).
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).
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.

体内研究

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Aged (21-month-old) and diabetic (12-week-old) C57BL/6J mice (excisional wound model).
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).
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.

体内研究

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Aged (21-month-old) and diabetic (12-week-old) C57BL/6J mice (excisional wound model).
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).
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.

性状

Solid

溶解性数据

In Vitro:

DMSO : 12.5 mg/mL (22.29 mM; ultrasonic and warming and heat to 60°C)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	1.7835 mL	8.9177 mL	17.8355 mL
5 mM	0.3567 mL	1.7835 mL	3.5671 mL
10 mM	0.1784 mL	0.8918 mL	1.7835 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°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 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： 10% DMSO 40% PEG300 5% Tween-80 45% saline
Solubility: ≥ 1.25 mg/mL (2.23 mM); Clear solution

此方案可获得 ≥ 1.25 mg/mL (2.23 mM，饱和度未知) 的澄清溶液。
以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。
将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液
2.

请依序添加每种溶剂： 10% DMSO 90% (20% SBE-β-CD in saline)
Solubility: ≥ 1.25 mg/mL (2.23 mM); Clear solution

此方案可获得 ≥ 1.25 mg/mL (2.23 mM，饱和度未知) 的澄清溶液。
以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
3.

请依序添加每种溶剂： 10% DMSO 90% corn oil
Solubility: ≥ 1.25 mg/mL (2.23 mM); Clear solution

此方案可获得 ≥ 1.25 mg/mL (2.23 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。
以 1 mL 工作液为例，取 100 μL 12.5 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在西域网站选购。

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

参考文献

. 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. [Content Brief]

. Dongiovanni P, et al. Iron depletion by deferoxamine up-regulates glucose uptake and insulin signaling in hepatoma cells and in rat liver. Am J Pathol. 2008 Mar;172(3):738-47. [Content Brief]

. 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. [Content Brief]

[4]. Wu Y, et al. Neuroprotection of deferoxamine on rotenone-induced injury via accumulation of HIF-1 alpha and induction of autophagy in SH-SY5Y cells. Neurochem Int. 2010 Oct;57(3):198-205. [Content Brief]

[5]. Bellotti D, et al. Deferoxamine B: A Natural, Excellent and Versatile Metal Chelator. Molecules. 2021 May 28;26(11):3255. [Content Brief]

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产品编号(Item Number)

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Deferoxamine 去铁胺; Deferoxamine B; Deferriferrioxamine B; Deferrioxamine,98.0%

Deferoxamine 去铁胺; Deferoxamine B; Deferriferrioxamine B; Deferrioxamine

化学品安全说明书(MSDS)

质检证书(COA)

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