70-51-9
70-51-9 structure
- Name: Deferoxamine
- Chemical Name: desferrioxamine B
- CAS Number: 70-51-9
- Molecular Formula: C25H48N6O8
- Molecular Weight: 560.68400
- Catalog: API Special medicine Antidote
- Create Date: 2018-07-14 17:06:24
- Modify Date: 2024-01-01 19:26:17
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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[1][2][3][4][5].
| Name | desferrioxamine B |
|---|---|
| Synonyms |
desferrioxamine mesylate
Deferoxamin EINECS 201-064-4 Desferal Deferrioxamine B Deferrioxamine Desferin DESFERRIOXAMINE deferoxamine MFCD00004679 Deferoxamine B Desferrioxamine B N-[5-[[4-[5-[acetyl(hydroxy)amino]pentylamino]-4-oxobutanoyl]-hydroxyamino]pentyl]-N'-(5-aminopentyl)-N'-hydroxybutanediamide Deferoxaminum |
| Description | 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[1][2][3][4][5]. |
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| Related Catalog | |
| In Vitro | Deferoxamine (1 mM; 16 h or 4 weeks) improves HIF-1α function under hypoxic and hyperglycemic conditions and decreases ROS in MEFs cells[1]. Deferoxamine (100 µM; 24 h) increases InsR expression and activity and also induces an increase in p-Akt/total Akt/PKB levels[2]. Deferoxamine (5, 10, 25, 50, 100 µM; 7 or 9 days) inhibits the proliferation of tumor-associated MSCs and bone marrow MSCs[3]. Deferoxamine (5, 10, 25, 50, 100 µM; 7 days) induces apoptosis of MSCs[3]. Deferoxamine (10 µM ; 3 days) influencs the expression of adhesion proteins on MSCs[3]. Deferoxamine (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 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. |
| 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[1]. 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[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. |
| References |
| Density | 1.212g/cm3 |
|---|---|
| Boiling Point | 627.9°C (rough estimate) |
| Melting Point | 139°C |
| Molecular Formula | C25H48N6O8 |
| Molecular Weight | 560.68400 |
| Exact Mass | 560.35300 |
| PSA | 205.84000 |
| LogP | 2.40420 |
| Index of Refraction | 1.537 |
| Storage condition | -20℃ |
CHEMICAL IDENTIFICATION
HEALTH HAZARD DATAACUTE TOXICITY DATA
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| HS Code | 2924199090 |
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| HS Code | 2924199090 |
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| Summary | 2924199090. other acyclic amides (including acyclic carbamates) and their derivatives; salts thereof. VAT:17.0%. Tax rebate rate:13.0%. . MFN tariff:6.5%. General tariff:30.0% |