138-14-7
138-14-7 structure
- Name: Deferoxamine (mesylate)
- Chemical Name: desferrioxamine B mesylate
- CAS Number: 138-14-7
- Molecular Formula: C26H52N6O11S
- Molecular Weight: 752.895
- Catalog: API Special medicine Antidote
- Create Date: 2018-07-12 23:01:13
- Modify Date: 2024-01-01 17:25:28
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Deferoxamine mesylate is an iron chelator that binds free iron in a stable complex, preventing it from engaging in chemical reactions.
| Name | desferrioxamine B mesylate |
|---|---|
| Synonyms |
Desferal methanesulfonate
DEFEROXAMINE MESYLATE Deferoxamine Methanesulfonate N'-{5-[Acetyl(hydroxy)amino]pentyl}-N-[5-({4-[(5-aminopentyl)(hydroxy)amino]-4-oxobutanoyl}amino)pentyl]-N-hydroxysuccinamide methanesulfonate (1:2) Deferoxamine mesylate salt DESFERAL MESYLATE EINECS 205-314-3 Butanediamide, N-[5-(acetylhydroxyamino)pentyl]-N-[5-[[4-[(5-aminopentyl)hydroxyamino]-1,4-dioxobutyl]amino]pentyl]-N-hydroxy-, methanesulfonate (1:2) (salt) MFCD00058605 DFOM,Deferoxamine methanesulfonate salt,Desferrioxamine mesylate salt Deferoxamine (mesylate) |
| Description | Deferoxamine mesylate is an iron chelator that binds free iron in a stable complex, preventing it from engaging in chemical reactions. |
|---|---|
| Related Catalog | |
| In Vitro | Deferoxamine treatment significantly increases HIF-1α binding under all culture conditions, including hypoxic and high-glucose. The mechanism of deferoxamine is through improving HIF-1α biological function through scavenging oxygen free radicals[1]. Deferoxamine (5 μM) has significant effect on the tumor-associated stromal cells cellular multiplication, and cells die at day 7 after exposure to 50 μM and 100 μM deferoxamine. Deferoxamine (5 μM-100 μM) inhibits the proliferation of BMMSCs, and induces apoptosis of MSCs in a dose-dependent manner. Deferoxamine influences the expression of adhesion proteins on MSCs[3]. Deferoxamine (30, 60, 120 μM) shows lower expression of HIF-1α in a concentration dependent way in AdMSCs[4]. |
| In Vivo | Deferoxamine (100 mg/kg, i.p.) lowers the mortality rate of subarachnoid hemorrhage (SAH) rat. Deferoxamine (100 mg/kg, i.p.) attenuates Evan’s blue extravasation in cortex, ameliorates the tight junction detachment and preserves the integrity of the base membrane examined in electron microscope at day 3 after SAH. Deferoxamine attenuates degradation of BBB proteins after SAH and significantly reduces ferritin expression at day 3 in the cortex, and improves neurologic behavior and cognitive deficits after experimental[1]. Ten µL of 1 mM deferoxamine-treated wounds display significantly accelerated healing from day 7 onward and heal significantly faster than control-treated wounds in diabetic mice. Deferoxamine-treated wounds and dimethyloxalylglycine-treated wounds heal significantly faster than control-treated wounds in aged mice[2]. In deferoxamine (10 mg/mL)-treated TG mice, there is a decrease in both soluble and insoluble Aβ40 and Aβ42. Both pGSK3β and β-catenin are significantly increased by approximately 50% in the deferoxamine-treated mice[5]. |
| Cell Assay | Harvested murine tumor and bone marrow-derived MSCs are exposed to varying doses of deferoxamine. Cell viability is assessed by trypan blue exclusion assay. The viable cells are more than 98% before enrolled for experiments. A total of 1.5×105 TAMSCs/well or 3×105 BMMSCs/well are seeded in 6-well plates. Then MSCs are exposed to 5, 10, 25, 50, and 100 μM deferoxamine on the following day. After 7 days, the number of TAMSCs is counted. To assess the cytotoxicity of deferoxamine to primary bone marrow MSCs, 2×106 bone marrow cells/well are seeded in 24-well plates. After 9 days, the number of survival cells is counted. To assess the cell cycle, TAMSCs are stained with propidium iodide, and cell cycle distribution is analyzed by flow cytometry. |
| Animal Admin | Mice are divided into three treatment groups of 17 each: (1) TG mice given IN Deferoxamine (TG-DFO), (2) TG mice given IN phosphate buffered saline (TG-PBS), and (3) WT mice given IN PBS (WT-PBS). At 30 weeks of age, mice are acclimated to handling and then treated intranasally every monday, wednesday, and friday, starting at 36 weeks of age. Mice are dosed for 18 weeks, until behavior tests at 54 weeks. Dosing continues during the 4 weeks of behavior to measure both chronic and acute effects. After behavior mice are dosed a final time, and 24 h later euthanized and tissues collected for biochemical analyses. These include soluble and insoluble amyloid as measured by ELISA and IHC, quantification of proteins with Western blot and oxidative markers. |
| References |
| Boiling Point | 966.9ºC at 760 mmHg |
|---|---|
| Melting Point | 148-149° |
| Molecular Formula | C26H52N6O11S |
| Molecular Weight | 752.895 |
| Flash Point | 538.5ºC |
| Exact Mass | 752.329590 |
| PSA | 268.59000 |
| LogP | 2.98900 |
| Vapour Pressure | 0mmHg at 25°C |
| Storage condition | −20°C |
| Water Solubility | H2O: 50 mg/mL |
CHEMICAL IDENTIFICATION
HEALTH HAZARD DATAACUTE TOXICITY DATA
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| Personal Protective Equipment | Eyeshields;Gloves;type N95 (US);type P1 (EN143) respirator filter |
|---|---|
| Safety Phrases | 22-24/25 |
| RIDADR | NONH for all modes of transport |
| WGK Germany | 2 |
| RTECS | UG5310000 |
