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D9533

Sigma-Aldrich

Deferoxamine mesylate salt

≥92.5% (TLC), powder, iron-chelating agent

Synonym(s):

DFX mesylate, DFOM, Deferoxamine methanesulfonate salt, Desferrioxamine mesylate salt

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About This Item

Empirical Formula (Hill Notation):
C25H48N6O8 · CH4O3S
CAS Number:
Molecular Weight:
656.79
EC Number:
MDL number:
UNSPSC Code:
12352116
PubChem Substance ID:
NACRES:
NA.32

product name

Deferoxamine mesylate salt, powder, ≥92.5% (TLC)

Quality Level

Assay

≥92.5% (TLC)

form

powder

color

white to off-white

solubility

H2O: 50 mg/mL

storage temp.

−20°C

SMILES string

CS(O)(=O)=O.CC(=O)N(O)CCCCCNC(=O)CCC(=O)N(O)CCCCCNC(=O)CCC(=O)N(O)CCCCCN

InChI

1S/C25H48N6O8.CH4O3S/c1-21(32)29(37)18-9-3-6-16-27-22(33)12-14-25(36)31(39)20-10-4-7-17-28-23(34)11-13-24(35)30(38)19-8-2-5-15-26;1-5(2,3)4/h37-39H,2-20,26H2,1H3,(H,27,33)(H,28,34);1H3,(H,2,3,4)

InChI key

IDDIJAWJANBQLJ-UHFFFAOYSA-N

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Application

Deferoxamine mesylate salt has been used



  • for cell pretreatment to assess its influenceon cell viability and its interactions with other compounds ()
  • to study the effect on Lipocalin 2(Lcn2) production triggered by amyloid-β(Aβ). ()
  • used to induce iron starvation in bacterial cultures.()

Biochem/physiol Actions

An iron chelator used often in the studies of cell proliferation and apoptosis. Has been shown to have anti-proliferative effects on vascular smooth muscle cells in vitro and in vivo and to arrest cells in the G1 phase. Also reported to induce p53. Induces apoptosis in HL-60 cells by chelating iron. After 48 hrs treatment with 1μM deferoxamine, DNA fragmentation was apparent. Cells treated with 0.1 μM deferoxamine for as little as 24 hours were committed to apoptosis; by 48 hrs nuclear collapse was observed. In some studies it has been shown to have antioxidant properties and to protect cells against H2O2-induced damage.
Deferoxamine is used as a hypoxia-mimetic agent to stabilize Hypoxia Inducible Factor 1 (HIF-1). Deferoxamine stabilizes HIF-1 through the inhibition of Prolyl Hydroxylases (PHDs) which target HIF-1 through degradation. The mechanism of deferoxamine inhibition is likely through the chelation of Fe2+ bound to the active site of PHD which is required for enzymatic activity.

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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E Porreca et al.
Arteriosclerosis and thrombosis : a journal of vascular biology, 14(2), 299-304 (1994-02-01)
Vascular smooth muscle cell (VSMC) growth is a primary component of accelerated and spontaneous atherosclerosis. Previous studies have shown that iron may be involved in the control of enzymatic activities that modulate DNA synthesis in human cells. In this study
S Bereswill et al.
Journal of bacteriology, 182(21), 5948-5953 (2000-10-13)
Homologs of the ferric uptake regulator Fur and the iron storage protein ferritin play a central role in maintaining iron homeostasis in bacteria. The gastric pathogen Helicobacter pylori contains an iron-induced prokaryotic ferritin (Pfr) which has been shown to be
Biodegradable hypoxia biomimicry microspheres for bone tissue regeneration.
Lina Hadidi et al.
Journal of biomaterials applications, 34(7), 1028-1037 (2019-10-28)
T Sánchez-Elsner et al.
The Journal of biological chemistry, 276(42), 38527-38535 (2001-08-04)
Signaling by transforming growth factor (TGF)-beta family members is mediated by Smad proteins that regulate gene transcription through functional cooperativity and association with other DNA-binding proteins. The hypoxia-inducible factor (HIF)-1 is a transcriptional complex that plays a key role in
Doortje W Dekens et al.
Neurochemistry international, 132, 104607-104607 (2019-11-25)
Lipocalin 2 (Lcn2) has been implicated to play a role in various neurodegenerative diseases, and normalizing its overexpression may be of therapeutic potential. Iron chelators were found to reduce Lcn2 levels in certain animal models of CNS injury. Focusing on

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