- DEFEROXAMINE MESYLATE
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- $8.00 / 1kg
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2025-09-25
- CAS:138-14-7
- Min. Order: 1kg
- Purity: 99%
- Supply Ability: g-kg-tons, free sample is available
- DeferoxaMine Mesylate
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- $0.00 / 1KG
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2022-02-19
- CAS:138-14-7
- Min. Order: 1KG
- Purity: 98.4%
- Supply Ability: 100 tons
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| | DEFEROXAMINE MESYLATE Basic information |
| | DEFEROXAMINE MESYLATE Chemical Properties |
| Melting point | 148-149° | | storage temp. | 2-8°C | | solubility | H2O: 50 mg/mL | | form | powder | | color | white to off-white | | Water Solubility | Soluble to 100 mM in water | | InChIKey | IDDIJAWJANBQLJ-UHFFFAOYSA-N | | SMILES | C(=O)(N(O)CCCCCNC(=O)CCC(=O)N(O)CCCCCN)CCC(=O)NCCCCCN(O)C(=O)C.S(=O)(=O)(O)C |
| Safety Statements | 22-24/25 | | WGK Germany | 2 | | RTECS | UG5310000 | | HS Code | 29280000 | | Storage Class | 11 - Combustible Solids | | Toxicity | man,TDLo,parenteral,16gm/kg/34W-I (16000mg/kg),CARDIAC: PERICARDITISGASTROINTESTINAL: ULCERATION OR BLEEDING FROM SMALL INTESTINEBLOOD: OTHER CHANGES,American Journal of Kidney Diseases. Vol. 10, Pg. 71, 1987. |
| | DEFEROXAMINE MESYLATE Usage And Synthesis |
| Description | Deferoxamine is a bacterial siderophore that chelates iron. It is used to experimentally inhibit iron-dependent prolyl hydroxylases (EC50 = 17.8 μM), thus preventing the degradation of isoforms of hypoxia inducible factor during normoxia. Deferoxamine has applications in diseases that are characterized by high levels of circulating iron, such as thalassemia major. | | Chemical Properties | DEFEROXAMINE MESYLATE is white or almost white powder. | | Uses | DEFEROXAMINE MESYLATE is an iron chelating agent used in therapy for patients with sickle cell diseases and iron overload. Studies suggest that it can exert potential antioxidant neuroprotective effects in stroke patients | | Uses | chelating agent (Fe & Al) | | Brand name | Desferal (Novartis). | | reaction suitability | reagent type: chelator | | 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. | | Clinical Use | Chelating agent:
Acute iron poisoning
Chronic iron or aluminium overload | | Veterinary Drugs and Treatments | Deferoxamine is used for the treatment of either acute or chronic
iron toxicity. It is being evaluated as an iron chelator for adjunctive
treatment of acute cardiac ischemia and as a chelator for aluminum
toxicity. Its efficacy in treating reperfusion injuries has been disappointing. | | Drug interactions | Potentially hazardous interactions with other drugs
Avoid prochlorperazine, levomepromazine and
methotrimeprazine (prolonged unconsciousness).
Do not administer with blood. | | Metabolism | When given parenterally desferrioxamine forms chelates
with iron and aluminium ions to form ferrioxamine and
aluminoxamine, respectively. The chelates are excreted
in the urine and faeces via the bile. Desferrioxamine is
metabolised, mainly in the plasma. Four metabolites of
desferrioxamine were isolated from urine of patients with
iron overload. The following biotransformation reactions
were found to occur with desferrioxamine: transamination
and oxidation yielding an acid metabolite, beta-oxidation
also yielding an acid metabolite, decarboxylation and
N-hydroxylation yielding neutral metabolites. | | storage | Store at -20°C | | References | [1] W L STEINMETZ T O O M R Glick. Modified aca method for determination of iron chelated by deferoxamine and other chelators.[J]. Clinical chemistry, 1980, 26 11: 1593-1597.
[2] JIMMY R. THERIAULT . Discovery of a new molecular probe ML228: An activator of the hypoxia inducible factor (HIF) pathway[J]. Bioorganic & Medicinal Chemistry Letters, 2012, 22 1: Pages 76-81. DOI: 10.1016/j.bmcl.2011.11.077
[3] PANU JAAKKOLA. Targeting of HIF-α to the von Hippel-Lindau Ubiquitylation Complex by O2-Regulated Prolyl Hydroxylation[J]. Science, 2001, 292 5516. DOI: 10.1126/science.1059796
[4] K. SANDAU. Regulation of the Hypoxia-inducible Factor 1α by the Inflammatory Mediators Nitric Oxide and Tumor Necrosis Factor-α in Contrast to Desferroxamine and Phenylarsine Oxide*[J]. The Journal of Biological Chemistry, 2001, 120 1: 39805-39811. DOI: 10.1074/jbc.m107689200
[5] NEUFELD E J. Update on iron chelators in thalassemia.[J]. Hematology. American Society of Hematology. Education Program, 2010: 451-455. DOI: 10.1182/asheducation-2010.1.451
[6] JOSEPH M. HENDRICKS. Identification of structurally diverse FSP1 inhibitors that sensitize cancer cells to ferroptosis[J]. bioRxiv?: the preprint server for biology, 2022, 6 1. DOI: 10.1101/2022.12.14.520445
[7] FENGXIANG WANG . PALP: A rapid imaging technique for stratifying ferroptosis sensitivity in normal and tumor tissues in situ[J]. Cell Chemical Biology, 2022, 29 1: Pages 157-170.e6. DOI: 10.1016/j.chembiol.2021.11.001
[8] DAVID A. ARMENTA . Ferroptosis inhibition by lysosome-dependent catabolism of extracellular protein[J]. Cell Chemical Biology, 2022, 29 11: Pages 1588-1600.e7. DOI: 10.1016/j.chembiol.2022.10.006
[9] ALEXANDER BEATTY. Ferroptotic cell death triggered by conjugated linolenic acids is mediated by ACSL1.[J]. ACS Combinatorial Science, 2021: 2244. DOI: 10.1038/s41467-021-22471-y
[10] WANLU DU. Lysosomal Zn2+ release triggers rapid, mitochondria-mediated, non-apoptotic cell death in metastatic melanoma.[J]. ACS Applied Polymer Materials, 2021: 109848. DOI: 10.1016/j.celrep.2021.109848
[11] PANDIAN NAGAKANNAN . Cathepsin B is an executioner of ferroptosis[J]. Biochimica et biophysica acta. Molecular cell research, 2021, 1868 3: Article 118928. DOI: 10.1016/j.bbamcr.2020.118928
[12] DANIEL M. KREMER. GOT1 Inhibition Primes Pancreatic Cancer for Ferroptosis through the Autophagic Release of Labile Iron[J]. bioRxiv?: the preprint server for biology, 2020, 8 1. DOI: 10.1101/2020.02.28.970228
[13] KIRILL BERSUKER. The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis[J]. Nature, 2019, 575 7784: 688-692. DOI: 10.1038/s41586-019-1705-2
[14] JENNIFER YINUO CAO. A Genome-wide Haploid Genetic Screen Identifies Regulators of Glutathione Abundance and Ferroptosis Sensitivity.[J]. Cell reports, 2019: 1544-1556.e8. DOI: 10.1016/j.celrep.2019.01.043
[15] ANAGHA SEN. MicroRNA-138 regulates hypoxia-induced endothelial cell dysfunction by targeting S100A1.[J]. PLoS ONE, 2013: e78684. DOI: 10.1371/journal.pone.0078684 |
| | DEFEROXAMINE MESYLATE Preparation Products And Raw materials |
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