InChI=1S/C25H48N6O8/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/h37-39H,2-20,26H2,1H3,(H,27,33)(H,28,34) Y
Deferoxamine is used to treat acute
iron poisoning, especially in small children.[7] This agent is also frequently used to treat
hemochromatosis, a disease of iron accumulation that can be either genetic or acquired. Acquired hemochromatosis is common in patients with certain types of chronic
anemia (e.g.
thalassemia and
myelodysplastic syndrome) who require many
blood transfusions, which can greatly increase the amount of iron in the body. Treatment with iron-chelating drugs such as deferoxamine reduces mortality in persons with sickle cell disease or β‐thalassemia who are transfusion dependent.[8]
Administration for chronic conditions is generally accomplished by
subcutaneous injection over a period of 8–12 hours each day. Administration of deferoxamine after acute intoxication may color the urine a pinkish red, a phenomenon termed "vin rosé urine". Apart from iron toxicity, deferoxamine can be used to treat
aluminium toxicity (an excess of aluminium in the body) in selected patients. In US, the drug is not FDA-approved for this use. Deferoxamine is also used to minimize
doxorubicin's cardiotoxic side effects and in the treatment of patients with
aceruloplasminemia.[9] Deferoxamine may be effective for improving neurologic outcomes in persons with
intracranial hemorrhage, although the evidence supporting the efficacy and safety for this indication was weak.[10]
Some published manuscripts suggesting the use of deferoxamine for patients diagnosed with COVID-19 because of the high level of ferritin among them.[11][12]
Adverse effects
It is unclear if use during
pregnancy is safe for the baby.[3]
Chronic use of deferoxamine may cause ocular symptoms,
growth retardation, local reactions and allergy.[14]
Mechanism
Deferoxamine is produced by removal of the trivalent iron moiety from ferrioxamine B, an iron-bearing
sideramine produced by the actinomycetes, Streptomyces pilosus. Its discovery was a serendipitous result of research conducted by scientists at Ciba in collaboration with scientists at the Swiss Federal Institute of Technology in Zurich and the University Hospital in Freiburg, Germany[15][4] Deferoxamine acts by binding free iron in the bloodstream and enhancing its elimination in the
urine. By removing excess iron from persons with
hemochromatosis, the agent reduces the damage done to various organs and tissues, such as the
liver. Also, it speeds healing of nerve damage (and minimizes the extent of recent nerve trauma).[citation needed] Deferoxamine may modulate expression[16] and release of inflammatory mediators by specific cell types.[17]
Research
Deferoxamine is being studied as a treatment for spinal cord injury[18] and intracerebral hemorrhage.[19][20] It is also used to induce hypoxia-like environment in mesenchymal stem cells.[21][22]
Since the terminal amine group of Deferoxamine does not participate in metal chelation, it has been used to immobilize Deferoxamine to surfaces and substrates for various industrial and biomedical applications.[23]
^
abcdef"Deferoxamine Mesylate". The American Society of Health-System Pharmacists.
Archived from the original on 21 December 2016. Retrieved 8 December 2016.
^
abGiardina PJ, Rivella S (2012).
"Thalassemia Syndromes". In Hoffman R, Benz Jr EJ, Silberstein LE, Heslop H, Weitz J, Anastasi J (eds.). Hematology: Diagnosis and Treatment (6th ed.). Elsevier Health Sciences. p. 515.
ISBN978-1-4557-4041-3.
Archived from the original on 2016-12-20.
^World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization.
hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
^Merlot AM, Kalinowski DS, Richardson DR (March 2013). "Novel chelators for cancer treatment: where are we now?". Antioxidants & Redox Signaling. 18 (8): 973–1006.
doi:
10.1089/ars.2012.4540.
PMID22424293.
^Miyajima H, Takahashi Y, Kamata T, Shimizu H, Sakai N, Gitlin JD (March 1997). "Use of desferrioxamine in the treatment of aceruloplasminemia". Annals of Neurology. 41 (3): 404–407.
doi:
10.1002/ana.410410318.
PMID9066364.
S2CID22425032.
^Yawalkar SJ (1993). "Milestones in the research and development of desferrioxamine". Nephrology, Dialysis, Transplantation. 8 (Suppl 1): 40–42.
doi:
10.1093/ndt/8.supp1.40.
PMID8389019.
^Ren H, Cao Y, Zhao Q, Li J, Zhou C, Liao L, et al. (August 2006). "Proliferation and differentiation of bone marrow stromal cells under hypoxic conditions". Biochemical and Biophysical Research Communications. 347 (1): 12–21.
doi:
10.1016/j.bbrc.2006.05.169.
PMID16814746.
^Woo KJ, Lee TJ, Park JW, Kwon TK (April 2006). "Desferrioxamine, an iron chelator, enhances HIF-1alpha accumulation via cyclooxygenase-2 signaling pathway". Biochemical and Biophysical Research Communications. 343 (1): 8–14.
doi:
10.1016/j.bbrc.2006.02.116.
PMID16527254.
^Touma JG, Kelly C, Coblyn M, Jovanovic GN, Schilke K (2023). "Reversible Covalent Binding of Desferrioxamine B (DFOB) to Polystyrene Microspheres for the Chelation of Aqueous Iron Citrate". Industrial & Engineering Chemistry Research. 62 (37): 15109–15119.
doi:
10.1021/acs.iecr.3c00812.