For research use only. Not for use in humans.

Catalog No.S1712 Synonyms: CGP-72670, ICL-670

2 publications

Deferasirox  Chemical Structure

Molecular Weight(MW): 373.36

Deferasirox is an iron chelator, also a cytochrome P450 3A4 inducer, Cytochrome P450 2C8 inhibitor, and Cytochrome P450 1A2 inhibitor.

Size Price Stock Quantity  
10mM (1mL in DMSO) USD 160 In stock
USD 70 In stock
USD 120 In stock
USD 210 In stock
USD 470 In stock
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Selleck's Deferasirox has been cited by 2 publications

1 Customer Review

  • U2OS cells were cultured with FAC for 24 hours, washed, followed by chelation with 2 chelators (DFO, DFX) -/+ lysosomal protease inhibitors (E-64d and PepstatinA) and analyzed as in panel A. DFX: Deferasirox.

    Nature, 2014, 509(7498):105-9.. Deferasirox purchased from Selleck.

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Choose Selective P450 (e.g. CYP17) Inhibitors

Biological Activity

Description Deferasirox is an iron chelator, also a cytochrome P450 3A4 inducer, Cytochrome P450 2C8 inhibitor, and Cytochrome P450 1A2 inhibitor.
In vitro

Deferasirox effectively chelates iron from Rhizopus oryzae and demonstrates cidal activity in vitro against 28 of 29 clinical isolates of Mucorales at concentrations well below clinically achievable serum levels. [1] Deferasirox incubation induces a significant inhibition of NF-κB activity and a cytoplasmic sequestration of its active subunit p65 in an inactive form in 28 of 40 peripheral blood samples. [2] Deferasirox inhibits three human myeloid cell lines (K562, U937, and HL60) with IC50 of 17-50 mM. [3] Deferasirox is cidal in vitro against A. fumigatus, with an MIC and MFC of 25 and 50 mg/L, respectively. [5]

Methods Test Index PMID
Western blot
CDK2 / CDK4 / CDK6 / Cyclin A / Cyclin B / Cyclin D1 / Cyclin E / p53 / p27 / p21 ; 

PubMed: 26965928     

Western blot analysis of cell cycle-related molecules showed that deferasirox upregulated p21, p27, and p53 and downregulated cyclin D1, cyclin B, and CDK4

TFR1 / Ferroportin ; 

PubMed: 26965928     

Treatment with deferasirox for 24 h resulted in an increased level of TFR1 and a decreased level of ferroportin

Pro-caspase-3 / Pro-caspase-8 / Pro-caspase-9 / BAX / NDRG1 / c-Myc / p-mTOR ; 

PubMed: 26965928     

Deferasirox also induced apoptosis, upregulated NDRG1, and downregulated p-mTOR and c-myc as assessed by Western blot analysis

Bax / TOM22 ; 

PubMed: 28139717     

Deferasirox for 24 hours induces Bax translocation to mitochondria, where it forms aggregates, and colocalizes with mitochondrial receptor TOM22 that appears aggregated (arrowhead). Confocal microscopy: Bax in red, TOM22 in green and DAPI in blue. Original magnification x63, detail x100. Images representative of three experiments.

Cytochrome c; 

PubMed: 28139717     

Localization of cytochrome c in tubular cells exposed to 10 μM deferasirox for 6 hours. Note the punctate mitochondrial pattern in control cells and diffuse labeling in deferasirox-exposed cells (arrowheads). Confocal microscopy. Cytochrome c in green and DAPI in blue, original magnification x63. Images representative of three experiments. 

Growth inhibition assay
Cell viability; 

PubMed: 26965928     

Cell viability was measured by the MTT assay. AGS, MKN-28, SNU-484, and SNU-638 cells were incubated with 0, 1, 10, 50, and 100 μM of deferasirox at 37 °C for 24, 48, or 72 h. Deferasirox treatment resulted in dose-dependent and time-dependent growth inhibition in all four gastric cancer cell lines.

Cell viability; 

PubMed: 28139717     

Analysis of tubular cell viability at 24 hours by MTT assay. Mean ± SEM of three independent experiments. *p < 0.001 vs control. 

26965928 28139717
In vivo Deferasirox significantly improves survival and decreased tissue fungal burden in diabetic ketoacidotic or neutropenic mice with mucormycosis, with an efficacy similar to that of liposomal amphotericin B. Deferasirox treatment also enhances the host inflammatory response to mucormycosis. Deferasirox synergistically improves survival and reduces tissue fungal burden when combined with liposomal amphotericin B. [1] Deferasirox administered p.o. to rats is absorbed to at least 75%, and the bioavailability is 26%.Deferasirox is present in the blood circulation mainly in the unchanged form and as its iron complex, Fe(deferasirox)2, after intravenous and p.o. administration. Deferasirox is 99.2% bound to plasma proteins. [4] Deferasirox monotherapy modestly prolongs survival of mice with IPA. [5]


Solubility (25°C)

In vitro DMSO 74 mg/mL (198.2 mM)
Ethanol 2 mg/mL (5.35 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 373.36


CAS No. 201530-41-8
Storage powder
in solvent
Synonyms CGP-72670, ICL-670
Smiles OC(=O)C1=CC=C(C=C1)[N]2N=C(N=C2C3=CC=CC=C3O)C4=CC=CC=C4O

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03920657 Recruiting Drug: Deferasirox Myelodysplastic Syndromes Fondazione Italiana Sindromi Mielodisplastiche Onlus July 2019 Phase 2
NCT02663752 Terminated Procedure: Bone marrow aspirate|Drug: Deferasirox Myelodysplastic Syndrome Novartis Pharmaceuticals|Novartis May 30 2016 Phase 2
NCT02069886 Withdrawn Drug: deferasirox Thalassemia (Transfusion Delendent) Novartis Pharmaceuticals|Novartis December 2014 Phase 4
NCT02038816 Terminated Drug: Deferasirox + Azacitidine|Drug: Azacitidine Myelodysplastic Syndromes Sunnybrook Health Sciences Centre|Novartis March 2014 Phase 2

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P450 (e.g. CYP17) Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID