product name Deferasirox
Description: Deferasirox (also known as CGP-72670, ICL-670) is an orally iron chelator used for the treatment of iron-overload disease. In DMS-53 lung carcinoma and SK-N-MC neuroepithelioma cell lines, deferasirox inhibited cells proliferation. Deferasirox inhibited iron uptake from human transferrin and mobilized cellular 59Fe. In two oesophageal adenocarcinoma cell lines OE33 and OE19, deferasirox with a standard chemotherapeutic agent inhibited cellular viability and proliferation. 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.
References: J Clin Invest. 2007 Sep;117(9):2649-57; Haematologica. 2010 Aug;95(8):1308-16.
373.36
Formula
C21H15N3O4
CAS No.
201530-41-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 74 mg/mL (198.2 mM)
Water: <1 mg/mL
Ethanol: 2 mg/mL (5.35 mM)
Solubility (In vivo)
30% PEG400+0.5% Tween80+5% Propylene glycol: 30 mg/mL
Synonyms
CGP-72670, ICL-670
other peoduct :
| In Vitro |
In vitro activity: 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. 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. Deferasirox inhibits three human myeloid cell lines (K562, U937, and HL60) with IC50 of 17-50 mM. Deferasirox is cidal in vitro against A. fumigatus, with an MIC and MFC of 25 and 50 mg/L, respectively. Kinase Assay: Cell Assay: In DMS-53 lung carcinoma and SK-N-MC neuroepithelioma cell lines, deferasirox inhibited cells proliferation. Deferasirox inhibited iron uptake from human transferrin and mobilized cellular 59Fe. In two oesophageal adenocarcinoma cell lines OE33 and OE19, deferasirox with a standard chemotherapeutic agent inhibited cellular viability and proliferation. |
|---|---|
| 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. 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. Deferasirox monotherapy modestly prolongs survival of mice with IPA. |
| Animal model | In nude mice bearing DMS-53 lung carcinoma xenografts, deferasirox inhibited tumor growth. Also, deferasirox increased cleaved caspase-3, cleaved poly(ADP-ribose) polymerase 1, the cyclin-dependent kinase inhibitor p21CIP1/WAF1 and the expression of the metastasis suppressor protein N-myc downstream-regulated gene 1 while reducing cyclin D1, which suggested deferasirox is an effective antitumor agent. In human xenograft models, deferasirox significantly inhibited tumour growth, which was associated with the decrease in iron levels. |
| Formulation & Dosage | |
| References | J Clin Invest. 2007 Sep;117(9):2649-57; Haematologica. 2010 Aug;95(8):1308-16. |
