product name Dexrazoxane HCl
Description: Dexrazoxane HCl (also known as ICRF-187, ADR-529) is an intracellular iron chelator, which decreases the formation of superoxide radicals, and is used as a cardioprotective agent. As a derivative of EDTA, dexrazoxane chelates iron, but the precise mechanism by which it protects the heart is not known. This agent is used to protect the heart against the cardiotoxic side effects. Dexrazoxane (10 mM), known clinically to limit anthracycline cardiac toxicity, prevents daunorubicin-induced myocyte apoptosis, but not necrosis induced by higher anthracycline concentrations in rat cardiac myocytes.
References: Circ Res. 1999 Feb 19;84(3):257-65; Cancer Res. 2007 Sep 15;67(18):8839-46.
304.73
Formula
C11H16N4O4.HCl
CAS No.
149003-01-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 60 mg/mL (196.9 mM)
Water: 60 mg/mL (196.9 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
ICRF-187 (ADR-529) HCl
other peoduct :
| In Vitro |
In vitro activity: Dexrazoxane (10 mM), known clinically to limit anthracycline cardiac toxicity, prevents daunorubicin-induced myocyte apoptosis, but not necrosis induced by higher anthracycline concentrations in rat cardiac myocytes. Dexrazoxane presumably exerts its cardioprotective effects by either binding free or loosely bound iron, or iron complexed to doxorubicin, thus preventing or reducing site-specific oxygen radical production that damages cellular components. Dexrazoxane specifically abolishes the DNA damage signal gamma-H2AX induced by doxorubicin, but not camptothecin or hydrogen peroxide, in H9C2 cardiomyocytes. Dexrazoxane also induces rapid degradation of Top2beta, which paralleles the reduction of doxorubicin-induced DNA damage. Dexrazoxane antagonizes doxorubicin-induced DNA damage through its interference with Top2beta, which could implicate Top2beta in doxorubicin cardiotoxicity. Dexrazoxane is hydrolyzed to its active form intracellularly and binds iron to prevent the formation of superhydroxide radicals, thus preventing mitochondrial destruction. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Dexrazoxane combined with doxorubicin, daunorubicin, or idarubicin reduces the tissue lesions in B6D2F1 mice (expressed as area under the curve of wound size times duration) by 96%, 70%, and 87%, respectively. Dexrazoxane combined with doxorubicin, daunorubicin, or idarubicin results in a statistically significant reduction in the fraction of mice with wounds as well as the duration of wounds. |
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| Formulation & Dosage | |
| References | Circ Res. 1999 Feb 19;84(3):257-65; Cancer Res. 2007 Sep 15;67(18):8839-46; Clin Cancer Res. 2000 Sep;6(9):3680-6. |
