Catalog No.S1228 Synonyms: 4-demethoxydaunorubicin (NSC256439, 4-DMDR) HCl
Molecular Weight(MW): 533.95
Idarubicin HCl is a hydrochloride salt form of Idarubicin which is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL in a cell-free assay.
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Sensitivity of AML cells to conventional induction treatment and small-molecule p53 activators. Cell viability in OCI-AML3 cells treated for 24 hours with cytarabin/idarubicin (CI) and Nultin-3A (Nut; A), CI and Leptomycin-B (LMB; B), or Nut and LMB (D), respectively. CI was tested at 0, 100, 200, and 300 nmol/L CI; Nutlin-3A at 0, 2.5, 5, 7.5; and LMB at 0, 2, 8, 32 ng/mL in dosages 0, 1, 2, and 3, respectively. Cell viability in normal and AML bone marrow cells.
Clin Cancer Res, 2016, 22(3):746-56.. Idarubicin HCl purchased from Selleck.
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|Description||Idarubicin HCl is a hydrochloride salt form of Idarubicin which is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL in a cell-free assay.|
|Features||Idarubicin is a substrate for CYP450 2D6 and 2C9.|
Idarubicin has significant cytotoxic activity against multicellular spheroids, comparable to the antiproliferative effects on monolayer cells.  Idarubicin inhibits CYP450 2D6. Idarubicin is about 57.5-fold and 25-fold more active than doxorubicin and epirubicin, respectively. Idarubicin is able to overcome P-glycoprotein-mediated multidrug resistance.  Idarubicin inhibits PMN superoxide radical formation.  Idarubicin could be coupled to the monoclonal antibodies (anti-Ly-2.1, anti-L3T4, or anti-Thy-1) with retention of protein solubility and antibody activity.  Idarubicin inhibits the proliferation of NALM-6 cells with an IC50 of 12 nM. 
|In vivo||Reduction of Idarubicin is dependent upon ketone reductases, and proceeds more stereoselectively than that of most ketones giving rise to the (13S)-epimer almost exclusively. The high stereospecificity in Idarubicin reduction might result from chiral induction due to the presence of asymmetric centres near to the carbonyl group in Idarubicin. |
CYP450 metabolism experiments:Evaluation of Idarubicin metabolism by the CYP450 isoenzymes 3A4, 2D6, 2C8, 2C9, and 1A2 is completed using isolated human CYP450 proteins for each isoform. The high throughput P450 inhibition testing method is utilized for these evaluations. The metabolism experiments are designed to investigate the following properties of each drug: (1) if Idarubicin is a substrate of the CYP450 3A4, 2C8, 2C9, 1A2 or 2D6 isoenzymes; (2) if metabolism is affected by known inhibitors of each isoenzyme; (3) if Idarubicin is inhibitors of CYP450 isoenzymes; and (4) if caspofungin or itraconazole inhibit the CYP450 metabolism of Idarubicin. Dibenzylfluorescein (DBF) (CYP3A4, CYP2C8, CYP2C9), 3-cyano-7-ethoxycoumarin (Cyp1A2), and 7-methoxy-4-(aminomethyl)-coumarin (MAMC) (CYP2D6) are the known substrates utilized as controls to confirm the respective isoenzyme activity and evaluate the effects of Idarubicin on the isoenzyme activity. In addition, ketoconazole, quercetin, suflaphenazole, furafylline, and quinidine are utilized as control CYP450 inhibitors for 3A4, 2C8, 2C9, 1A2 or 2D6 isoenzymes, respectively. The substrate, inhibitor plus Idarubicin as indicated are added to each protein sample are incubated for 20 minutes- 60 minutes, as recommend by manufacturer, at 37oC. Reactions are stopped with an organic solvent solution and then samples are analyzed by fluorescence plate reader as appropriate. For each experiment, control samples with a known amount of substrate and synthesized metabolite, in the absence of the isoenzyme, are prepared for qualitative comparisons. All experiments are performed in triplicate.
-  Orlandi P, et al. J Chemother. 2005, 17(6), 663-667.
-  Colburn DE, et al. Hematology. 2004, 9(3), 217-221.
-  Siegsmund MJ, et al. Eur Urol. 1997, 31(3), 365-370.
|In vitro||DMSO||100 mg/mL (187.28 mM)|
|Water||5 mg/mL warmed (9.36 mM)|
* 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.
|Synonyms||4-demethoxydaunorubicin (NSC256439, 4-DMDR) HCl|
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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02635074||Recruiting||Recurrent Adult Acute Myeloid Leukemia||Bruno C. Medeiros|National Cancer Institute (NCI)|Stanford University||November 2016||Phase 1|
|NCT02527174||Not yet recruiting||Leukemia, Myeloid, Acute|Leukemia, Monocytic, Acute|Leukemia, Myelomonocytic, Acute|Leukemia, Erythroblastic, Acute|Leukemia, Megakaryoblastic, Acute||University of Alberta||November 2016||Phase 1|
|NCT02937662||Not yet recruiting||Acute Myeloid Leukemia||Institute of Hematology & Blood Diseases Hospital||October 2016||Phase 2|
|NCT02905994||Not yet recruiting||AML||Massachusetts General Hospital|Boehringer Ingelheim||September 2016||Phase 1|
|NCT02668653||Recruiting||Acute Myeloid Leukemia|Leukemia||Daiichi Sankyo Inc.||September 2016||Phase 3|
|NCT02873338||Recruiting||Acute Myeloid Leukemia||Cantex Pharmaceuticals||August 2016||Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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