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.
1 Customer Review
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.
Purity & Quality Control
Choose Selective Topoisomerase Inhibitors
|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|
Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2
Instructions to calculate molar mass (molecular weight) of a chemical compound:
To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03226418||Recruiting||Adult Acute Myeloid Leukemia|Secondary Acute Myeloid Leukemia|Therapy-Related Acute Myeloid Leukemia||University of Nebraska|National Cancer Institute (NCI)||July 7 2017||Phase 2|
|NCT02236013||Recruiting||Acute Myeloid Leukemia||Astellas Pharma Global Development Inc.|Astellas Pharma Inc||January 7 2015||Phase 1|
|NCT03250338||Recruiting||Relapsed/Refractory Acute Myeloid Leukemia With FLT3 Activating Mutations||Arog Pharmaceuticals Inc.||June 5 2018||Phase 3|
|NCT02440568||Recruiting||Acute Myeloid Leukemia||University of Illinois at Chicago|Teva Pharmaceuticals USA||June 5 2015||Phase 1|Phase 2|
|NCT02096055||Active not recruiting||Leukemia||M.D. Anderson Cancer Center|Astex Pharmaceuticals||April 4 2014||Phase 2|
|NCT00801489||Recruiting||Acute Myeloid Leukemia With Inv(16)(p13.1q22); CBFB-MYH11|Acute Myeloid Leukemia With t(16;16)(p13.1;q22); CBFB-MYH11|Acute Myeloid Leukemia With t(8;21); (q22; q22.1); RUNX1-RUNX1T1|de Novo Myelodysplastic Syndrome|High Risk Myelodysplastic Syndrome|Inv(16)|Myelodysplastic Syndrome With Excess Blasts|t(16;16)|t(8;21)|Untreated Adult Acute Myeloid Leukemia||M.D. Anderson Cancer Center|National Cancer Institute (NCI)||April 4 2007||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.
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.