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    Daunorubicin HCl (Daunomycin)
    Daunorubicin HCl (Daunomycin)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1400
    CAS #: 23541-50-6 Purity ≥98%

    Description: Daunorubicin HCl (Daunomycin; RP-13057; Rubidomycin; Ondena; Rubilem; DNM; DNR; DRB; FI6339; RP13057), the hydrochloride salt of daunorubicin, is an anthracycline analog and a topoisomerase II inhibitor which is approved for use as an antibiotic and chemotherapeutic drug.

    References: Eur J Cancer. 1998 Sep;34(10):1514-21; Cancer Res. 1976 Aug;36(8):2891-5.

    Related CAS#: 23541-50-6 (free base); 74853-81-9 (Alanylleucyl-daunorubicin); 28008-54-0 (Daunosamnyl-daunorubicin, an antibody conjugate); 290304-24-4 (Daun02, a prodrug of the topoisomerase inhibitor Daunorubicin);  23541-50-6 (HCl)

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    Molecular Weight (MW)563.98 
    FormulaC27H29NO10 . HCl 
    CAS No.23541-50-6 (HCl); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 100 mg/mL (177.3 mM) 
    Water: 100 mg/mL (177.3 mM) 
    Ethanol: <1 mg/mL
    Solubility (In vivo)Saline: 30 mg/mL 
    SynonymsDaunomycin HCl;  RP 13057; Rubidomycin; RP-13057; RP13057; Daunomycin hydrochloride; daunomycin HCl; daunorubidomycine; US trade names: Cerubidine; Rubidomycin; Foreign brand names: Cerubidin; Daunoblastin; Daunoblastina; Ondena; Rubilem; Abbreviations: DNM; DNR; DRB; Code names: FI6339; RP13057.


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    In Vitro

    In vitro activity: At drug concentrations that reflect the peak plasma concentration after Daunorubicin administration, the primary mechanism is likely to be through interaction with topoisomerase II, which may be a primary triggering event for growth arrest and/or cell killing through a signalling pathway leading to apoptosis, at least in leukemic cells and thymocytes. The quinone structure permits daunorubicin to act as electron acceptors in reactions mediated by oxoreductive enzymes including cytochrome P450 reductase, NADH dehydrogenase, and xanthine oxidase. At Daunorubicin concentrations exceeding approximately 2–4 μM, free radical mediated toxicity and DNA cross-linking may become evident. Daunorubicin inhibits both DNA and RNA syntheses in HeLa cells over a concentration range of 0.2 through 2 μM. Daunorubicin inhibits both DNA syntheses in Ehrlich ascites tumor cells over a concentration range of 4 μM. Daunorubic triggers apoptosis at concentrations of 0.5 and 1 μM in either HL-60 or U-937 human leukemic cells. Daunorubicin stimulates ceramide elevation and apoptosis in P388 and U937 cells through de novo synthesis via activation of the enzyme ceramide synthase. Daunorubicin dose-dependently increases the phosphatidylserine exposure and consequent procoagulant activity of human umbilical vein endothelial cells. Daunorubicin (0.2 mM) significantly enhances the release of endothelial microparticles which are highly procoagulant in human umbilical vein endothelial cells.


    Cell Assay: When treated with leukemic cells isolated from acute lymphocytic leukemia patients, daunorubicin significantly inhibits the biosynthesis of the DNA and RNA macromolecules.

    In VivoUrinary protein excretion, serum creatinine, and blood urea nitrogen (BUN) level are significantly increased in group Daunorubicin Hydrochloride (RP 13057 Hydrochloride) (3 mg/kg, i.v.) compared with those in group Control. Administration of Daunorubicin (DNR) causes a significant increase in malondialdehyde (MDA) level in renal tissue compared with that in the control group.
    Animal modelSprague-Dawley rats
    Formulation & DosageEight-week-old male Sprague-Dawley rats are used. The animals are quarantined and acclimatized for the additional 2 weeks prior to the initiation of the experiments. On day 0, each animal receives a single intravenous injection of Daunorubicin at a dose of 3 mg/kg (i.v.). Daunorubicin is administered in three equal injections at 48 h intervals for a period of one week to achieve an accumulative dose of 9 mg/kg, which is well documented to produce cardiotoxicity and nephrotoxicity. Age-matched rats are injected with corresponding volumes of 0.9% NaCl and used as a control (group Control;n=5). Twenty-two DNR-treated rats are randomly divided into two groups and received oral administration of Telmisartan (10 mg/kg/day; group Daunorubicin+Telmisartan; n=10) or vehicle (group Daunorubicin; n=12). The dose of Telmisartan is chosen on the basis of a previous report. Administration of Telmisartan is started on the same day as Daunorubicin administration and continued for 5 additional weeks after cessation of Daunorubicin administration (6 weeks total period). This duration of study is chosen on the basis of previous reports. On day 41, rats are placed individually in metabolic cages for 24-h urine collections for the measurement of protein concentrations and body weight (BW) is measured. After the end of the study period (6 weeks), rats are sacrificed and kidney tissue is harvested for semi-quantitative immunoblotting and immunohistochemical studies.
    References Biochem Pharmacol. 1999 Apr 1;57(7):727-41; Eur J Cancer. 1998 Sep;34(10):1514-21; Cancer Res. 1976 Aug;36(8):2891-5.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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