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    Doxorubicin HCl (adriamycin; NSC 123127)
    Doxorubicin HCl (adriamycin; NSC 123127)

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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 #: V1389
    CAS #: 25316-40-9 Purity ≥98%

    Description: Doxorubicin HCl (formerly known as Adriamycin; FI 106; Adriblastina; DOXOCELL; Doxolem; NSC-123127 etc.) is an anthracycline antibiotic agent with anticancer activity. It inhibits DNA topoisomerase II and induces DNA damage and apoptosis in tumor cells. It was approved for use as an antineoplastic agent. Doxorubicin is isolated from the bacterium Streptomyces peucetius var. caesius, and is the hydroxylated congener of daunorubicin. Doxorubicin acts by intercalating between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II.           

    References: Cancer Res. 2009 May 15;69(10):4294-300; Food Chem Toxicol. 2010 Jun;48(6):1425-38.

    Related CAS#: 23214-92-8 (free base); 23214-92-8 (Doxorubicin free base); 480998-12-7 (MC-DOXHZN hydrochloride is an albumin-binding prodrug of Doxorubicin, with acid-sensitive properties); 151038-96-9 (MC-DOXHZN); 108852-90-0 [Nemorubicin,Methoxymorpholinyldoxorubicin; PNU 152243; PNU-152243A]; 56390-09-1 [Epirubicin hydrochloride, 4'-Epidoxorubicin hydrochloride]; 56420-45-2 (Epirubicin); 1361644-26-9 (Aldoxorubicin; INNO-206; DOXO-EMCH);

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    Molecular Weight (MW)579.98
    FormulaC27H29NO11.HCl
    CAS No.25316-40-9 (Doxorubicin HCl); 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 100 mg/mL (172.4 mM)
    Water: <1 mg/mL
    Ethanol: 20 mg/mL (34.5 mM)
    Technical InfoChemical Name: (8S,10S)-10-(((2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyltetrahydro-2H-pyran-2-yl)oxy)-6,8,11-trihydroxy-8-(2-hydroxyacetyl)-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione hydrochloride

    SMILES Code: O=C1C2=C(O)C(C[[email protected]](C(CO)=O)(O)C[[email protected]@H]3O[[email protected]]4C[[email protected]](N)[[email protected]](O)[[email protected]](C)O4)=C3C(O)=C2C(C5=C1C=CC=C5OC)=O.[H]Cl

    Exact Mass: 543.17406 

    SynonymsAdriamycin; Hydroxydaunorubicin hydrochloride; FI106; ADR; Doxo; Dox HCl; FI-106; FI 106; Adriamycin; Adriacin; Adriblastina; Adriblastine; Adrimedac; DOXOCELL; Doxolem; Doxorubin; Farmiblastina; Rubex.


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    In Vitro

    In vitro activity:  Doxorubicin, an antibiotic anthracycline, is commonly considered to exert its anti-tumor activity at two fundamental levels, altering DNA and producing free radicals to trigger apoptosis of cancer cells through DNA damage. Doxorubicin can block the synthesis of DNA by intercalating into the DNA strand, and inhibits DNA topoisomerase II (TOP2). Doxorubicin is most effective when cells are rapidly proliferating and expressing high levels of TOP2. Additionally, Doxorubicin can trigger apoptosis by producing ceramide (which prompts apoptosis by activating p53 or other downstream pathways such as JNK), the degradation of Akt by serine threonine proteases, the mitochondrial release of cytochrome c, increased FasL (death receptor Fas/CD95 ligand) mRNA production, and a greater production of free radicals. Pre-treatment with GSNO (nitrosoglutathione) suppresses the resistance in the doxorubicin-resistant breast cancer cell line MCF7/Dx, accompanied by enhanced protein glutathionylation and accumulation of doxorubicin in the nucleus. Doxorubicin induced G2/M checkpoint arrest are attributed to elevated cyclin G2 (CycG2) expression and phospho-modification of proteins in the ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) signaling pathways. Doxorubicin inhibits AMP-activated protein kinase (AMPK), resulting in SIRT1 dysfunction, p53 accumulation, and increased cell death in mouse embryonic fibroblasts (MEFs) and cardiomyocytes, which can be further sensitized by pre-inhibition of AMPK.  Doxorubicin elicits a marked heat shock response, and that either inhibition or silencing of heat shock proteins enhance the Doxorubicin apoptotic effect in neuroblastoma cells. Nanomolar Doxorubicin treatment of neuroblastoma cells causes dose-dependent over-ubiquitination of a specific set of proteins in the absence of measurable inhibition of proteasome, and loss of activity of ubiquitinated enzymes such as lactate dehydrogenase and α-enolase, the protein ubiquination patterns of which is similar to those with proteasome inhibitor Bortezomib, indicating that Doxorubicin may also exert its effect by damaging proteins.


    Cell Assay: H9c2 cells were treated with increased concentrations of Doxorubicin (0.1, 0.3, 0.5, and 1.0 μg/ml, equal to 0.17, 0.52, 0.85, and 1.71 μM separately) for 2 h, or treated with 0.3 μg/ml (equal to 0.52 μM) of Doxorubicin for the different time points. Doxorubicin induces strong AMPKα (Thr 172) and its downstream Acetyl-CoA carboxylase (ACC, Ser 79) phosphorylation in both time- and dose-dependent manner. AMPKα phosphorylation became obvious after 1 h of Doxorubicin treatment which was further sustained for at least 6 h. LKB1, the possible upstream kinase for AMPK, was also activated by Doxorubicin in H9c2 cells.

    In VivoIn vivo, Doxorubicin in combination with adenoviral MnSOD (AdMnSOD) plus 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) has the greatest effect in decreasing the volumes of MB231 tumors and prolonging survival of mice. Although its use is limited by the chronic and acute toxic side effects it produces, Doxorubicin is essential in treating breast and oesophageal carcinomas, solid tumours in childhood, osteosarcomas, Kaposi's sarcoma, soft tissue sarcomas, and Hodgkin and non-Hodgkin lymphomas.
    Animal modelFemale athymic nude mice injected s.c. with MB231 cells
    Formulation & DosageDissolved in DMSO; 3 mg/kg;  intratumorly injected
    ReferencesCancer Res. 2009 May 15;69(10):4294-300; Food Chem Toxicol. 2010 Jun;48(6):1425-38.


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


    Doxorubicin (Adriamycin)
    AdMnSOD infection + BCNU sensitized cells to adriamycin and radiation. Cancer Res. 2009 May 15;69(10):4294-300.


    Doxorubicin (Adriamycin)
    AdMnSOD infection plus BCNU sensitized the antitumor effect of adriamycin in vivo and increased animal survival. Cancer Res. 2009 May 15;69(10):4294-300.


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