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Doxorubicin (Alias: Hydroxydaunorubicin, DOX, Adriamycin)

Catalog No. T1456 Copy Product Info
Purity: 99.31%
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Doxorubicin (Adriamycin) is a fluorescent anthracycline antitumor antibiotic that inhibits Topoisomerase I/II, induces apoptosis and autophagy, downregulates the AMPK signaling pathway, and is commonly used in cancer chemotherapy as well as in models of nephritis and heart failure.

Doxorubicin

Copy Product Info
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Catalog No. T1456
Alias Hydroxydaunorubicin, DOX, Adriamycin

Doxorubicin (Adriamycin) is a fluorescent anthracycline antitumor antibiotic that inhibits Topoisomerase I/II, induces apoptosis and autophagy, downregulates the AMPK signaling pathway, and is commonly used in cancer chemotherapy as well as in models of nephritis and heart failure.

Doxorubicin
Cas No. 23214-92-8
Pack SizePriceUSA StockGlobal StockQuantity
25 mg$39In StockIn Stock
50 mg$54In StockIn Stock
In stock · Estimated delivery: USA Stock (1-2 days) Global Stock (5-7 days)
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For research use only—not for human use. No sales to individuals. Use as intended only.
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Purity:99.31%
Appearance:Solid
Color:Red
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Product Introduction

Bioactivity
Description
Doxorubicin (Adriamycin) is a fluorescent anthracycline antitumor antibiotic that inhibits Topoisomerase I/II, induces apoptosis and autophagy, downregulates the AMPK signaling pathway, and is commonly used in cancer chemotherapy as well as in models of nephritis and heart failure.
Targets&IC50
Topo I:0.8 μM (IC50), Topo II:2.67 μM (IC50)
In vitro
The combination of Doxorubicin and Simvastatin at the highest tested concentrations (2 μM and 10 μM, respec-tively) kills 97% of the Hela cells[2].
In vivo
In an experiment, mice with PC3 xenografts received injections of Doxorubicin at dosages of 2, 4, or 8 mg/kg, and tumor volume was monitored. The 2 mg/kg dose did not inhibit tumor growth, but doses of 4 mg/kg and 8 mg/kg initially delayed growth, significantly reducing c-FLIP levels in the tumors (p<0.05 on days 18 and 22)[3]. In a separate study with rats, treatments involved a single intraperitoneal injection of 10 mg/kg Doxorubicin, ten daily injections of 1 mg/kg, or five weekly injections of 2 mg/kg, resulting in an 80% mortality rate by day 28 for the first group, and on days 107 and 98 for the latter groups, respectively. Furthermore, fractional shortening—a measure of heart function—decreased by 30% in the first group at week 2, 55% in the second group at week 13, and 42% in the third group at week 13[4].
Disease Modeling Protocol
Cardiomyopathy model
  • Modeling Mechanism:

    Doxorubicin (DOX) induces cardiac damage through multiple pathways: ① It triggers oxidative stress, inhibiting NRF2-mediated antioxidant pathways (downregulation of genes such as NRF2, GST, and HO-1), leading to the accumulation of reactive oxygen species (ROS) and lipid peroxidation; ② It interferes with the protein ubiquitination system, disrupting cardiomyocyte protein homeostasis; ③ It inhibits the PI3K/AKT signaling pathway, promoting cardiomyocyte apoptosis and necrosis; ④ It damages mitochondrial function, affecting energy metabolism, ultimately leading to myocardial hypertrophy, fibrosis, and decreased cardiac function.

  • Related Products:

    Doxorubicin (T1456)

  • Modeling Method:

    Experimental Subject:

    Rats, Sprague-Dawley, Female

    Dosage and Administration Route:

    15 mg/kg Doxorubicin, dissolved in physiological saline, intraperitoneal injection (i.p.)

    Dosing Frequency and Duration Model:

    Single dose

  • Validation:

    1. Pathological Indicators: - Myocardial Injury: HE staining showed myocardial cell degeneration and necrosis; Masson staining revealed interstitial fibrosis. - Hematological Changes: Lymphopenia and thrombocytopenia were observed (48 hours after modeling). 2. Molecular Indicators: - Gene Expression: 2411 genes were synchronously differentially expressed (SDRG) in myocardial and peripheral blood mononuclear cells (PBMCs), including downregulation of antioxidant genes such as NRF2 (-2.085-fold) and HO-1 (-2.849-fold), and upregulation of S100A8/A9 (calcium-binding protein). - Signaling Pathways: Western blot showed decreased expression of PI3K/AKT pathway-related proteins and disordered expression of ubiquitination-related molecules. 3. Biochemical Indicators: - Serum Markers: Decreased albumin (ALB), increased alanine aminotransferase (ALT), total bilirubin (TBIL), and creatinine (CRE) (48 hours after modeling). - Tissue Drug Concentration: DOX in myocardial tissue. The concentration reached 0.342±0.22 μg/mg protein (p=0.051), and the blood concentration reached 0.591±0.041 μg/ml (p<0.01); 4. Functional indicators: - Cardiac function: Echocardiography of the chronic model showed a decrease in left ventricular ejection fraction (LVEF) and abnormal diastolic function.

*Precautions: All rats were euthanized within 48 hours of DOX administration under deep isoflurane anesthesia.

*References:Todorova VK,et,al. Transcriptome profiling of peripheral blood cells identifies potential biomarkers for doxorubicin cardiotoxicity in a rat model. PLoS One. 2012;7(11):e48398.

Cell Research
Doxorubicin is dissolved in stock solutions (1 mM) and serially diluted with RPMI 1640 media (0.1, 1, and 2 μM)[2]. 160 μL of Hela cells suspension (3×104 cell/mL) is dispensed into three 96-well U-bottom microplates and incubated for 24 h at 37°C in a fully humidified atmosphere of 5% CO2. In plate 1, serial dilutions of Doxorubicin (20 μL; final concentration, 0.1-2 μM) and Simvastatin (20 μL; final concentration, 0.25-2 μM) are added to a final volume of 200 μL and incubated for another 72 h. In plates 2 and 3 serial dilutions of each drug (Simvastatin or Doxorubicin, 40 μL) are added. After an incubation period of 24 h, the medium is aspirated and the cells are washed in PBS. Then, serial dilutions of other drug (40 μL) are added and supplemented with culture medium to a final volume of 200 μL, and incubated for 48 h. Doxorubicin and Simvastatin are used individually as positive controls (40 μL in each well), and the cells treated only with solvent are considered as negative controls. To evaluate cell survival, 20 μL of MTT solution (5 mg/mL in PBS) is added to each well and incubated for 3 h. Then the media is replaced with 150 μL of DMSO, and complete solubilization of formazan crystals is achieved by repeated pipetting of the solution. Absorbance is then determined at 540 nm by an ELISA plate reader. Each drug concentration is assayed in 4 or 8 wells and repeated 3 times. The cytotoxic/cytostatic effect of Doxorubicin is expressed as the relative viability (% control) and calculated. Percentage of cell survival in the negative control is assumed as 100. Relative viability=(experimental absorbance-background absorbance)/ (absorbance of untreated controls-background absorbance)×100 %[2].
SynonymsHydroxydaunorubicin, DOX, Adriamycin
Chemical Properties
Molecular Weight543.52
FormulaC27H29NO11
Cas No.23214-92-8
SmilesCOc1cccc2C(=O)c3c(O)c4C[C@](O)(C[C@H](O[C@H]5C[C@H](N)[C@H](O)[C@H](C)O5)c4c(O)c3C(=O)c12)C(=O)CO
Relative Density.1.61 g/cm3
Storage & Solubility Information
Storagekeep away from direct sunlight,keep away from moisture | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
Solubility Information
H2O: 50 mg/mL (91.99 mM), Sonication is recommended.
DMSO: 49 mg/mL (90.15 mM), Sonication is recommended.
Solution Preparation Table
DMSO/H2O
1mg5mg10mg50mg
1 mM1.8399 mL9.1993 mL18.3986 mL91.9929 mL
5 mM0.3680 mL1.8399 mL3.6797 mL18.3986 mL
10 mM0.1840 mL0.9199 mL1.8399 mL9.1993 mL
20 mM0.0920 mL0.4600 mL0.9199 mL4.5996 mL
50 mM0.0368 mL0.1840 mL0.3680 mL1.8399 mL
Note : The dilution table applies only to solid products. For liquid products, please calculate the stock solution based on the stated concentration and/or density.

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