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Doxorubicin (Adriamycin) HCl

Catalog No.
Antitumour antibiotic,inhibits TOPO II.
Grouped product items
SizePriceStock Qty
10mM (in 1mL DMSO)
In stock
In stock
In stock
In stock

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Doxorubicin is a semi-synthesized anticancer agent derived from bacterial culture [1]. It is an anthracycline antibiotic. It is been widely used in blood cancers, solid tumors and sarcomas.

Doxorubicin intercalates into DNA double strand and inhibits the progression of DNA topoisomerase II, stopping replication process [2]. Doxorubicin also induces histone eviction from open chromatin, causing DNA damage and epigenetic deregulation [3]. 

Doxorubicin is administrated intravenously. Approximately 75% of doxorubicin and its metabolites bind to plasma protein. Doxorubicin does not cross blood brain barrier. 50% of the drug is eliminated unchanged from the body mainly though bile excretion. The remaining undergoes one-electron reduction, two-electron reduction, and deglycosidation. The major metabolite is a potent membrane ion pump inhibitor, which is associated with cardiomyopathy [4].

[1] Brayfield, A., et al. (2013). Doxorubicin. Martindale: The Complete Drug Reference. Pharmaceutical Press. Retrieved 15 April 2014.
[2] Pommier Y., et al. (2010). DNA topoisomerases and their poisoning by anticancer and antibacterial drugs. Chemistry & Biology 17 (5): 421-433.
[3] Pang, B., et al. (2013). Drug-induced histone eviction from open chromatin contributes to the chemotherapeutic effects of doxorubicin. Nature Communications 4 (5): 1908
[4] Boucek R J., et al. (1987). The major metabolite of doxorubicin is a potent inhibitor of membrane-associated ion pumps. A correlative study of cardiac muscle with isolated membrane fractions. J of Biol Chem 262: 15851-15856.

Product Citation

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
Cas No.25316-40-9
Solubility≥29 mg/mL in DMSO; ≥57.2 mg/mL in H2O; insoluble in EtOH
Chemical Name(7S,9S)-7-[(2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyloxan-2-yl]oxy-6,9,11-trihydroxy-9-(2-hydroxyacetyl)-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione;hydrochloride
SDFDownload SDF
Canonical SMILESCC1C(C(CC(O1)OC2CC(CC3=C(C4=C(C(=C23)O)C(=O)C5=C(C4=O)C=CC=C5OC)O)(C(=O)CO)O)N)O.Cl
Shipping ConditionShip with blue ice, or upon other requests.
General tipsFor obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while. We do not recommend long-term storage for the solution, please use it up soon.


Cell experiment: [1]

Cell lines

H9c2 cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37°C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months.

Reaction Conditions

1 μg/mL, 2 hours


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.

Animal experiment: [2]

Animal models

C57BL/10 mice

Dosage form

Intraperitoneal injection, 20 mg/kg


Five days after doxorubicin injection, mice displayed significantly impaired systolic (LVP, -29%; dP/dtmax, -45%), diastolic (dP/dtmin, -44%; stiffness, +275%), and global (SV, -61%; HR, -18%; CO,-68%) left ventricular (LV) function when compared with the placebo group. Both cardiac lipid peroxidation activity (+37%) and cardiac nitrotyrosine protein expression (+204%) were increased when compared with placebo mice.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Chen M B, Wu X Y, Gu J H, et al. Activation of AMP-activated protein kinase contributes to doxorubicin-induced cell death and apoptosis in cultured myocardial H9c2 cells. Cell biochemistry and biophysics, 2011, 60 (3): 311-322.

[2] Riad A, Bien S, Westermann D, et al. Pretreatment with statin attenuates the cardiotoxicity of Doxorubicin in mice. Cancer research, 2009, 69 (2): 695-699.

Biological Activity

Description Doxorubicin is an antitumor antibiotic agent and shows inhibition against DNA topoisomerase II.
Targets MCF-7          
IC50 100 nM          

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