Doxorubicin (Adriamycin) Licensed by Pfizer

Doxorubicin (Adriamycin) is an antibiotic agent that inhibits DNA topoisomerase II and induces DNA damage and apoptosis.

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Doxorubicin (Adriamycin) Chemical Structure

Doxorubicin (Adriamycin) Chemical Structure
Molecular Weight: 579.98

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Customer Reviews(4)

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Product Description

Biological Activity

Description Doxorubicin (Adriamycin) is an antibiotic agent that inhibits DNA topoisomerase II and induces DNA damage and apoptosis.
Targets Topo II [1]
In vitro 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. [2] 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. [3] 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. [5] 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. [6] 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. [8]
In vivo In 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. [1] 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. [2]

Protocol(Only for Reference)

Animal Study: [1]

Animal Models Female athymic nude mice injected s.c. with MB231 cells
Formulation Dissolved in DMSO, and diluted in saline
Dosages 3 mg/kg/day
Administration Delivered intratumorly
Solubility 30% PEG400/0.5% Tween80/5% propylene glycol, 30 mg/mL
* 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.


[1] Sun W, et al. Cancer Res, 2009, 69(10), 4294-4300.

[2] Granados-Principal S, et al. Food Chem Toxicol, 2010, 48(6), 1425-1438.

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Clinical Trial Information( data from

NCT Number Recruitment Conditions Sponsor
Start Date Phases
NCT02116530 Not yet recruiting Hematopoietic/Lymphoid Cancer|Nausea and Vomiting|Unspecified Adult Solid Tumor, Protocol Specific Alliance for Clinical Trials in Oncology|National Cancer Institute (NCI)|Mayo Clinic 2014-05 Phase 3
NCT02112656 Not yet recruiting Hepatocellular Carcinoma Celsion 2014-06 Phase 3
NCT01969578 Not yet recruiting Salivary Gland Cancer European Organisation for Research and Treatment of Cancer - EORTC 2014-06 Phase 2
NCT01775475 Not yet recruiting AIDS-related Diffuse Large Cell Lymphoma|AIDS-related Diffuse Mixed Cell Lymphoma|AIDS-related Diffuse Small Cleaved Cell Lymphoma|AIDS-related Immunoblastic Large Cell Lymphoma|AIDS-related Lymphoblastic Lymphoma|AIDS-related Peripheral/Systemic Lymphoma|AIDS-related Small Noncleaved Cell Lymphoma|Stage III AIDS-related Lymphoma|Stage IV AIDS-related Lymphoma AIDS Malignancy Clinical Trials Consortium|National Cancer Institute (NCI) 2014-06 Phase 2
NCT01539174 Not yet recruiting Contiguous Stage II Adult Diffuse Large Cell Lymphoma|Noncontiguous Stage II Adult Diffuse Large Cell Lymphoma|Stage I Adult Diffuse Large Cell Lymphoma|Stage III Adult Diffuse Large Cell Lymphoma|Stage IV Adult Diffuse Large Cell Lymphoma Fox Chase Cancer Center|Genentech 2014-07 Phase 2

Chemical Information

Download Doxorubicin (Adriamycin) SDF
Molecular Weight (MW) 579.98


CAS No. 25316-40-9
Storage 3 years -20℃Powder
6 months-80℃in DMSO
Solubility (25°C) * In vitro DMSO 100 mg/mL (172 mM)
Water 20 mg/mL (34 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 30% PEG400/0.5% Tween80/5% propylene glycol 30 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* 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.
Chemical Name (8S,10S)-10-((2R,4S,5S,6S)-4-amino-5-hydroxy-6-methyl-tetrahydro-2H-pyran-2-yloxy)-6,8,11-trihydroxy-8-(2-hydroxyacetyl)-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione hydrochloride

Research Area

Customer Reviews (4)

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Source J Biomed Mater Res Part A 2012:00A:000–000.. Doxorubicin (Adriamycin) purchased from Selleck
Method Release experiment
Cell Lines N.A.
Concentrations 0.25mg/mL
Incubation Time 2-10 h
Results Doxorubicin was loaded by equilibrium partitioning in the following manner: a stock solution of doxorubicin was prepared in 2 wt % DMSO in 1 PBS (pH 7.4) at a concentration of 0.25 mg/mL. A 5 mg/mL concentration of crushed particles (75–150 um) of P(MAA-g-EG) or P(MAA-g-EG) containing PMMA nanoparticles to doxorubicin stock solution was allowed to stir slowly for 2 h.

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Source PLoS One, 2013, 8(1):e54595.. Doxorubicin (Adriamycin) purchased from Selleck
Method MTT assay
Cell Lines Huh7, THLE2, Hep5B cells
Concentrations 0.016-52 uM
Incubation Time 74 h
Results Cytotoxicity by doxorubicin was measured by MTT assay at varying concentrations on the HCC lines Huh7, THLE2, Hep3B.

Click to enlarge
Source Cancer Res, 2014, 74(1):298-308. Doxorubicin (Adriamycin) purchased from Selleck
Method MTT assay
Cell Lines H1299, A549, Hep3B, HT1080, HCT116, MCF7
Incubation Time 48 h
Results Hypoxic (1% O2 ) conditions for 48 hours. The IC50 value for cisplatin or doxorubicin significantly increased under hypoxia in H1299, A549, Hep3B, and HT1080, but did not in HCT116 and MCF7

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Source Mol Cancer Ther 2011 10, 1846-56. Doxorubicin (Adriamycin) purchased from Selleck
Method Viability screen
Cell Lines SK-ES-1 cell, A673 cell
Concentrations 0-10000 nM
Incubation Time
Results In both cell lines, SK-ES-1 and A673, Doxorubicin proved to be effective of the 3 agents.

Product Citations (17)

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