Doxorubicin (DOX) HCl

Catalog No.S1208 Batch:S120816

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Technical Data

Formula

C27H29NO11.HCl
Molecular Weight 579.98 CAS No. 25316-40-9
Solubility (25°C)* In vitro DMSO 100 mg/mL (172.41 mM)
Water 100 mg/mL (172.41 mM)
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O
5.0mg/ml Taking the 1 mL working solution as an example, add 50 μL of 100 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify it; then continue to add 500 μL ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Doxorubicin (DOX) HCl is an antibiotic agent that inhibits human DNA topoisomerase I and topoisomerase II with IC50s of 0.8 μM and 2.67 μM, respectively. Doxorubicin reduces basal phosphorylation of AMPK. Doxorubicin is used in the concomitant treatment of HIV-infected patients but is found to be at high risk of HBV reactivation.This product may precipitate when dissolved in PBS solution. It is recommended to prepare the stock solution in pure water and dilute with either pure water or saline to obtain the working solution.
Targets
AMPK [6] Topo II [1]
(Tumor cells)
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 (from reference)

Cell Assay:

[9]
  • Cell lines

    ID8 cells

  • Concentrations

    5 uM

  • Incubation Time

    24 h

  • Method

    Parental ID8 or erastin-resistant ID8 cells were treated with different concentrations of doxorubicin for 24 hours.
Animal Study:

[1]
  • Animal Models

    Female athymic nude mice injected s.c. with MB231 cells

  • Dosages

    3 mg/kg/day

  • Administration

    Delivered intratumorly

Customer Product Validation

Data from [Cancer Res, 2014, 74, 298-308]

Data from [Data independently produced by PLoS One, 2014, 9, e94309]

Data independently produced by , 2014, Dr Milica Pesic from Institute for Biological Research

Data from [PLoS One, 2013, 8(1), e54595]

Selleck's Doxorubicin (DOX) HCl has been cited by 1016 publications

A novel role for the ROS-ATM-Chk2 axis mediated metabolic and cell cycle reprogramming in the M1 macrophage polarization [ Redox Biol, 2024, 70:103059] PubMed: 38316066
An oncolytic vaccinia virus encoding hyaluronidase reshapes the extracellular matrix to enhance cancer chemotherapy and immunotherapy [ J Immunother Cancer, 2024, 12(3)e008431] PubMed: 38458640
Targeting high circDNA2v levels in colorectal cancer induces cellular senescence and elicits an anti-tumor secretome [ Cell Rep, 2024, 43(4):114111] PubMed: 38615319
Neutrophil extracellular traps mediate cardiomyocyte ferroptosis via the Hippo-Yap pathway to exacerbate doxorubicin-induced cardiotoxicity [ Cell Mol Life Sci, 2024, 81(1):122] PubMed: 38456997
HIF-1α Mediates Immunosuppression and Chemoresistance in Colorectal Cancer by Inhibiting CXCL9, -10 and -11 [ Biomed Pharmacother, 2024, 173:116427] PubMed: 38484558
Acquired NF2 mutation confers resistance to TRK inhibition in an ex vivo LMNA::NTRK1-rearranged soft-tissue sarcoma cell model [ J Pathol, 2024, 10.1002/path.6282] PubMed: 38613194
miR-218-5p and doxorubicin combination enhances anticancer activity in breast cancer cells through Parkin-dependent mitophagy inhibition [ Cell Death Discov, 2024, 10(1):149] PubMed: 38514650
Targeting TRIP13 in favorable histology Wilms tumor with nuclear export inhibitors synergizes with doxorubicin [ Commun Biol, 2024, 7(1):426] PubMed: 38589567
EFNB1 levels determine distinct drug response patterns guiding precision therapy for B-cell neoplasms [ iScience, 2024, 27(1):108667] PubMed: 38155773
Therapy-induced normal tissue damage promotes breast cancer metastasis [ iScience, 2024, 27(1):108503] PubMed: 38161426

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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