Doxorubicin (Adriamycin) Hydrochloride

N° de catalogueS1208 Lot :S120813

Imprimer

Données techniques

Formule

C27H29NO11.HCl
Poids moléculaire 579.98 Numéro CAS 25316-40-9
Solubilité (25°C)* In vitro DMSO 100 mg/mL (172.41 mM)
Water 100 mg/mL (172.41 mM)
Ethanol Insoluble
In vivo (Ajouter les solvants au produit individuellement et dans l'ordre.)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml signifie légèrement soluble ou insoluble.
* Veuillez noter que Selleck teste la solubilité de tous les composés en interne, et la solubilité réelle peut différer légèrement des valeurs publiées. Ceci est normal et est dû à de légères variations d'un lot à l'autre.
* Expédition à température ambiante (les tests de stabilité montrent que ce produit peut être expédié sans aucune mesure de refroidissement.)

Préparation des solutions mères

Activité biologique

Description Doxorubicin Hydrochloride est un agent antibiotique et un inhibiteur de la DNA Topoisomerase II avec une CI50 de 2,67 μM contre la DNA Topoisomerase II humaine. Ce composé réduit la phosphorylation basale de AMPK et est utilisé dans le traitement concomitant des patients infectés par le HIV, mais présente un risque élevé de réactivation du HBV. Ce produit peut précipiter lorsqu'il est dissous dans une solution de PBS. Il est recommandé de préparer la solution mère dans de l'eau pure et de la diluer avec de l'eau pure ou une solution saline pour obtenir la solution de travail. Il peut être utilisé pour induire des modèles animaux de maladie rénale.Les solutions sont instables et doivent être préparées fraîches.
Cibles
AMPK Topo II
(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.

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, indicating that Doxorubicin may also exert its effect by damaging proteins.

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.

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.

Protocole (de référence)

Test cellulaire :

[9]
  • Lignées cellulaires

    ID8 cells

  • Concentrations

    5 uM

  • Temps d'incubation

    24 h

  • Méthode

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

[1]
  • Modèles animaux

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

  • Posologies

    3 mg/kg/day

  • Administration

    Delivered intratumorly

Références

  • https://pubmed.ncbi.nlm.nih.gov/19401447/
  • https://pubmed.ncbi.nlm.nih.gov/20385199/
  • https://pubmed.ncbi.nlm.nih.gov/21834791/
  • https://pubmed.ncbi.nlm.nih.gov/21364585/
  • https://pubmed.ncbi.nlm.nih.gov/22589537/
  • https://pubmed.ncbi.nlm.nih.gov/22267730/
  • https://pubmed.ncbi.nlm.nih.gov/22374332/
  • https://pubmed.ncbi.nlm.nih.gov/22536838/
  • https://pubmed.ncbi.nlm.nih.gov/19377506/
  • https://pubmed.ncbi.nlm.nih.gov/17194596/
  • https://pubmed.ncbi.nlm.nih.gov/1318169/

Validation du produit par le client

<p>Cell viabilities with increasing concentrations of cisplatin (CP) and doxorubicin (DOXO) under normoxic and hypoxic condition for 48 hours were determined by MTT assay. IC50 values are presented as the means ?SDs (n=4) and * denotes p<0.05.</p>

Données de [ Cancer Res , 2014 , 74, 298-308 ]

Temporal uptake of free DOX or DOX-PCL63-b-PNVP90 micelles into K-562 (I) and DL (J) cells were studied by incubating in 24-well plates at a concentration of 50,000 cells per well. Representative images shown were obtained using a fluorescence microscope Eclipse 80i (Nikon, Japan) (Plan Fluor, 40X, NA 0.75 objective) equipped with blue and red filters for, Hoechst and Doxorubicin respectively (n = 3).

Données de [ PLoS One , 2014 , 9, e94309 ]

CON+ -positive control (with FBS as chemoattractant); CON- - negative control (without chemoattractant); DOX -doxorubicin; WZ -WZ811; PF- PF-573228; * -significant difference compared to positive control: p<0.05; ** -significant difference compared to positive control: p<0.01; # -significant difference between combination and inhibitor only: p<0.05. Cancer cell invasion was analyzed using Transwell membranes assembled in 24-well plates and covered with a layer of Matrigel. COR-L23 cells were treated for 24 h with 50 nM DOX, 10 uM WZ811, 5 uM PF-573228 and combinations of inhibitors with 50 nM DOX. Similarly, RH460 cells were treated for 24 h with 1 uM DOX, 10 uM WZ811, 2.5 uM PF-573228 and combinations of inhibitors with 1 uM DOX. Applied doses were the ones that exerted the most pronounced synergistic effect on cytotoxicity level. After the incubation period, cells that invaded through matrigel and membranes were fixed in 4% paraformaldehyde-PBS and stained with Hoechst 33342 nuclear stain. Cells were visualized and counted under a fluorescent microscope at 10x magnification.

, 2014 , Dr Milica Pesic from Institute for Biological Research

Données de [ PLoS One , 2013 , 8(1), e54595 ]

Selleck's Doxorubicin (Adriamycin) Hydrochloride A été cité par 1038 Publications

Tritrichomonas muris sensitizes the intestinal epithelium to doxorubicin-induced apoptosis [ American Journal of Physiology-Gastrointestinal and Liver Physiology, May 1, 2025, G594-G609] PubMed: 39149272
Indirect targeting of MYC and direct targeting in combination with chemotherapies are more effective than direct mono-targeting in triple negative breast cancer [ Translational Oncology, January 2025, 102204] PubMed: 39631207
Targeting ACSS2 activity suspends the formation of chemoresistance through suppressed histone H3 acetylation in human breast cancer [ Research Square, February 21, 2024, nan]
Hyperglutaminolysis drives senescence and aging through arginine-mTORC1 axis activation [ Signal Transduct Target Ther, 2026, 11(1):64] PubMed: 41708609
Polθ activity modulates sensitivity to standard therapies in DNMT3A-deficient leukemia [ Cell Rep Med, 2026, 7(3):102687] PubMed: 41850232
Regularized Single-Cell Imaging Enables Generalizable AI Models for Stain-Free Cell Viability Screening [ Small Methods, 2026, 10(4):e01369] PubMed: 41574984
NPM1 phosphorylation-mediated telomere maintenance via stabilization of POLD3 in ALT-positive osteosarcoma: unraveling mechanisms and therapeutic opportunities [ Theranostics, 2026, 16(8):4224-4244] PubMed: 41695477
Targeting senescence-like tumor-associated macrophages sensitizes chemotherapy in triple-negative breast cancer [ Cell Oncol (Dordr), 2026, 49(2)61] PubMed: 41870812
The OtR tumor recurrence and metastasis model reveals doxorubicin-induced tumor shrinkage doesnt guarantee prolonged survival [ Animal Models and Experimental Medicine, 2026, Online ahead of print] PubMed: 41492919
Protocol to quantify cell-surface vimentin on senescent human chondrocytes and other cell types via a cell-based ELISA [ STAR Protoc, 2026, 7(2):104451] PubMed: 41865378

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