Doxorubicinone
Based on 2 publication(s) in Google Scholar
Doxorubicinone (Adriamycin aglycone) is the aglycone of the antibiotic Doxorubicin (HY-15142A), i.e., its sugar-free parent nucleus structure. Doxorubicinone does not induce DNA damage or bind to RelA, but still downregulates the expression of pro-inflammatory cytokines (such as TNF, IL-12, etc.) regulated by the NF-κB pathway. Doxorubicinone can be used in sepsis-related research.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 98.29%
- CAS. Nr.: 24385-10-2
- Formel: C21H18O9
- Molecular Weight:414.36
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Speicherung:
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Publications Citing Use of MedChemExpress (MCE) Doxorubicinone
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Biologische Aktivität
Beschreibung
In Vitro
Doxorubicinone (2 μM) weakly stabilizes CT DNA, increasing its melting temperature by 2.5 °C, which suggests minimal or no intercalation[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Chemical Information
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CAS. Nr. 24385-10-2
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Appearance Solid
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Molecular Weight 414.36
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Formel C21H18O9
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Color Purple to purplish red
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SMILES
OC1=C(C2=C(C(C3=O)=C1C(C4=CC=CC(OC)=C34)=O)O)C[C@](O)(C[C@@H]2O)C(CO)=O
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Synonyms
Adriamycin aglycone; Adriamycinone
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Publications (2)
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Journal Impact Factor
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Most Recent
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Cell Death Dis
HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer. [Abstract]2022 Apr 22;13(4):396. PMID: 35459269 -
Exp Ther Med
miR-199b-5p mediates adriamycin-induced podocyte apoptosis by inhibiting the expression of RGS10. [Abstract]2021 Dec;22(6):1469. PMID: 34737809
Protokoll
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Reinheit & Dokumentation
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Data Sheet (274 KB)
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SDS (644 KB)
- English - EN (644 KB)
- Français - FR (644 KB)
- Deutsch - DE (644 KB)
- Norwegian - NO (644 KB)
- Español - ES (644 KB)
- Swedish - SV (644 KB)
- Italian - IT (644 KB)
- Korean - KR (644 KB)
- Portuguese - PT (644 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Chora AF, et al. DNA damage independent inhibition of NF-κB transcription by anthracyclines. Elife. 2022;11:e77443. Published 2022 Dec 7. [Content Brief]
[2]. Tartakoff SS, et al. Investigations into the DNA-binding mode of doxorubicinone. Org Biomol Chem. 2019;17(7):1992-1998. [Content Brief]
[3]. Qian L, et al. Identification of Gut Bacterial Enzymes for Keto-Reductive Metabolism of Xenobiotics. ACS Chem Biol. 2022;17(7):1665-1671. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)