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Doxorubicin


CAS No. : 23214-92-8

(Synonyms: Hydroxydaunorubicin)

23214-92-8
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Cat. No. : HY-15142A
M.Wt: 543.52
Formula: C27H29NO11
Purity: >98 %
Solubility: 10 mM in DMSO
Introduction of 23214-92-8 :

Doxorubicin (Hydroxydaunorubicin), a cytotoxic anthracycline antibiotic, is an anti-cancer chemotherapy agent. Doxorubicin is a potent human DNA topoisomerase I and topoisomerase II inhibitor with IC50s of 0.8 μM and 2.67 μM, respectively. Doxorubicin reduces basal phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Doxorubicin induces apoptosis and autophagy[1][2][3]. IC50 & Target:Topoisomerase II[1] In Vitro:Doxorubicin (1-8 μM; 24 and 48 hours) decreases the viability of MCF-10F, MCF-7 and MDA-MB-231 cells in a time- and dose-dependent manner[4].
Doxorubicin (1 μM; 3 and 24 hours) results in Hct-116 human colon carcinoma cells reduction in G0/G1 phase and accumulation in G2 phase[5].
Doxorubicin (1 μM for MCF-10F and MDA-MB-231 cells, 4 μM for MCF-7 cells; 48 hours) induces apoptosis by upregulating Bax, caspase-8 and caspase-3 and downregulation of Bcl-2 protein expression[4].
Doxorubicin (5 μM; 10-30 min) can be accumulated in B16-F10 melanoma cell line CRL-6475 in a time-dependent manner, and can be detected by green or red fluorescence (green fluorescence has higher detection sensitivity) with a maximum excitation wavelength (λex) and a maximum emission wavelength (λem) of 470 nm and 560 nm, respectively[8].
In Vivo:Doxorubicin (2 mg/kg; i.v.; once a week; 6 weeks) inhibits MDA-G8 breast tumor growth in mice[6].
Doxorubicin (4%-20%; Intrastriatal injection; Single dose) is neurotoxic in Sprague-Dawley rats[7].

Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Doxorubicin hydrochloride can be used to induce models of cardiotoxicity and heart failure.

1. Inducing cardiotoxicity[10]
Background
The mechanism of short-term induction of cardiotoxicity: promoting extracellular remodeling of myocardium to induce heart failure, and also works at the molecular level. Including: interacting with iron, changing the activity of oxidases in cells or mitochondria, and binding to topoisomerases.
Specific Modeling Methods
Mice: Female C57BL/6j mice • 20-22 g • 6 weeks old
Administration: 2 mg/kg, 10 mg/kg • ip • once every the other day for 2 or 3 times
Note
Mice were sacrificed 3 days after the first injection.
Modeling Indicators
molecular level: (1) Pro-inflammatory cytokines (such as TNF-α and IL-6) increase significantly, while anti-inflammatory cytokine IL-10 decreases; (2) Inducible - Nitric oxide synthase (iNOS) was overexpressed and serum nitrite levels were elevated; nitrotyrosine expression was significantly increased.
2. Induction of heart failure[11]
Background
The long-term mechanisms inducing heart failure remain to be carefully elucidated.
Specific Modeling Methods
Rat: Male Wistar rats • 180-200 g
Administration: 2.5 mg/kg • ip • once every week, for 6 weeks • treated at 4 weeks later.
Modeling Indicators
Cellular/tissue level: Myocardial sarcomeres are destroyed, mitochondria are swollen and damaged, Myocardial cells showed inflammation and apoptosis (transmission electron microscopy results); myocardial fibrosis, and left ventricular collagen I and II levels were downregulated (immunohistochemistry results).
Changes in macroscopic indicators: Hemodynamic parameters and echocardiography show cardiac insufficiency and impaired left ventricular function; such as increases in LVIDd, LVIDs and LVEDP.
Opposite Product(s): Captopril (HY-B0368)

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