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Doxorubicin (hydrochloride) (Standard)


CAS No. : 25316-40-9

(Synonyms: Hydroxydaunorubicin (hydrochloride) (Standard); ADR (Standard))

25316-40-9
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Cat. No. : HY-15142R
M.Wt: 579.98
Formula: C27H30ClNO11
Purity: >98 %
Solubility:
Introduction of 25316-40-9 :

Doxorubicin hydrochloride (Standard) is the analytical standard of Doxorubicin hydrochloride. This product is intended for research and analytical applications. Doxorubicin (Hydroxydaunorubicin) hydrochloride, a cytotoxic anthracycline antibiotic, is an anti-cancer chemotherapy agent. Doxorubicin hydrochloride is a potent human DNA topoisomerase I and topoisomerase II inhibitor with IC50s of 0.8 μM and 2.67 μM, respectively. Doxorubicin hydrochloride reduces basal phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Doxorubicin hydrochloride induces apoptosis and autophagy[1][2][3]. IC50 & Target:IC50: 0.8 μM (Topoisomerase I)[3], 2.67 μM (Topoisomerase II)[1] In Vitro:Doxorubicin (1-8 μM; 24 and 48 hours) hydrochloride 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) hydrochloride 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) hydrochloride induces apoptosis by upregulating Bax, caspase-8 and caspase-3 and downregulation of Bcl-2 protein expression[4].
Doxorubicin (5 μM; 10-30 min) hydrochloride 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].
Note:
Doxorubicin hydrochloride is suitable for neutral or weakly acidic solvents; PBS (PH 7.4) is not recommended for dissolution, which may affect the dissolution effect. In Vivo:Doxorubicin hydrochloride can be used to induce models of cardiotoxicity and heart failure.

1. Inducing cardiotoxicity[10][11]
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 Mmodeling 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.
Correlated Product(s): /
Opposite Product(s): /

2. Induction of heart failure[11][12]
Background
The long-term mechanisms inducing heart failure remain to be carefully elucidated.
Specific Mmodeling 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.
Note
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.
Correlated Product(s): /
Opposite Product(s): Captopril (HY-B0368)

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